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Psychology Biological Psychology
by
James Kalat

Introduction

Biological psychology approaches behavior and experience with the assumption that they are products of the nervous system, as it has been molded through evolution. This field encompasses studies of genetics, evolution, hormones, the nervous system, and the physiology of other organs, as they relate to perception, movement, learning and memory, motivation and emotion, consciousness, and abnormal behavior. The term biological psychology” is approximately synonymous with biopsychology, psychobiology, behavioral neuroscience, and physiological psychology. Research methods include examining behavioral changes after brain damage, brain stimulation, and drug injections. Methods also include recordings from the brain during behavior, genetic analyses of behavior, and comparisons of behavior in different species. Traditionally, and still to a fair extent, researchers have relied on studies of laboratory animals. However, because of advances in brain imaging, today’s researchers also conduct much research on humans.

Textbooks

Several textbooks are available, with varying levels and emphases. Any of these could be consulted for more detailed information. Expect each of them to be revised periodically. Biological psychology heavily overlaps neuroscience, but as a rule, textbooks with the word neuroscience in the title—such as Bear, et al. 2007, Carlson 2011, and Purves 2008—tend to put more emphasis on the physiology and biochemistry of the nervous system. Those with the title biological psychology—such as Breedlove, et al. 2010, Kalat 2009, and Pinel 2009—tend to put more emphasis on application to behavior.

Data Sources

Of the huge number of websites relevant to biological psychology, the following are especially recommended. The Dana Foundation provides insightful reviews addressed to a general audience. The Society for Neuroscience also provides up-to-date information, some of it at a more technical level. The Whole Brain Atlas and Brain Museum provide excellent anatomical information. Researchers should not overlook Neuroscience for Kids. That site explains complex background information in simple terms.

Results of Brain Damage

According to the philosophical position of dualism, dating back at least to René Descartes, minds and brains are fundamentally different kinds of existence. Nearly all neuroscientists and philosophers today reject that idea in favor of monism—the idea that your brain activity is your experience. Brain activity does not cause mental experience any more than mental experience causes brain activity. They are simply the same, even though they seem so different. One of the main lines of evidence to support this conclusion is the wide variety of specific losses that occur after brain damage. To lose part of your brain is to lose part of your experience or mental ability. Here are some interesting examples.

Face Recognition

After certain types of brain damage, people maintain apparently normal vision in other regards, but have great difficulty recognizing faces. The technical term for inability to recognize faces is prosopagnosia. Many types of brain damage impair facial recognition in one way or another, but the strongest and most specific deficits arise after damage to the fusiform gyrus, an area within the temporal lobe of the cerebral cortex that responds strongly and selectively to the sight of particular faces, as documented by Kriegeskorte, et al. 2007. Thomas, et al. 2009 reports on people born with fewer than normal connections to the fusiform gyrus, who also show poor ability to recognize faces. People with prosopagnosia still recognize people by tone of voice, so overall memory is not the problem. They fail to recognize faces not only by vision, but also by touch, as reported by Kilgour, et al. 2004. The exact role of the fusiform gyrus has been controversial. Is it devoted to faces, or to any and all kinds of visual expertise? Tarr and Gauthier 2000 reports that acquired expertise of any sort requires activity of the fusiform gyrus. The other side of this controversy, as persuasively summarized by Kanwisher and Yovel 2006, holds that the human fusiform gyrus is evolutionarily specialized for facial recognition.

  • Kanwisher, N., and G. Yovel. 2006. The fusiform face area: A cortical region specialized for the perception of faces. Philosophical Transactions of the Royal Society B 361:2109–2128.

    DOI: 10.1098/rstb.2006.1934Save Citation »Export Citation »E-mail Citation »

    Even after someone has developed other kinds of visual expertise, many cells in the fusiform gyrus respond more vigorously and more selectively to faces than to anything else. This article summarizes evidence for regarding the fusiform gyrus as responding specifically to facial recognition.

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  • Kilgour, A. R., B. de Gelder, and S. J. Lederman. 2004. Haptic face recognition and prosopagnosia. Neuropsychologia 42:707–712.

    DOI: 10.1016/j.neuropsychologia.2003.11.021Save Citation »Export Citation »E-mail Citation »

    People with prosopagnosia also have trouble finding similarities and differences between clay models of faces. Therefore the problem pertains to face recognition, and not to vision itself.

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  • Kriegeskorte, N., E. Formisano, B. Sorger, and R. Goebel. 2007. Individual faces elicit distinct response patterns in human anterior temporal cortex. Proceedings of the National Academy of Sciences of the United States of America 104:20600–20605.

    DOI: 10.1073/pnas.0705654104Save Citation »Export Citation »E-mail Citation »

    Recordings from cells in the fusiform gyrus of the inferior temporal cortex in the right hemisphere show consistent responses to particular faces.

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  • Tarr, M. J., and I. Gauthier. 2000. FFA: A flexible fusiform area for subordinate-level visual processing automatized by experience. Nature Neuroscience 3:764–769.

    DOI: 10.1038/77666Save Citation »Export Citation »E-mail Citation »

    This article argues that acquired visual expertise of any sort requires activity of the fusiform gyrus. After people become experts at recognizing birds, judging dogs for a dog show, or any other item, seeing that type of item activates the fusiform gyrus.

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  • Thomas, C., G. Avidan, K. Humphreys, K. Jung, F. Gao, and M. Behrmann. 2009. Reduced structural connectivity in ventral visual cortex in congenital prosopagnosia. Nature Neuroscience 12:29–31.

    DOI: 10.1038/nn.2224Save Citation »Export Citation »E-mail Citation »

    Prosopagnosia occurs in some people from birth because they were born with a deficiency of connections to and from the fusiform gyrus. The natural variation among people in their ability to recognize faces may have an underlying anatomical basis.

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Motion Perception

One of the most surprising results of brain damage is motion blindness. It is easy to imagine what it would be like to become color blind, but it is hard to imagine seeing an object without seeing that it is moving. Examples of this phenomenon had been reported in the neurology literature for decades, but nearly all theorists ignored these reports until the same deficit was documented in monkeys under controlled laboratory conditions. Many areas in the primate visual cortex analyze specific aspects of visual information. Cells in the middle temporal cortex (area MT) respond selectively when an object moves in a particular direction and speed, as documented by Perrone and Thiele 2001. Those cells ordinarily do not respond to a stationary object, although Kourtzi and Kanwisher 2000 found that they respond to a photograph of a running person. Both monkeys and people with damage to area MT fail on tasks where they need to respond to the speed or direction of movement, as in the article by Marcar, et al. 1997. People with motion blindness are impaired on a wide variety of everyday tasks, as reported by Zihl, et al. 1983, and by Duffy, et al. 2000. Although it is difficult to imagine the permanent experience of motion blindness, all people become motion blind for a fraction of a second before and during a voluntary eye movement. Vallines and Greenlee 2006 explains how the brain briefly shuts down the middle temporal cortex during an eye movement.

  • Duffy, C. J., S. J. Tetewsky, and H. O’Brien. 2000. Cortical motion blindness in visuospatial AD. Neurobiology of Aging 21:867–869.

    DOI: 10.1016/S0197-4580(00)00187-1Save Citation »Export Citation »E-mail Citation »

    Many people with Alzheimer’s disease have a mild case of motion blindness, manifested as difficulty finding their way around.

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  • Kourtzi, Z., and N. Kanwisher. 2000. Activation in human MT/MST by static images with implied motion. Journal of Cognitive Neuroscience 12:48–55.

    DOI: 10.1162/08989290051137594Save Citation »Export Citation »E-mail Citation »

    Cells in the middle temporal cortex also respond to a still photograph if the picture implies motion—for example, a photo of someone running.

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  • Marcar, V. L., J. Zihl, and A. Cowey. 1997. Comparing the visual deficits of a motion blind patient with the visual deficits of monkeys with area MT removed. Neuropsychologia 35:1459–1465.

    DOI: 10.1016/S0028-3932(97)00057-2Save Citation »Export Citation »E-mail Citation »

    Monkeys with damage in the middle temporal cortex fail on tasks where they have to respond one way to an object moving one direction and a different way to an object moving a different direction. People with damage in this area have similar difficulties in reporting the speed or direction of visual movement. This is a rare condition.

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  • Perrone, J. A., and A. Thiele. 2001. Speed skills: Measuring the visual speed analyzing properties of primate MT neurons. Nature Neuroscience 4:526–532.

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    In the middle temporal cortex (area MT) of monkeys, cells respond selectively when an object moves in a particular direction at a particular speed. These neurons do not respond to the sight of a stationary object.

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  • Vallines, I., and M. W. Greenlee. 2006. Saccadic suppression of retinotopically localized blood oxygen level-dependent responses in human primary visual area V1. Journal of Neuroscience 26:5965–5969.

    DOI: 10.1523/JNEUROSCI.0817-06.2006Save Citation »Export Citation »E-mail Citation »

    Normal people experience motion blindness briefly during voluntary eye movements (saccades). Beginning 75ms before a saccade, the brain inhibits activity in the middle temporal cortex, presumably to avoid apparent motion during the eye movement. To demonstrate, fixate on one eye in a mirror, and then look at the other eye. The eyes moved, but you do not perceive the movement.

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  • Zihl, J., D. von Cramon, and N. Mai. 1983. Selective disturbance of movement vision after bilateral brain damage. Brain 106:313–340.

    DOI: 10.1093/brain/106.2.313Save Citation »Export Citation »E-mail Citation »

    A fascinating case report of a woman with motion blindness. She has trouble crossing a road, because she cannot tell how fast the cars are approaching, if at all. She has trouble pouring coffee, because she does not see how fast the cup is filling.

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Spatial Memory

A later section discusses several other aspects of memory. Here let’s consider spatial memory, as measured by the oculomotor delayed response task in monkeys. In this task, a monkey fixates its eyes on a central point. At some point in time, a target is briefly illuminated at an unpredictable location in a circle surrounding the central point. To receive reward (such as a few drops of water to drink), the monkey has to continue fixating on the central point until several seconds after the end of the illuminated target, and then look at the place where it remembers the target had been. Chafee and Goldman-Rakic 1998 demonstrated that particular cells in the prefrontal cortex are active during the delay, and different cells become active depending on the location of the target. Sawaguchi and Iba 2001 temporarily inactivated cells in various sites in the prefrontal cortex and found specific memory deficits. Depending on the location of inactivation, a monkey might fail the memory task only if the target had been in the upper right corner of the screen, the lower central area, and so forth. On a task where the monkey could respond immediately to the target without a delay, the inactivation had no effect. Evidently inactivating a spot in the prefrontal cortex did not impair vision or eye movement, but it prevented memory of a stimulus in a particular location. This finding has potentially broad implications. Psychologists often think of intelligence as a general process. This study suggests that intelligence encompasses a huge number of specific intelligent processes, and it is possible to lose a specific type of functioning without impairing anything else.

  • Chafee, M. V., and P. S. Goldman-Rakic. 1998. Matching patterns of activity in primate prefrontal area 8a and parietal area 7ip neurons during a spatial working memory task. Journal of Neurophysiology 79:2919–2940.

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    Recordings in both the prefrontal cortex and the parietal cortex of monkeys find cells that are active while monkeys remember a particular location and move their eyes to that location after a short delay.

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  • Sawaguchi, T., and M. Iba. 2001. Prefrontal cortical representation of visuospatial working memory in monkeys examined by local inactivation with muscimol. Journal of Neurophysiology 86:2041–2053.

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    Temporary inactivation of neurons in a small area of the prefrontal cortex of a monkey leads to temporary impairment of memory for stimuli in a particular location.

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Spatial Neglect

After a stroke in the right hemisphere, many people at least in the first weeks show spatial neglect, a tendency to ignore the left side of the body and the left side of the world, especially in the presence of stimuli on the right side. (Damage to the left hemisphere seldom produces equal neglect of the right side.) For example, if asked to point straight ahead, the person points to the right of center. If asked to find the center of a line, the person bisects it to the right of center, as described by Richard, et al. 2004. The exact nature of the neglect varies, depending on the location of damage within the right hemisphere. Some people ignore everything to the left side of the body, whereas others ignore the left half of any object, regardless of its location. Hillis, et al. 2005 describes some of these differences. As documented in a review by Buxbaum 2006, neglect is usually due more to a loss of attention than a sensory loss. Someone looking at two objects may describe only the one on the right, but may be able to answer whether the two objects are the same or different. Ability to describe an object on the left is decreased by the presence of an object to its right, but is increased by the presence of an object still farther to the left. Hearing something on the left side increases the person’s ability to see something on the left side, as documented by Frassinetti, et al. 2002. Marshall and Halligan 1995 showed people display such as a series of As arranged in a circle. People with neglect saw it as a circle, but when asked to cross off all the As, they crossed off only the ones on the right. They had to see all the As to see the circle as a whole, but when focusing on the details, they attended only to those on the right. In short, after right-hemisphere damage, the left hemisphere directs attention strongly to the right side, although it is capable of detecting something to the left.

  • Buxbaum, L. J. 2006. On the right (and left) track: Twenty years of progress in studying hemispatial neglect. Cognitive Neuropsychology 23:184–201.

    DOI: 10.1080/02643290500202698Save Citation »Export Citation »E-mail Citation »

    This is a thorough review of spatial neglect, covering the types of neurological damage that lead to it, and the variations in behavioral outcomes.

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  • Frassinetti, F., F. Pavani, and E. Làdavas. 2002. Acoustical vision of neglected stimuli: Interaction among spatially converging audiovisual inputs in neglect patients. Journal of Cognitive Neuroscience 14:62–69.

    DOI: 10.1162/089892902317205320Save Citation »Export Citation »E-mail Citation »

    People showing left-side neglect are capable of responding to objects on the left side with sufficient effort, or if some stimulus directs attention toward the left. One way to do so is by sounds coming from the left.

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  • Hillis, A. E., M. Newhart, J. Heidler, P. B. Barker, E. H. Herskovits, and M. Degaonkar. 2005. Anatomy of spatial attention: Insights from perfusion imaging and hemispatial neglect in acute stroke. Journal of Neuroscience 25:3161–3167.

    DOI: 10.1523/JNEUROSCI.4468-04.2005Save Citation »Export Citation »E-mail Citation »

    In most cases, people with damage to the right parietal cortex neglect everything on the left side of the body. People with damage to the right superior temporal cortex neglect the left side of any object, regardless of its location.

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  • Marshall, J. C., and P. W. Halligan. 1995. Seeing the forest but only half the trees? Nature 373:521–523.

    DOI: 10.1038/373521a0Save Citation »Export Citation »E-mail Citation »

    People with left neglect viewed objects made of smaller objects, such as a circle made of many copies of the letter A. Although they could identify the object as a whole, when they tried to cross out all the A’s, they found only those on the right side of the object.

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  • Richard, C., J. Honoré, T. Bernati, and M. Rousseaux. 2004. Straight-ahead pointing correlates with long-line bisection in neglect patients. Cortex 40:75–83.

    DOI: 10.1016/S0010-9452(08)70921-3Save Citation »Export Citation »E-mail Citation »

    When people with neglect try to point straight ahead, they point to the right of center, as if the left field were irrelevant. When asked to bisect a line, they draw a mark to the right of center. (A later study found that this tendency disappears or reverses with very short lines.)

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The Binding Problem/Long-Range Integration

As evidence accumulated that different brain areas perform different functions, neuroscientists beginning in the 1980s began to recognize a theoretical problem that they had previously ignored. Different brain areas control different senses, and even within a given sense, such as vision, different areas mediate different aspects of the sensation—for example, perception of shape, color, movement, and location. Nevertheless, you perceive a unified object. Given that different brain areas control different sensations, and given that they do not all funnel their information into a central processor, how do you put the object together? One hypothesis is that it depends on precisely simultaneous activity in different brain areas. Several research groups have confirmed that when a viewer recognizes a blurry or otherwise ambiguous figure, gamma waves at 30–80Hz emerge in high synchrony in several brain areas. Among those advancing this hypothesis are Gray, et al. 1989; Rodriguez, et al. 1999; and Roelfsema, et al. 1997. In addition to synchrony, another essential element for binding is localization of a stimulus. When you, for example, perceive the dog you touch as being also the dog you see and hear, you localize the direction and distance of each of those stimuli. People with damage to the parietal cortex have trouble localizing objects, and as a result they often fail to bind objects. Treisman 1999 and others have reported that people with parietal damage sometimes might see a red square and a blue triangle but be uncertain which shape was which color. They see the shapes and colors, but because they are uncertain of the location of each, they do not bind them. People with intact brains also sometimes fail to bind shape with color if they see objects briefly under conditions of distracted attention, as Holcombe and Cavanagh 2001 reported. Robertson 2003 provides an excellent review of the research on binding.

  • Gray, C. M., P. König, A. K. Engel, and W. Singer. 1989. Oscillatory responses in cat visual cortex exhibit inter-columnar synchronization which reflects global stimulus properties. Nature 338:334–337.

    DOI: 10.1038/338334a0Save Citation »Export Citation »E-mail Citation »

    This article was one of the first to demonstrate synchronized activity in separate brain areas during perception of a complex stimulus, arguing for the importance of synchrony in binding.

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  • Holcombe, A. O., and P. Cavanagh. 2001. Early binding of feature pairs for visual perception. Nature Neuroscience 4:127–128.

    DOI: 10.1038/83945Save Citation »Export Citation »E-mail Citation »

    Binding various aspects of a stimulus into a single object takes a certain amount of time and effort. When a viewer is distracted and a complex stimulus appears only briefly, the viewer may be unable to bind the various aspects successfully.

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  • Robertson, L. C. 2003. Binding, spatial attention and perceptual awareness. Nature Reviews Neuroscience 4:93–102.

    DOI: 10.1038/nrn1030Save Citation »Export Citation »E-mail Citation »

    An excellent review of research on binding and possible explanations for it.

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  • Rodriguez, E., N. George, J. -P. Lachaux, J. Martinerie, B. Renault, and F. J. Varela. 1999. Perception’s shadow: Long-distance synchronization of human brain activity. Nature 397:430–433.

    DOI: 10.1038/17120Save Citation »Export Citation »E-mail Citation »

    Demonstrated that synchronized activity in separate brain areas emerges when a viewer makes sense of a complex ambiguous stimulus.

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  • Roelfsema, P. R., A. K. Engel, P. König, and W. Singer. 1997. Visuomotor integration is associated with zero time-lag synchronization among cortical areas. Nature 385:157–161.

    DOI: 10.1038/385157a0Save Citation »Export Citation »E-mail Citation »

    This article provides another demonstration of accurate synchrony of activity in separate brain areas during perception.

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  • Treisman, A. 1999. Feature binding, attention and object perception. In Attention, space, and action: Studies in cognitive neuroscience. Drawn from papers reported to two linked meetings, a discussion meeting of the Royal Society and a meeting at the Novartis Foundation held in November 1997. Edited by G. W. Humphreys, J. Duncan, and A. Treisman, 91–111. Oxford: Oxford Univ. Press.

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    This chapter describes research on the conditions when binding does and does not take place.

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Brain Areas in Emotion

Neuroscientists have long known that the sympathetic nervous system responds to emotional arousal. They have also long known that the limbic system (forebrain areas surrounding the thalamus) is particularly important for emotional processing. Since the 1990s, research has focused heavily on the amygdala (a limbic system structure in each temporal lobe) and parts of the prefrontal cortex. Research on the amygdala has relied on converging evidence from both humans and laboratory animals.

Amygdala and the Startle Reflex

A sudden loud noise evokes a startle reflex, marked by tensing of the muscles. This reflex, universal among mammals that hear, depends on a circuit from the ears to the cochlear nucleus of the medulla, then to the pons, and finally to the muscles. Although the reflex itself is unlearned, it varies in intensity depending on genetics and previous experiences. In rats, the intensity of this reflex increases in a setting previously associated with shock, and decreases in a setting associated with safety or pleasure, as demonstrated by Schmid, et al. 1995. This type of learning depends on the amygdala. Hitchcock and Davis 1991 found that animals with damage to the amygdala fail to show modifications of the startle reflex under the influence of various signals. These data imply that the amygdala is responsible for variations in anxiety. Support for this view in humans comes from several observations on post-traumatic stress disorder (PTSD). Grillon, et al. 1998 found that people with PTSD show an enhanced startle response. Also, Admon and colleagues tested Israeli soldiers at induction, using functional magnetic resonance imaging (fMRI) to measure the responsiveness of their amygdala to unpleasant photographs (see Amdon, et al. 2009). These measurements predicted the amount of stress they reported during combat experiences, with a correlation of .67. Finally, as reported by Koenigs, et al. 2008, Vietnam vets who suffered brain damage were highly likely to develop PTSD, unless the damage included the amygdala, in which case none of them developed PTSD. Evidently a person without an amygdala cannot develop strong anxiety. Finally, a study by Oxley, et al. 2008 linked startle responses (as measures of amygdala response) to political leanings. They asked people about their level of support for military action, police action, and so forth. People with high levels of support tended to show stronger than average startle responses, and they did not show as much habituation (weakening) of these responses as other people did after many repetitions of the startling sound.

  • Admon, R., G. Lubin, O. Stern, K. Rosenberg, L. Sela, H. Ben-Ami, et al. 2009. Human vulnerability to stress depends on amygdala’s predisposition and hippocampal plasticity. Proceedings of the National Academy of Sciences of the United States of America 106:14120–14125.

    DOI: 10.1073/pnas.0903183106Save Citation »Export Citation »E-mail Citation »

    Of those being inducted into the military, some show greater amygdala responses than others do to unpleasant photos. The level of amygdala response correlates strongly with stress symptoms after potentially traumatic experiences.

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  • Grillon, C., C. A. Morgan III, M. Davis, and S. M. Southwick. 1998. Effect of darkness on acoustic startle in Vietnam veterans with PTSD. American Journal of Psychiatry 155:812–817.

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    People with post-traumatic stress disorder show an enhanced startle response to loud noises. This observation is consistent with the use of the startle response as a measure of anxiety.

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  • Hitchcock, J. M., and M. Davis. 1991. Efferent pathway of the amygdala involved in conditioned fear as measured with the fear-potentiated startle paradigm. Behavioral Neuroscience 105:826–842.

    DOI: 10.1037/0735-7044.105.6.826Save Citation »Export Citation »E-mail Citation »

    Rats with damage to outputs from the amygdala show a normal startle reflex. However, a light that predicts shock does not enhance their startle reflex. That is, they do not show learned anxiety.

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  • Koenigs, M., E. D. Huey, V. Raymont, B. Cheon, J. Solomon, E. M. Wassermann. 2008. Focal brain damage protects against post-traumatic stress disorder in combat veterans. Nature Neuroscience 11:232–237.

    DOI: 10.1038/nn2032Save Citation »Export Citation »E-mail Citation »

    Of soldiers who suffered brain damage not including the amygdala, 40 percent developed PTSD. Of those whose brain damage included the amygdala, none developed PTSD. Evidently the amygdala is necessary for strong anxiety.

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  • Oxley, D. R., K. B. Smith, J. R. Alford, M. V. Hibbing, J. L. Miller, M. Scalora. 2008. Political attitudes vary with physiological traits. Science 321:1667–1670.

    DOI: 10.1126/science.1157627Save Citation »Export Citation »E-mail Citation »

    These researchers measured political beliefs consistent with fear of a dangerous world, such as support for reliance on military force, use of the death penalty, and prohibitions against immigration. People with strong support of such views tended to show an enhanced startle reflex that was slow to habituate even after many repetitions.

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  • Schmid, A., M. Koch, and H. -U. Schnitzler. 1995. Conditioned pleasure attenuates the startle response in rats. Neurobiology of Learning and Memory 64:1–3.

    DOI: 10.1006/nlme.1995.1037Save Citation »Export Citation »E-mail Citation »

    Previous studies showed that a signal predicting shock increases the intensity of the startle reflex in rats. This article showed that a signal of safety or pleasure decreases the intensity.

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Damage to the Amygdale

Many people suffer a stroke that damages the amygdala in one hemisphere or the other. Those people, of course, suffer varying amounts of damage to other brain structures also. From a theoretical standpoint, the most interesting cases are the rare individuals with Urbach-Wiethe disease, a little-understood condition in which calcium accumulates specifically in the amygdala, essentially destroying it in both hemispheres. Do such people lose all fear and anxiety? It depends on how we define these terms. Most psychologists define emotion as a complex of cognition, feelings, physiological changes, and behavior. The assumption is that all these aspects necessarily go together. In people with amygdala damage, perhaps they do not. Anderson and Phelps 2002 reported that people with amygdala damage report experiencing fear and other emotions in normal ways during everyday life. However, it may be that they were reporting the cognitive aspect of fear without the full feeling. In the study Berntson, et al. 2007, people with amygdala damage reported much lower than normal arousal to many types of unpleasant photographs. Also, after hearing a list of words, people with amygdala damage are no more likely to remember emotionally charged words such as “kill” than any other word. After hearing a story, they do not show the enhanced memory other people show for the emotionally arousing or disturbing episodes in the story. Adolphs, et al. 2005 reported these studies. According to a beautifully simple demonstration reported in Kennedy, et al. 2009, one patient with Urbach-Wiethe disease stands much closer to other people than is typical. Even if a stranger approaches her nose-to-nose with direct eye contact, she feels no discomfort. This woman has a long history of walking into dangerous situations without the usual anxiety.

  • Adolphs, R., D. Tranel, and T. W. Buchanan. 2005. Amygdala damage impairs emotional memory for gist but not details of complex stimuli. Nature Neuroscience 8:512–518.

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    People with damage to the amygdala show approximately normal overall memory, but unlike other people, they fail to show enhanced memory for the emotionally arousing or disturbing items.

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  • Anderson, A. K., and E. A. Phelps. 2002. Is the human amygdala critical for the subjective experience of emotion? Evidence of intact dispositional affect in patients with amygdala lesions. Journal of Cognitive Neuroscience 14:709–720.

    DOI: 10.1162/08989290260138618Save Citation »Export Citation »E-mail Citation »

    People with damage to the amygdala report experiencing fear and other emotions during everyday life. However, reporting fear may not be the same as fully feeling it.

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  • Berntson, G. G., A. Bechara, H. Damasio, D. Tranel, and J. T. Cacioppo. 2007. Amygdala contribution to selective dimensions of emotion. Social Cognitive & Affective Neuroscience 2:123–129.

    DOI: 10.1093/scan/nsm008Save Citation »Export Citation »E-mail Citation »

    People with brain damage that included the amygdala gave ratings of emotional arousal to a variety of photographs. Compared to people with damage to other brain areas, those with amygdala damage gave normal reports of arousal to pleasant or neutral photographs, but much lower reports of arousal to unpleasant photographs.

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  • Kennedy, D. P., J. Gläscher, J. M. Tyszka, and R. Adolphs. 2009. Personal space regulation by the human amygdala. Nature Neuroscience 12:1226–1227.

    DOI: 10.1038/nn.2381Save Citation »Export Citation »E-mail Citation »

    A forty-two-year-old woman with Urbach-Wiethe disease typically stands 0.34m from another person, about half the usual distance, and she reports feeling comfortable with any distance including nose-to-nose with a stranger.

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Prefrontal Cortex and Emotion

The famous patient Phineas Gage first called attention to the possible role of the prefrontal cortex. In 1848 he amazingly survived an explosion that sent an iron rod through his prefrontal cortex. During the subsequent months his behavior became impulsive. Unfortunately, his progress was poorly documented. As Kotowicz 2007 argued, most of the later retellings of his story were exaggerated and imaginative. Nevertheless, the prefrontal cortex is important for regulating emotional responses. Greene, et al. 2001 found increased activity in the prefrontal cortex when people contemplated moral dilemmas, such as under what circumstances it might be right to kill one person in order to save several others. As people grow older, connections tend to strengthen between the prefrontal cortex and the amygdala. Theorists believe these connections help to regulate and suppress emotional responses. St. Jacques, et al. 2009 attributes to these connections the greater ability of older adults to keep their emotional responses in check. At the opposite extreme, people with frontotemporal lobar degeneration, a degenerative disease, have a gradual weakening of activity in both frontal and temporal cortices. Although certain aspects of their emotional experience appear to remain normal, such as happiness and fear, they are impaired at emotional responses that require more extensive cognitive processing. In particular, they become nearly indifferent to the reactions of other people. The results include a weakening of moral restraints and an almost complete loss of embarrassment. Two good reviews of this condition are reported by Levenson and Miller 2007 and by Sturm, et al. 2008.

  • Greene, J. D., R. B. Sommerville, L. E. Nystrom, J. M. Darley, and J. D. Cohen. 2001. An fMRI investigation of emotional engagement in moral judgment. Science 293:2105–2108.

    DOI: 10.1126/science.1062872Save Citation »Export Citation »E-mail Citation »

    While people pondered difficult moral dilemmas, brain scans revealed increased activity in parts of the prefrontal cortex and the cingulate gyrus of the cortex.

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  • Kotowicz, Z. 2007. The strange case of Phineas Gage. History of the Human Sciences 20:115–131.

    DOI: 10.1177/0952695106075178Save Citation »Export Citation »E-mail Citation »

    This article describes a search for historical documents concerning Phineas Gage. The medical reports at the time were sketchy. Newspaper and other accounts provide no support for claims that Gage became a dissolute drunkard, that he traveled with Barnum’s freak show, or many other later retellings of his life.

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  • Levenson, R. W., and B. L. Miller. 2007. Loss of cells—loss of self. Current Directions in Psychological Science 16:289–294.

    DOI: 10.1111/j.1467-8721.2007.00523.xSave Citation »Export Citation »E-mail Citation »

    People with frontotemporal lobar degeneration become impulsive, indifferent to other people’s suffering, and unembarrassed by their own errors. They make poor decisions in many aspects of life.

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  • St. Jacques, P. L., F. Dolcos, and R. Cabeza. 2009. Effects of aging on functional connectivity of the amygdala for subsequent memory of negative pictures. Psychological Science 20:74–84.

    DOI: 10.1111/j.1467-9280.2008.02258.xSave Citation »Export Citation »E-mail Citation »

    On the average, older adults show stronger functional connections between the dorsolateral prefrontal cortex and the amygdala. These connections may be important in regulating and inhibiting unwanted emotional responses.

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  • Sturm, V. E., E. A. Ascher, B. L. Miller, and R. W. Levenson. 2008. Diminished self-conscious emotional responding in frontotemporal lobar degeneration patients. Emotion 8:861–869.

    DOI: 10.1037/a0013765Save Citation »Export Citation »E-mail Citation »

    People with frontotemporal lobar degeneration become poor at recognizing other people’s emotional expressions. They are unembarrassed by their own social blunders and they give low ratings to the severity of moral transgressions.

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Experiential Influences on Brain Development

Although a great deal of brain development occurs before birth, much continues long afterward. Myelin continues forming for decades, and synaptic changes continue throughout life. Prolonged experiences induce structural changes, some of them far more extensive than we might have imagined.

Reorganization in Response to Congenital Blindness

People often say that blind or deaf people develop greater acuity of their other senses. The receptors themselves do not change, but the cerebral cortex does reorganize to make greater use of the remaining senses. In sighted people, the occipital cortex responds vigorously to visual input and weakly or not at all to other modalities. In people blind since birth or early childhood, the occipital cortex responds strongly to other inputs. Sadato, et al. 1996 demonstrated strong responses to Braille. Gougoux, et al. 2009 showed strong responses to auditory stimuli. Amedi, et al. 2003 found strong responses while blind people were performing verbal memory tasks. These responses to nonvisual stimuli are functional. Suppressing activity in the occipital cortex by use of a strong magnet interferes with Braille perception, auditory perception, and verbal memory in blind people. The same suppression has little or no effect when sighted people perform these same tasks. Cohen, et al. 1997 documented this finding. Although the biggest changes occur in people who were blind from birth or infancy, even in sighted adults, a few days of visual deprivation increases the response of the occipital cortex to touch stimuli, as reported by Merabet, et al. 2008. Evidently connections of touch and other stimuli to the occipital cortex are present in everyone, but usually inhibited by the much stronger connections from vision.

  • Amedi, A., N. Raz, P. Pianka, R. Malach, and E. Zohary. 2003. Early “visual” cortex activation correlates with superior verbal memory performance in the blind. Nature Neuroscience 6:758–766.

    DOI: 10.1038/nn1072Save Citation »Export Citation »E-mail Citation »

    While blind people are performing verbal memory tasks, the amount of activation in the occipital cortex (usually devoted to vision) correlated significantly with their memory performance. Evidently they were using their occipital cortex to help with the memory. On the average, congenitally blind people show better verbal memory than sighted people do.

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  • Cohen, L. G., P. Celnik, A. Pascual-Leone, B. Corwell, L. Faiz, J. Dambrosia. 1997. Functional relevance of cross-modal plasticity in blind humans. Nature 389:180–183.

    DOI: 10.1038/38278Save Citation »Export Citation »E-mail Citation »

    A strong magnetic field temporarily blocks activity in the cortical area under the magnet. Applying this procedure to the occipital cortex interferes with several kinds of nonvisual processing in blind people, but has no effect on the same tasks performed by sighted people.

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  • Gougoux, F., P. Belin, P. Voss, F. Lepore, M. Lassonde, and R. J. Zatorre. 2009. Voice perception in blind persons: A functional magnetic resonance imaging study. Neuropsychologia 47:2967–2974.

    DOI: 10.1016/j.neuropsychologia.2009.06.027Save Citation »Export Citation »E-mail Citation »

    The primary visual cortex in the occipital lobe shows little or no response to sound stimuli in sighted people, but fMRI scans show significant responses to sounds in people blind since early childhood.

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  • Merabet, L. B., R. Hamilton, G. Schlaug, J. D. Swisher, E. T. Kiriakopoulos, N. B. Pitskel. 2008. Rapid and reversible recruitment of early visual cortex for touch. PLoS One 3:e3046.

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    Sighted adults, voluntarily kept in visual deprivation for a few days, showed responses to Braille stimuli in the occipital cortex, usually reserved for visual stimuli.

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  • Sadato, N., A. Pascual-Leone, J. Grafman, V. Ibañez, M. -P. Deiber, G. Dold. 1996. Activation of the primary visual cortex by Braille reading in blind subjects. Nature 380:526–528.

    DOI: 10.1038/380526a0Save Citation »Export Citation »E-mail Citation »

    The primary visual cortex in the occipital lobe shows little or no response to touch stimuli in sighted people, but brain scans show significant responses to Braille stimuli in people blind since early childhood.

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Reorganization in Musicians

In many ways, musicians are excellent for studies of the effects of experience on the brain. Serious musicians practice for a few hours almost every day, and most began this habit in childhood. Furthermore, musicians are numerous and easy to find in most cities. One of the earliest studies of musicians’ brains, by Elbert, et al. 1995, found that stringed-instrument players devote a larger than average portion of the right hemisphere to sensations and control of the fingers of the left hand. Those are the fingers responsible for playing the strings of the instrument. Later studies found that several brain areas are larger—up to 30 percent larger—in musicians than in nonmusicians. These changes were reported by Schneider, et al. 2002 for the right temporal cortex and by Gaser and Schlaug 2003 for areas responsible for vision and hand control. From those studies it is not clear whether practicing music alters brain anatomy, or whether people with certain kinds of brain anatomy are more likely than others to become musicians. However, a longitudinal study by Hyde, et al. 2009 of children who were starting music lessons found that their brains were at the start of music lessons the same as those of other children, but within fifteen months, significant changes had already emerged. That result implies that brain differences are the result of musical practice and not the cause of it.

  • Elbert, T., C. Pantev, C. Wienbruch, B. Rockstroh, and E. Taub. 1995. Increased cortical representation of the fingers of the left hand in string players. Science 270:305–307.

    DOI: 10.1126/science.270.5234.305Save Citation »Export Citation »E-mail Citation »

    Recordings from the surface of the scalp show that long-time players of violins and similar instruments have a wider than average portion of their right cortex devoted to the fingers of the left hand.

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  • Gaser, C., and G. Schlaug. 2003. Brain structures differ between musicians and non-musicians. Journal of Neuroscience 23:9240–9245.

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    Several brain areas responsible for hand control and vision are, on the average, larger in professional musicians than in amateur musicians, and larger in amateurs than in nonmusicians.

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  • Hyde, K. L., J. Lerch, A. Norton, M. Forgeard, E. Winner, A. C. Evans. 2009. Musical training shapes structural brain development. Journal of Neuroscience 29:3019–3025.

    DOI: 10.1523/JNEUROSCI.5118-08.2009Save Citation »Export Citation »E-mail Citation »

    The brains of six-year-olds who were or were not starting music lessons did not differ significantly. However, fifteen months later, the brains of the children taking music lessons were already changing in the direction seen for adults who are serious musicians.

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  • Schneider, P., M. Scherg, G. Dosch, H. J. Specht, A. Gutschalk, and A. Rupp. 2002. Morphology of Heschl’s gyrus reflects enhanced activation in the auditory cortex of musicians. Nature Neuroscience 5:688–694.

    DOI: 10.1038/nn871Save Citation »Export Citation »E-mail Citation »

    On the average, Heschl’s gyrus is 30 percent larger in the right hemisphere of musicians than in nonmusicians.

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Reorganization and the Phantom Limb

Phantom limb is the continued perception of a limb after its amputation. For decades, any explanation eluded researchers until a study of monkeys serendipitously shed light on the matter. After amputation of a single finger, the area of sensory cortex previously responsive to that finger becomes more responsive to the neighboring fingers. After loss of sensory input from the entire hand or arm, what would happen? Researchers assumed that no axons from elsewhere in the cortex could form collaterals long enough to reach the vacated synapses. However, a follow-up by Pons, et al. 1991 on monkeys long after they lost arm, input found that axons representing the face had come to innervate the cortical areas previously responsive to the arm. Similar reorganization occurs in the human cortex. Davis, et al. 1998 tested people with phantom limbs and stimulated thalamic areas known to respond to the face. They found that face stimulation produced facial sensations and simultaneous arm or hand sensations. That is, the axons from the face stimulated their own cortical area and the cortical areas responsible for the arm and hand. Stimulating the arm and hand areas gave rise to arm and hand experiences. Ramachandran and Blakeslee 1998 provides an excellent, fascinating discussion of phantom limbs and their relationship to brain reorganization.

  • Davis, K. D., Z. H. T. Kiss, L. Luo, R. R. Tasker, A. M. Lozano, and J. O. Dostrovsky. 1998. Phantom sensations generated by thalamic microstimulation. Nature 391:385–387.

    DOI: 10.1038/34905Save Citation »Export Citation »E-mail Citation »

    In people with phantom limbs, stimulating areas of the thalamus responsible for one body area can induce simultaneous sensations from that area and the other, phantom area.

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  • Pons, T. P., P. E. Garraghty, A. K. Ommaya, J. H. Kaas, E. Taub, and M. Mishkin. 1991. Massive cortical reorganization after sensory deafferentation in adult macaques. Science 252:1857–1860.

    DOI: 10.1126/science.1843843Save Citation »Export Citation »E-mail Citation »

    Axons representing the face terminate in a cortical area that neighbors the area responsive to the arm and hand. Long after loss of sensory input from the arm and hand, monkeys showed strong responses to face stimulation in the cortical areas previously responsive to the hand and arm.

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  • Ramachandran, V. S., and S. Blakeslee. 1998. Phantoms in the brain: Probing the mysteries of the human mind. New York: Morrow.

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    This book describes fascinating clinical cases of phantom limbs, and relates them to reorganization of synaptic contacts in the sensory cortex.

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Learning to Read

In most people, learning to read occurs during childhood, where many other brain changes are occurring for other reasons. Carreiras, et al. 2009 used brain scans to examine the effects of learning to read in adulthood. Studying Colombian guerrillas returning to society, they compared those who subsequently learned to read and those who didn’t. Those who learned to read had more gray matter in five gyri of the cerebral cortex and greater thickness in part of the corpus callosum. This finding strongly suggests brain changes in adulthood as a result of learning to read.

Brain Activity and Consciousness

It is one thing to identify which brain area is associated with which behavioral function. It is another to discover how and why brain activity is associated with consciousness. The question of why consciousness exists at all, and how it relates to brain function, is what the philosopher David Chalmers calls the “hard problem” (see Chalmers 1995). Although nearly all scientists and philosophers who have addressed the problem endorse some version of monism—the idea that mental activity and brain activity are inseparable—no one has yet explained convincingly why brain activity is (sometimes) conscious. Nevertheless, research has made progress on subordinate questions, such as what aspects of brain activity are associated with consciousness and what role consciousness does or does not play in planning behavior.

  • Chalmers, D. J. 1995. Facing up to the problem of consciousness. Journal of Consciousness Studies 2: 200–219.

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    Chalmers points out the inadequacies of many claims to have solved the mind-body problem. He argues that we don’t even know where to begin in trying to explain the existence of consciousness and why it is associated with brain activity.

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Conscious and Unconscious Activity

Consciousness is difficult to define. For research purposes, the usual operational definition is that someone who verbally reports a stimulus must have been conscious of it. Failure to report a stimulus does not necessarily indicate unconsciousness, as should be clear from considering preverbal infants, nonhuman animals, and so forth. However, if a cooperative person reports awareness of certain stimuli and not others, most researchers are satisfied to consider the reported ones as conscious and the others as unconscious. What brain activity occurs during consciousness? Researchers have found clever ways to present an identical stimulus under different conditions, such that consciousness results in some cases and not others. Dehaene, et al. 2001 flashed words on a screen for 29ms. If the screen was blank before and after the word, viewers identified the word on 90 percent of trials. If the screen had an interfering pattern before and after the word, viewers almost never identified the word, reporting that they saw no word at all. Many other researchers—such as Cosmelli, et al. 2004 and Lee, et al. 2005—have relied on the phenomenon of binocular rivalry: Suppose one eye sees red and black vertical stripes while the other eye sees green and black horizontal stripes. Many other displays work equally well, such as seeing a face in one eye and a pulsating circle in the other. The brain, unable to fuse the two into a single perception, alternates perceptions. For several seconds the viewer is aware of one display, and then it disappears and the viewer is aware of the other. In binocular rivalry, both stimuli reach the visual cortex, but the viewer is conscious of one of them and not the other. All these studies have found that the difference between conscious and unconscious stimuli is quantitative. While someone is conscious of a stimulus, that stimulus evokes activity strong enough to spread to many other brain areas. When the viewer is unconscious of the stimulus, it evokes lesser, briefer, and more confined activity. However, even while the viewer is not conscious of one stimulus, the brain unconsciously processes it. Evidence for this conclusion comes from a study by Jiang, et al. 2007. Participants viewed different displays in the two eyes, experiencing binocular rivalry. If a word gradually faded into view in one eye while the person was conscious of the other eye, consciousness shifted toward the eye with the changing display. Consciousness shifted faster if the word was meaningful in the participant’s own language. If it was a word from a different alphabet, in a language unfamiliar to the viewer, consciousness shifted more slowly. Evidently the brain could identify whether the stimulus was meaningful or not, before the viewer had become conscious of the stimulus.

  • Cosmelli, D., O. David, J. -P. Lachaux, J. Martinerie, L. Garnero, B. Renault. 2004. Waves of consciousness: Ongoing cortical patterns during binocular rivalry. NeuroImage 23:128–140.

    DOI: 10.1016/j.neuroimage.2004.05.008Save Citation »Export Citation »E-mail Citation »

    Participants viewed a stationary face in one eye and a circle that pulsated seven times per second in the other eye. Conscious perception alternated between the two displays. While people were aware of the pulsating circle, high-amplitude waves of activity at seven cycles per second were recorded in much of the brain. When people were aware of the face, the 7Hz responses were muted.

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  • Dehaene, S., L. Naccache, L. Cohen, D. LeBihan, J. -F. Mangin, J. -B. Poline. 2001. Cerebral mechanisms of word masking and unconscious repetition priming. Nature Neuroscience 4:752–758.

    DOI: 10.1038/89551Save Citation »Export Citation »E-mail Citation »

    A word flashed on the screen for 29ms stimulates cells in the retina, lateral geniculate nucleus of the thalamus, and primary visual cortex, regardless of what other stimuli come before and after it. However, if an interfering pattern before and after the word masks it, the activity evoked in the primary visual cortex does not spread to other cortical areas, and the person cannot consciously identify the word.

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  • Jiang, Y., P. Costello, and S. He. 2007. Processing of invisible stimuli. Psychological Science 18:349–355.

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    Participants viewed different displays in the two eyes, producing binocular rivalry. If a word gradually faded into view in the eye that was not producing conscious perception at the moment, attention shifted to that eye faster if it was a meaningful word than if it was a word from a language the viewer did not know.

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  • Lee, S. -H., R. Blake, and D. J. Heeger. 2005. Traveling waves of activity in primary visual cortex during binocular rivalry. Nature Neuroscience 8:22–23.

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    During binocular rivalry, each visible stimulus evokes a distinct pattern of brain activity. When one stimulus is conscious, its pattern dominates much of the brain. As consciousness shifts to the other stimulus, the other pattern spreads in the brain.

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Using Brain Recordings to Infer Consciousness

Given that conscious brain activity differs from unconscious activity, it may be possible to use brain recordings to infer consciousness in people (and perhaps animals) that are unable to give verbal responses. Owen, et al. 2006 studied a young woman in a persistent vegetative state following a traffic accident. She could not speak and she made no overt response to any verbal instruction. Researchers used fMRI to monitor her brain activity after telling her to imagine playing tennis or to imagine walking through her house. The instructions evoked brain activity similar to that of healthy people who were given the same instructions. These results suggest consciousness.

  • Owen, A. M., M. R. Coleman, M. Boly, M. H. Davis, S. Laureys, and J. D. Pickard. 2006. Detecting awareness in the vegetative state. Science 313:1402.

    DOI: 10.1126/science.1130197Save Citation »Export Citation »E-mail Citation »

    A woman in a persistent vegetative state was given two kinds of instruction. Instruction to imagine playing tennis evoked activity in her motor cortex, as it would in a healthy, conscious person. Instruction to imagine walking around her house evoked activity in the hippocampus, again similar to the result for healthy people. The results suggest consciousness, although we cannot be sure.

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Blindsight as an Example of Unconscious Perception

People with complete damage to the primary visual cortex in the occipital lobe report no conscious vision, not even in their dreams or imagination. If the damage includes only part of the primary visual cortex, people lose conscious perception in only part of the visual field, such as the upper left quadrant, depending on the location of the damage. However, within a field where the person reports no conscious perception, some people can make movements directed toward a stimulus, such as moving their eyes toward it or pointing toward it. This persistence of directed movement despite a lack of conscious vision is known as blindsight. People with blindsight insist that they are only guessing, and they are surprised to be told of their accuracy. One explanation, proposed by Fendrich, et al. 1992 and supported by Radoeva, et al. 2008, holds that the spared functions depend on surviving islands of spared tissue in the primary visual cortex. These islands might suffice to control a few behaviors without producing the spread of activity that is necessary for consciousness. That explanation deals with the fact that many people show blindsight in part of their damaged visual field but not in another part. A competing explanation points to continuing input from the thalamus to other visual areas outside the primary visual cortex. Blocking the connections from the thalamus to other cortical areas abolishes blindsight, as Schmid, et al. 2010 demonstrated. It is possible that both of these explanations is correct and that both processes contribute to the final result.

  • Fendrich, R., C. M. Wessinger, and M. S. Gazzaniga. 1992. Residual vision in a scotoma: Implications for blindsight. Science 258:1489–1491.

    DOI: 10.1126/science.1439839Save Citation »Export Citation »E-mail Citation »

    This was the first article to argue for an explanation of blindsight in terms of surviving islands of healthy tissue in an otherwise damaged primary visual cortex.

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  • Radoeva, P. D., S. Prasad, D. H. Brainard, and G. K. Aguirre. 2008. Neural activity within area V1 reflects unconscious visual performance in a case of blindsight. Journal of Cognitive Neuroscience 20:1927–1939.

    DOI: 10.1162/jocn.2008.20139Save Citation »Export Citation »E-mail Citation »

    These researchers recorded activity in the primary visual cortex that correlated with the evidence for blindsight.

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  • Schmid, M. C., S. W. Mrowka, J. Turchi, R. C. Saunders, M. Wilke, A. J. Peters. 2010. Blindsight depends on the lateral geniculate nucleus. Nature 466:373–377.

    DOI: 10.1038/nature09179Save Citation »Export Citation »E-mail Citation »

    In people with blindsight, the lateral geniculate nucleus continues sending some of its output to areas of the cortex outside the primary visual cortex. Suppressing this output abolishes blindsight.

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Consciousness and Voluntary Behavior

People have the impression that they decide what to do consciously and that the consciousness is instrumental in initiating the action. However, a study by Libet, et al. 1983 casts doubt on that impression. Participants in their study observed a dot moving rapidly around a clocklike display. Each was instructed to make a wrist flexion as spontaneously as possible, without any advance planning of the time, and to remember the position of the dot at the time of the decision. The researchers asked for a report of the dot position and compared it to the measured times of the movement itself and the onset of activity (the “readiness potential”) in the motor cortex. On the average, the brain activity in preparation for the movement began about 300ms before the reported time of the conscious decision, which in turn occurred 200ms before the movement. Several other researchers have replicated this result, but the issue remains of what it means. It apparently indicates that consciousness is more an observer of decisions than a cause of them. Banks and Isham 2009 conducted a somewhat complex study that questions whether people can at all accurately report the time of a conscious decision. If in fact people are just guessing, then the study by Libet, et al. 1983 is not decisive. Nevertheless, an additional study by Soon, et al. 2008 is noteworthy. Participants were told to make a spontaneous decision to press a button on the left or one on the right. Letters appeared on a screen once every half second, and participants identified the time of their decision by recalling the letter displayed at the time of the decision. As in Libet’s study, Soon, et al. 2008 recorded the onset of enhanced activity in motor areas of the cortex. Based on the letter reported, people said they had decided when to press and which button to press half a second to one second before the action. However, the brain activity indicated the choice of left or right seven to ten seconds before the response. Evidently what we perceive as a spontaneous decision builds up gradually for a few seconds before we become conscious of having made the decision.

  • Banks, W. P., and E. A. Isham. 2009. We infer rather than perceive the moment we decided to act. Psychological Science 20:17–21.

    DOI: 10.1111/j.1467-9280.2008.02254.xSave Citation »Export Citation »E-mail Citation »

    We probably had no reason to evolve the ability to report accurately the time of a conscious decision. Changes in procedure can induce people to misestimate the time of a muscle response, and similarly can induce people to alter their reports of a conscious decision. Perhaps people are only guessing when they try to report the time of a conscious decision.

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  • Libet, B., C. A. Gleason, E. W. Wright, and D. K. Pearl. 1983. Time of conscious intention to act in relation to onset of cerebral activities (readiness potential): The unconscious initiation of a freely voluntary act. Brain 106:623–642.

    DOI: 10.1093/brain/106.3.623Save Citation »Export Citation »E-mail Citation »

    The reported time of a conscious decision precedes a voluntary act by 200ms, but activity in the motor cortex begins 300ms before the reported decision. This result has become well known in philosophy as well as psychology.

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  • Soon, C. S., M. Brass, H. -J. Heinze, and J. -D. Haynes. 2008. Unconscious determinants of free decisions in the human brain. Nature Neuroscience 11:543–545.

    DOI: 10.1038/nn.2112Save Citation »Export Citation »E-mail Citation »

    Participants viewed a letter on a screen that changed every half second. Each participant reported the letter that was present at the time he or she decided whether to press a button on the left or on the right. Brain recordings predicted the choice of left or right seven to ten seconds before the action, whereas the participant was conscious of the choice only in the final second.

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Sleep

Before the 1950s, nearly everyone assumed that sleep was a passive process that consisted of little more than decreased activity of brain and body. We now regard sleep as a process in which certain brain areas rhythmically generate a period of inhibition of other brain areas.

Stages

In the 1950s, Nathaniel Kleitman in the United States and Michel Jouvet in France virtually simultaneously discovered that sleep has several stages, instead of being uniform. In particular, they discovered the stage known as rapid eye movement sleep (REM) in humans, generally referred to as paradoxical sleep in research on nonhumans. REM is characterized by higher brain activity than other sleep stages but involves complete relaxation of the body’s postural muscles. An excellent book Dement 1972 describes the early research on sleep stages. The early research found that people awakened from an REM state usually report dreams, and for a while people believed that REM and dreaming were virtually synonymous. However, as reported in the review Solms 2000, many dreams occur during non-REM sleep, and people with certain kinds of brain damage lose all REM sleep but continue reporting dreams. That is, REM and dreaming overlap to some extent but not entirely.

As Inhibition of Brain Activity

Sleep is an interruption or alteration of consciousness. During sleep, body temperature decreases slightly and spontaneous activity decreases in the brain, but less than we might have guessed. The primary change is an increase in inhibitory output to synapses throughout the cortex. Because of this inhibition, neurons’ activity cannot spread substantially to other cells. Massimini, et al. 2005 and Esser, et al. 2009 have documented this conclusion. As described in the previous section, consciousness occurs when a pattern of activity spreads to a large portion of the brain. Preventing the spread of messages means that even when many neurons are active, the sleeper remains unconscious. Thinking of sleep as an inhibitory process led to the interesting insight, described by Krueger, et al. 2008, that sleep can be a local process. That is, certain brain areas may wake up or go to sleep before others do. Dolphins and several other marine mammals sleep on one side of the brain at a time. In sleepwalkers, part of the brain is awake enough to walk around while other parts remain asleep. People sometimes awaken but find themselves temporarily unable to move. The reason is that an area in the pons, responsible for paralyzing the postural muscles of the body during REM sleep, has remained asleep while other brain areas have awakened.

  • Esser, S. K., S. Hill, and G. Tononi. 2009. Breakdown of effective connectivity during slow wave sleep: Investigating the mechanism underlying a cortical gate using large-scale modeling. Journal of Neurophysiology 102:2096–2111.

    DOI: 10.1152/jn.00059.2009Save Citation »Export Citation »E-mail Citation »

    During sleep, activity does not spread from one brain area to another in nearly the same way that it does during wakefulness.

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  • Krueger, J. M., D. M. Rector, S. Roy, H. P. A. Van Dongen, G. Belenky, and J. Panksepp. 2008. Sleep as a fundamental property of neuronal assemblies. Nature Reviews Neuroscience 9:910–919.

    DOI: 10.1038/nrn2521Save Citation »Export Citation »E-mail Citation »

    Because sleep depends on inhibition of brain activity, it can be a local process. That is, certain parts of the brain can go to sleep or wake up before others do.

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  • Massimini, M., F. Ferrarelli, R. Huber, S. K. Esser, H. Singh, and G. Tononi. 2005. Breakdown of cortical effective connectivity during sleep. Science 309:2228–2232.

    DOI: 10.1126/science.1117256Save Citation »Export Citation »E-mail Citation »

    During sleep, neurons continue spontaneous activity at a rate only slightly less than usual, and they respond to sensory stimuli. However, because of the increased inhibition at this time, the activity does not spread enough to become conscious.

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Circadian Rhythms of Sleep and Wakefulness

People and nearly all species of animals continue generating a sleep-wake rhythm of approximately twenty-four hours, even if they live in an unchanging environment. In mammals, that rhythm is generated by one nucleus of the hypothalamus, the suprachiasmatic nucleus (SCN). Strong evidence for that role of the SCN comes from the report by Inouye and Kawamura 1979 that SCN cells maintained in cell culture, separated from the rest of the body, continue generating a nearly twenty-four-hour rhythm. Although these cells produce the rhythm by themselves, light is important for resetting the rhythm to keep it in phase with the outside world. Researchers have detailed much about the biochemical pathways that produce the circadian rhythm, and they have identified several genes that control it. Those genes are virtually identical across species, ranging from humans to fruit flies. A mutation in one of those genes causes people to produce a sleep-wake cycle closer to twenty-three than twenty-four hours. They consistently get sleep early at night and awaken early the next morning, as if they were moving one time zone west every day. Xu, et al. 2005 describes one family in which many members have this genetic mutation.

  • Inouye, S. T., and H. Kawamura. 1979. Persistence of circadian rhythmicity in a mammalian hypothalamic “island” containing the suprachiasmatic nucleus. Proceedings of the National Academy of Sciences, USA 76:5962–5966.

    DOI: 10.1073/pnas.76.11.5962Save Citation »Export Citation »E-mail Citation »

    This was the first report that cells of the suprachiasmatic nucleus continue generating a twenty-four-hour rhythm after being disconnected from the rest of the body.

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  • Xu, Y., Q. S. Padiath, R. E. Shapiro, C. R. Jones, S. C. Wu, N. Saigoh, et al. 2005. Functional consequences of a δCK1 mutation causing familial advanced sleep phase syndrome. Nature 434:640–644.

    DOI: 10.1038/nature03453Save Citation »Export Citation »E-mail Citation »

    One family includes many members with a mutation in one of the genes controlling their circadian rhythms. As a result, they constantly fight the tendency to go to bed earlier every night and awaken earlier every morning.

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Learning and Memory

Learning and memory are complex, and so is their brain representation. Research in biological psychology has shed light on several important aspects of learning and memory.

Localization

Karl Lashley, one of the dominant figures in psychology during the early to mid-20th century, conducted extensive research to localize learning in animals. He trained rats in simple mazes and then made cuts in their cortex or removed part of their cortex. None of the cuts impaired the rats’ memory and the ablations produced deficits related more to the size of the ablation than to the location. His failure to localize memory, as described in Lashley 1950, discouraged other researchers for decades. We now note two assumptions that impeded Lashley. He assumed that any one example of learning was as good as any other, and he assumed that learning takes place in the cerebral cortex. Thompson 1986 succeeded where Lashley had failed, by abandoning both of Lashley’s assumptions. Thompson studied classical conditioning of eye blinks in rabbits and demonstrated that this type of learning depends on a small area in the cerebellum, the lateral interpositus nucleus. That study was important for identifying the location for one example of learning, and thus enabling researchers to explore in detail what happens in that area as it relates to learning. However, most learning depends on multiple changes in many brain areas.

  • Lashley, K. S. 1950. In search of the engram. Symposia of the Society for Experimental Biology 4:454–482.

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    Here Lashley summarized his long and largely fruitless attempts to localize memory in the brain.

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  • Thompson, R. F. 1986. The neurobiology of learning and memory. Science 233:941–947.

    DOI: 10.1126/science.3738519Save Citation »Export Citation »E-mail Citation »

    By temporarily inactivating different brain areas, Thompson demonstrated that the lateral interpositus nucleus of the cerebellum must be active for classical conditioning of a particular response. However, the areas receiving output from this nucleus did not need to be active. He inferred that the lateral interpositus nucleus mediated learning, whereas the other areas controlled muscle responses.

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Role of the Hippocampus

In 1953 Henry Molaison, generally known by his initials H.M., underwent surgery to control his severe epilepsy. The surgeons removed the hippocampus from both hemispheres. As a result, H.M. suffered severe anterograde amnesia (inability to form new memories). Corkin 2002 and Eichenbaum 2002 provide good accounts of H.M. and his memory loss. However, it gradually became apparent that H.M. was impaired on some aspects of learning and memory much more than others, and this discovery highlighted the importance of distinguishing among different types of memory. H.M. could form new short-term memories and retain them without trouble until he was distracted. However, the memories faded quickly after any distraction. He and many other people with amnesia appear to be normal in learning new motor skills, although they do not remember learning them. The most profound loss is in episodic memory, the recall of specific life events. H.M. could not recall any specific event in his life after the operation and had trouble recalling many events from earlier in his life. Rosenbaum, et al. 2005 describes another patient who lost memory for all events in his life. Research with laboratory animals has led to several competing, but not entirely incompatible, theories of the role of the hippocampus in learning and memory. Squire 1992 proposed that the hippocampus is essential for declarative memory, the ability to recall a specific memory in words. Obviously, it is difficult to apply that concept to nonhuman animals, although researchers have developed many clever analogues to declarative memory that do not require language. A second view links the hippocampus with spatial memory. When an animal explores an environment, different hippocampal cells become active in different locations, forming a map of the environment. Hippocampal damage is highly disruptive for spatial memory. A book edited by Mizumori 2008 provides chapters by many researchers in this field. Third, a growing consensus focuses on the role of the hippocampus in episodic memory. The hippocampus binds together the details and context of a memory, enabling the individual to recall the sequence of events. An article by Winocur, et al. 2007 outlines research supporting this view.

Role of the Basal Ganglia

Suppose we ask people to learn to choose symbol A over symbol B, C over D, and so forth, with eight or so pairs. Whereas intact people learn quickly, those with amnesia show no progress at first, and may not even remember the instructions from one session to the next. However, with many repetitions over days, patients with amnesia make gradual progress, even while saying that they do not know the answers and are just guessing. Evidently it is possible to learn the same task in more than one way. The more efficient way uses declarative memory that depends on the hippocampus. When that method fails, an individual can gradually learn a habit, dependent on the basal ganglia. Bayley, et al. 2005 provided one of the first clear demonstrations of gradual habit learning after hippocampal damage, and Foerde, et al. 2006 used fMRI to demonstrate that it depends on the basal ganglia. Moody, et al. 2010 confirmed this conclusion with a study of patients with Parkinson’s disease, associated with impairment of the basal ganglia. People learned a complex discrimination that is generally difficult to verbalize. Intact people showed gradual improvement, despite poor ability to describe what they had learned. People with Parkinson’s disease failed to improve at all, except in those few cases in which they could describe explicitly what they had learned.

  • Bayley, P. J., J. C. Frascino, and L. R. Squire. 2005. Robust habit learning in the absence of awareness and independent of the medial temporal lobe. Nature 436:550–553.

    DOI: 10.1038/nature03857Save Citation »Export Citation »E-mail Citation »

    After damage to the hippocampus and neighboring brain structures, people have trouble with what is usually fairly easy learning. They do make gradual progress, but even after learning, they are unaware that they have learned.

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  • Foerde, K., B. J. Knowlton, and R. A. Poldrack. 2006. Modulation of competing memory systems by distraction. Proceedings of the National Academy of Sciences, USA 103:11778–11783.

    DOI: 10.1073/pnas.0602659103Save Citation »Export Citation »E-mail Citation »

    When people are concentrating on a task, they learn quickly and describe what they have learned. When they are distracted, they learn slowly and have trouble verbalizing what they have learned. Here, an fMRI study shows that this second type of learning depends on activation of the basal ganglia.

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  • Moody, T. D., G. Y. Chang, Z. F. Vanek, and B. J. Knowlton. 2010. Concurrent discrimination learning in Parkinson’s disease. Behavioral Neuroscience 124:1–8.

    DOI: 10.1037/a0018414Save Citation »Export Citation »E-mail Citation »

    People received simultaneous training on thirty visual discriminations using complex stimuli difficult to describe. Under these conditions, most people learn slowly and can verbalize the correct answer to few of the items. People with Parkinson’s disease, which damages the basal ganglia, showed no progress except on the items they could verbalize. This study confirms the idea that gradual nonverbal habit learning depends on the basal ganglia.

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Language

Although nearly all animal species communicate in various ways, human language is unique in its productivity—that is, its ability to express a wide variety of new ideas. How did it evolve? A simple idea is that it evolved accidentally as a by-product of selection for overall intelligence. However, people with Williams syndrome are mentally retarded in many regards, but most of them have surprisingly good language skills. Martens, et al. 2008 provides a thorough review of Williams syndrome. Furthermore, people with a mutation of the FOXP2 gene are intellectually normal in most regards but seriously disadvantaged in language. Gopnik and Crago 1991 describes the behavioral deficits. Evidently, language represents a specific adaptation that organized the human brain to perform differently from other species. Since the 1800s, neurologists have identified two brain areas as especially important for language. Damage in the left temporal lobe leads to Wernicke’s aphasia, marked by impaired language comprehension and impaired ability to think of the names of objects. Damage in the left frontal lobe leads to Broca’s aphasia, marked by impaired language production, as well as impaired use and comprehension of prepositions, conjunctions, and sentences whose meaning depends on complex grammar. A study by Sahin, et al. 2009 found that different locations within Broca’s area have different functions. Thus, future research may be able to describe language production in more detail.

  • Gopnik, M., and M. B. Crago. 1991. Familial aggregation of a developmental language disorder. Cognition 39:1–50.

    DOI: 10.1016/0010-0277(91)90058-CSave Citation »Export Citation »E-mail Citation »

    People with a particular gene, later identified as a mutation of the FOXP2 gene, have multiple language problems, including pronunciation and simple aspects of grammar, such as forming plurals.

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  • Martens, M. A., S. J. Wilson, and D. C. Reutens. 2008. Research review: Williams syndrome: A critical review of the cognitive, behavioral, and neuroanatomical phenotype. Journal of Child Psychology and Psychiatry 49:576–608.

    DOI: 10.1111/j.1469-7610.2008.01887.xSave Citation »Export Citation »E-mail Citation »

    This review highlights the abilities and disabilities associated with Williams syndrome. It also calls attention to limitations of many of the studies that have been published so far.

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  • Sahin, N. T., S. Pinker, S. S. Cash, D. Schomer, and E. Halgren. 2009. Sequential processing of lexical, grammatical, and phonological information within Broca’s area. Science 326:445–449.

    DOI: 10.1126/science.1174481Save Citation »Export Citation »E-mail Citation »

    Researchers recorded from Broca’s area in patients undergoing brain surgery under local anesthesia. Cells at the most superior location responded first, and equally to any words the person read. Cells at a lower location responded later, and more strongly as the person imagined grammatically changing a word. Cells at the lowest location responded latest, and were most active in preparation for speaking.

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Drug Effects on Behavior

Drugs that affect behavior and experience act on the brain, and drugs that act on the brain affect behavior and experience. That fact underlines the identity of mind and brain. With a few exceptions, such as Novocain and related drugs that block sodium passage through axons, the drugs that affect behavior act at synapses—the points at which one neuron communicates with another. Thus the study of drug effects is closely related to the study of synapses. Research on drug effects also sheds light on addictions. One unifying principle across addictions is that they increase activity in the nucleus accumbens, an area at the base of the forebrain. In most cases they act by increasing release of dopamine or norepinephrine, as reported by Dalley and Everitt 2009 and by Weinshenker and Schroeder 2007. The nucleus accumbens also responds to a wide variety of other reinforcing experiences, as Damsma, et al. 1992 demonstrated for sex, Breiter, et al. 2001 demonstrated for gambling, and Ko, et al. 2009 demonstrated for videogame playing. Here we consider just a few examples of drugs and then focus on the phenomenon of addiction.

Stimulants

Stimulant drugs increase alertness and activity. At low levels they enhance attention, and amphetamine has been used as a therapy for attention deficit disorder. However, at higher levels, stimulants interfere with attention and learning. Stimulants act on the brain via the dopamine and norepinephrine transporters. After a neuron releases either of the neurotransmitters dopamine or norepinephrine, the transmitters activate receptors on the postsynaptic cell and then transporter molecules on the presynaptic neuron return many or most of the released transmitter molecules to the presynaptic cell, in a recycling system. Amphetamine, methamphetamine, and cocaine block this reuptake process, prolonging the presence of the transmitters in the synaptic cleft and enabling them to restimulate their receptors. Many researchers have demonstrated this process; Schmitt and Reith 2010 provides a good review. Methylphenidate (Ritalin) acts at the same receptors as cocaine, in the same way. However, as Volkow, et al. 1997 demonstrated, cocaine’s effects on the brain increase and decrease much faster.

  • Schmitt, K. C., and M. E. A. Reith. 2010. Regulation of the dopamine transporter. Annals of the New York Academy of Sciences 1187:316–340.

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    Amphetamine, cocaine, and methamphetamine bind to the dopamine transporter on the presynaptic neuron, thereby blocking the path for dopamine to enter the neuron. Dopamine remains in the synaptic cleft, where it restimulates its receptors, perhaps many times. Methamphetamine is similar to amphetamine but exerts stronger effects.

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  • Volkow, N. D., G. -J. Wang, and J. S. Fowler. 1997. Imaging studies of cocaine in the human brain and studies of the cocaine addict. Annals of the New York Academy of Sciences 820:41–55.

    DOI: 10.1111/j.1749-6632.1997.tb46188.xSave Citation »Export Citation »E-mail Citation »

    Whereas methylphenidate taken in pill form reaches its maximum concentration in the brain about an hour later, and its effects decline with a half-life of an hour and a half, the effects of cocaine are much faster and briefer. As a result, cocaine produces a “rush” that leads to addiction, whereas methylphenidate does not. The results are different, however, if someone injects methylphenidate.

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Opiates

Decades ago it was not clear whether opiates had their main effects on the brain or in the periphery of the body. Pert and Snyder 1973 reported brain receptors sensitive to opiate drugs such as morphine and heroin. Soon after, other researchers found the brain’s endogenous chemicals that stimulate these receptors, chemicals now known as endorphins. Endorphins indirectly increase dopamine release in the nucleus accumbens, by inhibiting other neurons that inhibit dopamine release. However, as Hnasko, et al. 2005 demonstrated, opiates are rewarding even to mice that lack dopamine. Evidently endorphins are reinforcing on their own, and not just by enhancing dopamine.

  • Hnasko, T. S., B. N. Sotak, and R. D. Palmiter. 2005. Morphine reward in dopamine-deficient mice. Nature 438:854–857.

    DOI: 10.1038/nature04172Save Citation »Export Citation »E-mail Citation »

    These researchers studied mice that were severely deficient in dopamine. The mice learned a preference for places where they received morphine, demonstrating the ability of endorphin receptors to mediate reinforcement on their own, and not just by enhancing dopamine release.

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  • Pert, C. B., and S. H. Snyder. 1973. The opiate receptor: Demonstration in nervous tissue. Science 179:1011–1014.

    DOI: 10.1126/science.179.4077.1011Save Citation »Export Citation »E-mail Citation »

    This was the groundbreaking article that demonstrated opiate receptors in the brain. It led the way to the discovery of endorphins and other neurotrophins that alter brain activity.

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Cannabinoids

Cannabinoids, the psychoactive chemicals in marijuana, exert their effects in an unusual way. In many brain areas, after one neuron releases neurotransmitters that stimulate receptors on a second cell, the second cell sends a reverse message to provide negative feedback to the first cell. In effect, it says, “I received your message. You can stop sending it.” Cannabinoids mimic this effect, attaching to the negative feedback sites on presynaptic cells. Wilson and Nicoll 2001 demonstrated that cannabinoids decrease glutamate release in the hippocampus. Földy, et al. 2006 demonstrated that cannabinoids decrease GABA release. Because glutamate is the brain’s main excitatory transmitter and GABA is its main inhibitory transmitter, the conclusion is that cannabinoids put the brakes on both excitatory and inhibitory transmission.

Addiction

Addiction is a puzzling phenomenon. People who have become addicted to a drug, or to gambling, overeating, or other habits, recognize that the addiction’s harm greatly outweighs the occasional pleasures. Nevertheless, they find it difficult or impossible to quit. One proposed explanation is that someone with an addiction continues using the substance as a way to avoid withdrawal symptoms. However, cravings emerge long after the end of withdrawal symptoms, and cigarette smoking is one of the most persistent addictions, although nicotine withdrawal symptoms are relatively mild. One proposed explanation is that a user learns an association between certain cues and the drug, and later exposure to one of those cues triggers a renewed craving. Hutchison, et al. 2002 found that the sight of a lit cigarette triggers a craving in an abstinent smoker. Thalemann, et al. 2007 found that the sight of a popular videogame triggers a craving in people who are trying to decrease their time spent on videogames. Another explanation is that people learn that they can use their abused substance or other habit to reduce stress. Hutcheson, et al. 2001 established heroin habits in rats and then allowed some of them to bar-press for heroin during withdrawal symptoms. Later, those rats worked especially hard for heroin when they were again suffering withdrawal. The idea is that rats or people might learn that a substance relieves one kind of distress and then turn to it during other kinds of distress. Still another explanation is that certain drugs reorganize synapses in the brain, particularly the nucleus accumbens. Mameli, et al. 2009 found that cocaine alters synapses in the nucleus accumbens in such a way that cocaine continues to stimulate them but other types of reinforcement, even sex, fail to do so or stimulate them less than usual. Kenny, et al. 2006 found similar results for heroin.

  • Hutcheson, D. M., B. J. Everitt, T. W. Robbins, and A. Dickinson. 2001. The role of withdrawal in heroin addiction: Enhances reward or promotes avoidance? Nature Neuroscience 4:943–947.

    DOI: 10.1038/nn0901-943Save Citation »Export Citation »E-mail Citation »

    Rats going through heroin withdrawal work moderately for heroin. However, after they have experienced the relief that heroin provides under those conditions, they work especially vigorously for heroin when they are again in withdrawal. That is, they learn that heroin can be extremely effective in relieving distress.

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  • Hutchison, K. E., H. LaChance, R. Niaura, A. Bryan, and A. Smolen. 2002. The DRD4 VNTR polymorphism influences reactivity to smoking cues. Journal of Abnormal Psychology 111:134–143.

    DOI: 10.1037/0021-843X.111.1.134Save Citation »Export Citation »E-mail Citation »

    The sight of a lit cigarette enhances the desire to smoke in some abstinent cigarette smokers. The effect varies depending on their genetics.

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  • Kenny, P. J., S. A. Chen, O. Kitamura, A. Markou, and G. F. Koob. 2006. Conditioned withdrawal drives heroin consumption and decreases reward sensitivity. Journal of Neuroscience 26:5894–5900.

    DOI: 10.1523/JNEUROSCI.0740-06.2006Save Citation »Export Citation »E-mail Citation »

    Repeated use of heroin makes rats less sensitive than usual to other types of reinforcement, such as rewarding self-stimulation of the brain. It has been said that an addiction hijacks the brain’s reward system, making the reward system respond to the addictive act and to little else.

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  • Mameli, M., B. Halbout, C. Creton, D. Engblom, J. R. Parkitna, R. Spanagel. 2009. Cocaine-evoked synaptic plasticity: Persistence in the VTA triggers adaptations in the NAc. Nature Neuroscience 12:1036–1041.

    DOI: 10.1038/nn.2367Save Citation »Export Citation »E-mail Citation »

    As in the case of heroin, cocaine alters the synapses in the nucleus accumbens so that they respond strongly to cocaine and weakly to other types of reinforcement.

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  • Thalemann, R., K. Wölfling, and S. M. Grüsser. 2007. Specific cue reactivity on computer game-related cues in excessive gamers. Behavioral Neuroscience 121:614–618.

    DOI: 10.1037/0735-7044.121.3.614Save Citation »Export Citation »E-mail Citation »

    People who have an excessive habit of playing videogames experience a strong craving when they see a popular videogame. In this and other regards, videogame playing is similar to a drug addiction.

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Sex Hormones and Behavior

Androgens such as testosterone and estrogens such as estradiol produce two types of effects on behavior. Early in development, and to some extent also during puberty, these hormones produce organizing effects—long-lasting structural changes in the brain, genitals, and other organs. At all times, they also produce activating effects that temporarily increase one reaction or another. Arnold 2009 provides an excellent review of organizing and activating effects.

  • Arnold, A. P. 2009. The organizational-activational hypothesis as the foundation for a unified theory of sexual differentiation of all mammalian tissues. Hormones and Behavior 55:570–578.

    DOI: 10.1016/j.yhbeh.2009.03.011Save Citation »Export Citation »E-mail Citation »

    Distinguishing between long-term organizing effects of hormones and their shorter-term activating effects is useful for understanding development of body structure and sex-related behaviors.

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Organizing Effects

For mammals, genes on the X and Y chromosomes induce sex-related differences mostly but not entirely by altering hormone production. During an early stage of development—prenatally in humans—a gene on the male’s Y chromosome, known as SRY (for sex-determining region on the Y chromosome) causes the primitive undifferentiated gonads to develop into testes that produce much androgens. The androgens induce the external genitals to develop into penis and scrotum. The female’s estrogens are important for development of internal female anatomy but not for external genitals. Development of penis versus clitoris depends on high versus low amounts of androgens, not on androgens versus estrogens. Prenatal androgens also alter the development of certain nuclei of the hypothalamus and other brain areas. Of psychological interest is the effect of this brain development on behavior. Several studies suggest an influence on interests, beginning in early childhood. Although it is undeniable that parents treat daughters differently from sons, biological factors may also influence children’s interests. Alexander, et al. 2009 found that girls showed more interest than boys did in dolls at ages three to eight months. Alexander and Hines 2002 found that male monkeys played more with balls and toy cars, whereas female monkeys played more with dolls. More direct evidence comes from a study by Hines, et al. 2002 in which researchers measured the testosterone levels of pregnant women and examined their daughters’ play behavior at age three and half. The level of testosterone to which the fetus was exposed in utero correlated significantly with the time that the girls spent playing with toy trucks and other typically boys’ toys. All of these girls were anatomically normal, and neither the girls nor their mothers knew the mothers’ testosterone levels during pregnancy. Swan, et al. 2010 found that boys whose mothers had high levels of phthalates during pregnancy (chemicals that inhibit testosterone production) showed elevated interest in girls’ toys and decreased interest in boys’ toys at ages three to six years, compared to other boys. All these results suggest an influence of prenatal hormones on gender-differentiated behaviors even in a non-reproductive setting.

  • Alexander, G. M., and M. Hines. 2002. Sex differences in response to children’s toys in nonhuman primates (Cercopithecus aethiops sebaeus). Evolution and Human Behavior 23:467–479.

    DOI: 10.1016/S1090-5138(02)00107-1Save Citation »Export Citation »E-mail Citation »

    At their first exposure to human toys, male monkeys spend more time with toy cars and female monkeys spend more time with dolls.

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  • Alexander, G. M., T. Wilcox, and R. Woods. 2009. Sex differences in infants’ visual interest in toys. Archives of Sexual Behavior 38:427–433.

    DOI: 10.1007/s10508-008-9430-1Save Citation »Export Citation »E-mail Citation »

    At ages three to eight months, before they have enough coordination to play with toys, girls look at dolls more than they look at toy cars and trucks. Boys looked at both types of item about equally.

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  • Hines, M., S. Golombok, J. Rust, K. J. Johnston, J. Golding, and the Avon Longitudinal Study of Parents and Children Study Team. 2002. Testosterone during pregnancy and gender role behavior of preschool children: A longitudinal, population study. Child Development 73:1678–1687.

    DOI: 10.1111/1467-8624.00498Save Citation »Export Citation »E-mail Citation »

    Researchers measured testosterone levels in the blood of pregnant women. Some of that testosterone would enter the fetus. At age three and half, the daughters who had been exposed to higher testosterone levels spent more time playing with what are typically boys’ toys than did girls who had been exposed to lower testosterone levels.

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  • Swan, S. H., F. Liu, M. Hines, R. L. Kruse, C. Wang, J. B. Redmon. 2010. Prenatal phthalate exposure and reduced masculine play in boys. International Journal of Andrology 33:259–269.

    DOI: 10.1111/j.1365-2605.2009.01019.xSave Citation »Export Citation »E-mail Citation »

    Phthalates are environmental chemicals that interfere with testosterone production. Sons whose mothers had higher phthalate levels during pregnancy showed lower than average interest in typical boys’ toys and higher than average interest in typical girls’ toys, when tested at ages three to six years.

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Activating Effects

The activating effects of sex hormones on sexual behavior have been explored extensively in rodents, where sex hormones prime the hypothalamus to release dopamine. Hull and Dominguez 2007 provides a thorough review. In humans, testosterone levels correlate with a tendency to seek sexual partners, especially to seek multiple partners. A study by van Anders, et al. 2007 found this tendency in women as well as men. Testosterone also has significant, although not always large, effects on nonsexual behaviors as well. Bos, et al. 2010 reported a placebo-controlled study in which temporarily increasing women’s testosterone levels made them less likely to trust other people. A similar study by van Honk and Schutter 2007 found that increasing women’s testosterone levels impaired their ability to recognize emotional expressions in faces.

  • Bos, P. A., D. Terburg, and J. van Honk. 2010. Testosterone decreases trust in socially naïve humans. Proceedings of the National Academy of Sciences of the United States of America 107:9991–9995.

    DOI: 10.1073/pnas.0911700107Save Citation »Export Citation »E-mail Citation »

    Experimenters administered testosterone or a placebo to women by sublingual absorption. Then the women looked at photos of faces and rated their trustworthiness. On the average, women gave lower ratings while under the influence of increased testosterone.

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  • Hull, E. M., and J. M. Dominquez. 2007. Sexual behavior in male rodents. Hormones and Behavior 52:45–55.

    DOI: 10.1016/j.yhbeh.2007.03.030Save Citation »Export Citation »E-mail Citation »

    This article reviews research on the role of hormones and neurotransmitters in the mating behavior of male rodents.

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  • van Anders, S. M., L. D. Hamilton, and N. V. Watson. 2007. Multiple partners are associated with higher testosterone in North American men and women. Hormones and Behavior 51:454–459.

    DOI: 10.1016/j.yhbeh.2007.01.002Save Citation »Export Citation »E-mail Citation »

    Men and women with multiple sexual partners have higher testosterone levels than those with one partner or none.

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  • van Honk, J., and D. J. L. G. Schutter. 2007. Testosterone reduces conscious detection of signals serving social correction. Psychological Science 18:663–667.

    DOI: 10.1111/j.1467-9280.2007.01955.xSave Citation »Export Citation »E-mail Citation »

    Women received either testosterone or a placebo. Then they viewed a series of faces that morphed gradually from a neutral expression to an emotional expression, and indicated as soon as they could which emotion was expressed. Women under the influence of increased testosterone were slower to identify the facial expressions.

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Sexual Orientation

Most people become aware of their sexual orientation early in life, and most—especially men—could hardly imagine changing. The many influences on sexual orientation apparently include genetics and prenatal environment, although the research so far is not definitive. LeVay 2011 provides a good review of this literature.

Abnormal Psychology

Given that behavior and experience are products of brain activity, a study of brain activity should shed light on abnormal psychology. Progress has focused on genetics and brain function. This section concentrates on depression and schizophrenia. Some of the material in the section on Brain Areas in Emotion is also relevant.

Genetic Factors

As reported in a review by Shih, et al. 2004, for every type of abnormal behavior that has been analyzed for genetic influences, genes play an important role, but no one gene is decisive. In the case of depression, people with depression have greater than the average percentage of relatives with anxiety disorders, addictions, migraine headaches, and a wide variety of other problems, as described by Hudson, et al. 2003. Evidently the genes and other factors predisposing to depression are not unique for depression. Rather, they increase vulnerability to many problems. People with late-onset depression are likely to have relatives with circulatory problems, as described by Kendler, et al. 2009. The study suggests we should distinguish early-onset from late-onset depression in future research, including research on treatment. In the case of schizophrenia, researchers have identified at least fourteen genes that appear to be more common among people with schizophrenia than in the general population. However, according to the review by Sanders, et al. 2008, none of these findings can be consistently replicated from one population sample to another. Currently, the most promising hypothesis is that the probability of schizophrenia increases after mutations, deletions, or duplications to any of two or three hundred genes affecting brain development. Given the large number of possibilities, new mutations and deletions may be occurring as fast as natural selection can eliminate them. Walsh, et al. 2008 provides evidence in support of this view.

  • Hudson, J. I., B. Mangweth, H. G. Pope, Jr., C. De Col, A. Hausmann, S. Gutweniger. 2003. Family study of affective spectrum disorder. Archives of General Psychiatry 60:170–177.

    DOI: 10.1001/archpsyc.60.2.170Save Citation »Export Citation »E-mail Citation »

    Someone with depression is likely to have relatives with depression and also likely to have relatives with a wide variety of other psychiatric and medical disorders. Evidently whatever predisposes to depression is a general predisposition that makes the person vulnerable, rather than anything specific to depression.

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  • Kendler, K. S., A. Fiske, C. O. Gardner, and M. Gatz. 2009. Delineation of two genetic pathways to major depression. Biological Psychiatry 65:808–811.

    DOI: 10.1016/j.biopsych.2008.11.015Save Citation »Export Citation »E-mail Citation »

    People with early-onset depression are likely to have relatives with depression. Those with late-onset depression are more likely to have relatives with circulatory problems.

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  • Sanders, A. R., J. Duan, D. F. Levinson, J. Shi, D. He, C. Hou. 2008. No significant association of 14 candidate genes with schizophrenia in a large European ancestry sample: Implications for psychiatric genetics. American Journal of Psychiatry 165:497–506.

    DOI: 10.1176/appi.ajp.2007.07101573Save Citation »Export Citation »E-mail Citation »

    Researchers have identified fourteen genes that appear linked to schizophrenia in at least one population sample. However, none of them shows a significant effect when all populations are combined.

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  • Shih, R. A., P. L. Belmonte, and P. P. Zandi. 2004. A review of the evidence from family, twin and adoption studies for a genetic contribution to adult psychiatric disorders. International Review of Psychiatry 16:260–283.

    DOI: 10.1080/09540260400014401Save Citation »Export Citation »E-mail Citation »

    Genetic factors are important for obsessive-compulsive disorder, panic disorder, depression, bipolar disorder, schizophrenia, and Alzheimer’s disease. However, in no case can we trace the disorder to one or two genes.

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  • Walsh, T., J. M. McClellan, S. E. McCarthy, A. M. Addington, S. B. Pierce, and G. M. Cooper. 2008. Rare structural variants disrupt multiple genes in neurodevelopmental pathways in schizophrenia. Science 320:539–543.

    DOI: 10.1126/science.1155174Save Citation »Export Citation »E-mail Citation »

    Researchers examined people’s chromosomes looking for duplications or deletions of small parts. They found such reproductive errors in 15 percent of people with schizophrenia, as compared to 5 percent of other people.

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Brain Function

The common antidepressant drugs in one way or another prolong or increase the presence of certain neurotransmitters at their synapses, especially the neurotransmitters dopamine, norepinephrine, and serotonin. Some affect one of these transmitters more than others. For decades, researchers have assumed that this observation provides a clue to the nature of depression. That is, they assumed that depression relates to a deficiency of one or more of these transmitters. However, the time course does not fit. Drugs enhance the presence of the transmitters in the synapse within minutes to hours, depending on the drug, but the behavioral improvement does not start until weeks later. To the extent that the drugs alleviate depression, their effects on these neurotransmitters may be irrelevant. A promising hypothesis is that depression relates to shrinkage of cells in the hippocampus and elsewhere, and that antidepressant drugs slowly enhance their growth and connections to other cells. Castrén and Rantamäki 2010 reviews evidence regarding this hypothesis. However, Kirsch 2010 has increased skepticism about antidepressant drugs by highlighting how much of the apparent benefit can be mimicked by placebos. Schizophrenia is, on the average, associated with mild brain abnormalities, which vary from one study to another, as described in Honea, et al. 2005. However, because many people with schizophrenia are also drug abusers, some of the studies have not adequately separated the effects of schizophrenia itself from those of drugs. Rais, et al. 2008 is one article raising this issue. Most current researchers favor the neurodevelopmental hypothesis. According to this hypothesis, abnormalities in brain development, mostly in the second and third trimesters of pregnancy, increase the individual’s vulnerability to developing schizophrenia decades later. Fatemi and Folsom 2009 reviews the status of this hypothesis.

  • Castrén, E., and T. Rantamäki. 2010. The role of BDNF and its receptors in depression and antidepressant drug action: Reactivation of developmental plasticity.

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    Antidepressant drugs lead to increased growth and connections of neurons in the hippocampus and prefrontal cortex, partly by increasing release of a neurotrophic (nerve-growing) factor called BDNF (brain-derived neurotrophic factor).

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  • Fatemi, S. H., and T. D. Folsom. 2009. The neurodevelopmental hypothesis of schizophrenia, revisited. Schizophrenia Bulletin 35:528–548.

    DOI: 10.1093/schbul/sbn187Save Citation »Export Citation »E-mail Citation »

    According to the neurodevelopmental hypothesis, schizophrenia begins with abnormalities of brain development before birth, partly based on genetics and partly based on prenatal environment. This article reviews evidence for this hypothesis.

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  • Honea, R., T. J. Crow, D. Passingham, and C. E. Mackay. 2005. Regional deficits in brain volume in schizophrenia: A meta-analysis of voxel-based morphometry studies. American Journal of Psychiatry 162:2233–2245.

    DOI: 10.1176/appi.ajp.162.12.2233Save Citation »Export Citation »E-mail Citation »

    This article summarizes many studies on brain abnormalities in schizophrenia, showing which brain areas show abnormalities in the largest and fewest studies.

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  • Kirsch, I. 2010. The emperor’s new drugs: Exploding the antidepressant myth. New York: Basic Books.

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    For people with mild to moderate depression, antidepressant drugs do not produce benefits that are statistically superior to those of placebos. Even for people with severe depression, Kirsch finds reason for skepticism about the effectiveness of antidepressant drugs.

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  • Rais, M., W. Cahn, N. Van Haren, H. Schnack, E. Caspers, H. Hulshoff. 2008. Excessive brain volume loss over time in cannabis-using first-episode schizophrenia patients. American Journal of Psychiatry 165:490–496.

    DOI: 10.1176/appi.ajp.2007.07071110Save Citation »Export Citation »E-mail Citation »

    A high percentage of people with schizophrenia abuse drugs. When brain abnormalities are reported among people with schizophrenia, at least part of those deficits may be attributed to the effects of the drugs.

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LAST MODIFIED: 11/29/2011

DOI: 10.1093/OBO/9780199828340-0012

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