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Showing papers in "Behavioral and Brain Sciences in 1982"


Journal ArticleDOI
TL;DR: It is proposed that these drugs reduce anxiety by impairing the functioning of a widespread neural system including the septo-hippocampal system (SHS), the Papez circuit, the prefrontal cortex, and ascending monoaminergic and cholinergic pathways which innervate these forebrain structures.
Abstract: A model of the neuropsychology of anxiety is proposed. The model is based in the first instance upon an analysis of the behavioural effects of the antianxiety drugs (benzodiazepines, barbiturates, and alcohol) in animals. From such psychopharmacologi-cal experiments the concept of a “behavioural inhibition system” (BIS) has been developed. This system responds to novel stimuli or to those associated with punishment or nonreward by inhibiting ongoing behaviour and increasing arousal and attention to the environment. It is activity in the BIS that constitutes anxiety and that is reduced by antianxiety drugs. The effects of the antianxiety drugs in the brain also suggest hypotheses concerning the neural substrate of anxiety. Although the benzodiazepines and barbiturates facilitate the effects of γ-aminobutyrate, this is insufficient to explain their highly specific behavioural effects. Because of similarities between the behavioural effects of certain lesions and those of the antianxiety drugs, it is proposed that these drugs reduce anxiety by impairing the functioning of a widespread neural system including the septo-hippocampal system (SHS), the Papez circuit, the prefrontal cortex, and ascending monoaminergic and cholinergic pathways which innervate these forebrain structures. Analysis of the functions of this system (based on anatomical, physiological, and behavioural data) suggests that it acts as a comparator: it compares predicted to actual sensory events and activates the outputs of the BIS when there is a mismatch or when the predicted event is aversive. Suggestions are made as to the functions of particular pathways within this overall brain system. The resulting theory is applied to the symptoms and treatment of anxiety in man, its relations to depression, and the personality of individuals who are susceptible to anxiety or depression.

4,725 citations


Journal ArticleDOI
Roy A. Wise1
TL;DR: For example, the authors found that the most subtle and interesting effect of neuroleptics is a selective attenuation of motivational arousal which is critical for goal-directed behavior, normally induced by reinforcers and associated environmental stimuli, and normally accompanied by the subjective experience of pleasure.
Abstract: Neuroleptic drugs disrupt the learning and performance of operant habits motivated by a variety of positive reinforcers, including food, water, brain stimulation, intravenous opiates, stimulants, and barbiturates. This disruption has been demonstrated in several kinds of experiments with doses that do not significantly limit normal response capacity. With continuous reinforcement neuroleptics gradually cause responding to cease, as in extinction or satiation. This pattern is not due to satiation, however, because it also occurs with nonsatiating reinforcement (such as saccharin or brain stimulation). Repeated tests with neuroleptics result in earlier and earlier response cessation reminiscent of the kind of decreased resistance to extinction caused by repeated tests without the expected reward. Indeed, withholding reward can have the same effect on responding under later neuroleptic treatment as prior experience with neuroleptics themselves; this suggests that there is a transfer of learning (really unlearning) from nonreward to neuroleptic conditions. These tests under continuous reinforcement schedules suggest that neuroleptics blunt the ability of reinforcers to sustain responding at doses which largely spare the ability of the animal to initiate responding. Animals trained under partial reinforcement, however, do not respond as well during neuroleptic testing as animals trained under continuous reinforcement. Thus, neuroleptics can also impair responding (though not response capacity) that is normally sustained by environmental stimuli (and associated expectancies) in the absence of the primary reinforcer. Neuroleptics also blunt the euphoric impact of amphetamine in humans. These data suggest that the most subtle and interesting effect of neuroleptics is a selective attenuation of motivational arousal which is (a) critical for goal-directed behavior, (b) normally induced by reinforcers and associated environmental stimuli, and (c) normally accompanied by the subjective experience of pleasure. Because these drugs are used to treat schizophrenia and because they cause parkinsonian-like side effects, this action has implications for a better understanding of human pathology as well as normal motivational processes.

1,027 citations


Journal ArticleDOI
TL;DR: The possibility that emotions are elaborated by transhypothalamic executive circuits that concurrently activate related behavior patterns is assessed and the manner in which learning and psychiatric disorders may arise from activities of such circuits is discussed.
Abstract: Emotions seem to arise ultimately from hard-wired neural circuits in the visceral-limbic brain that facilitate diverse and adaptive behavioral and physiological responses to major classes of environmental challenges. Presumably these circuits developed early in mammalian brain evolution, and the underlying control mechanisms remain similar in humans and “lower” mammals. This would suggest that theoretically guided studies of the animal brain can reveal how primitive emotions are organized in the human brain. Conversely, granted this cross-species heritage, it is arguable that human introspective access to emotional states may provide direct information concerning operations of emotive circuits and thus be a primary source of hypotheses for animal brain research. In this article the possibility that emotions are elaborated by transhypothalamic executive (command) circuits that concurrently activate related behavior patterns is assessed. Current neurobehavioral evidence indicates that there are at least four executive circuits of this type – those which elaborate central states of expectancy, rage, fear, and panic. The manner in which learning and psychiatric disorders may arise from activities of such circuits is also discussed.

880 citations


Journal ArticleDOI
TL;DR: In this article, an attempt to study the peer-review process directly, in the natural setting of actual journal referee evaluations of submitted manuscripts, was made. But the results showed that only three (8%) of the 38 editors and reviewers detected the resubmissions.
Abstract: A growing interest in and concern about the adequacy and fairness of modern peer-review practices in publication and funding are apparent across a wide range of scientific disciplines. Although questions about reliability, accountability, reviewer bias, and competence have been raised, there has been very little direct research on these variables.The present investigation was an attempt to study the peer-review process directly, in the natural setting of actual journal referee evaluations of submitted manuscripts. As test materials we selected 12 already published research articles by investigators from prestigious and highly productive American psychology departments, one article from each of 12 highly regarded and widely read American psychology journals with high rejection rates (80%) and nonblind refereeing practices.With fictitious names and institutions substituted for the original ones (e.g., Tri-Valley Center for Human Potential), the altered manuscripts were formally resubmitted to the journals that had originally refereed and published them 18 to 32 months earlier. Of the sample of 38 editors and reviewers, only three (8%) detected the resubmissions. This result allowed nine of the 12 articles to continue through the review process to receive an actual evaluation: eight of the nine were rejected. Sixteen of the 18 referees (89%) recommended against publication and the editors concurred. The grounds for rejection were in many cases described as “serious methodological flaws.” A number of possible interpretations of these data are reviewed and evaluated.

879 citations


Journal ArticleDOI
TL;DR: It is concluded that different physical variables can be controlled depending on the type of limb movement required, and the concept of stiffness regulation should probably be extended to the regulation of the visco-elastic properties of a muscle or joint.
Abstract: To control force accurately under a wide range of behavioral conditions, the central nervous system would either require a detailed, continuously updated representation of the state of each muscle (and the load against which each is acting) or else force feedback with sufficient gain to cope with variations in the properties of the muscles and loads. The evidence for force feedback with adequate gain or for an appropriate central representation is not sufficient to conclude that force is the major controlled variable in normal limb movements.Morton's hypothesis, that length is controlled by a follow-up servo, has a number of difficulties related to the delays, gains, variability, and specificity in feedback pathways comprising potential servo loops. However, experimental evidence is consistent with these pathways providing servo assistance for some movements produced by coactivation of α- and static γ-motoneurons. Dynamic γ-motoneurons may provide an additional input for adaptive control of different types of movements.The idea that feedback is used to compensate for changes in muscle stiffness has received experimental support under static postural conditions. However, reflexes tend to increase rather than decrease the range of variation in muscle stiffness during some cyclic movements. Theoretical problems associated with the regulation of stiffness are also discussed. The possibilities of separate control systems for velocity or viscosity are considered, but the evidence is either negative or lacking. I conclude that different physical variables can be controlled depending on the type of limb movement required. The concept of stiffness regulation is also useful under some conditions, but should probably be extended to the regulation of the visco-elastic properties (i.e., the mechanical impedance) of a muscle or joint.

425 citations


Journal ArticleDOI
TL;DR: It is suggested that the effects of stressful experiences on affective state may be related to depletion of several neurotransmitters, including norepinephrine, dopamine, and serotonin, which contributes to behavioral depression.
Abstract: Aversive experiences have been thought to provoke or exacerbate clinical depression. The present review provides a brief survey of the stress-depression literature and suggests that the effects of stressful experiences on affective state may be related to depletion of several neurotransmitters, including norepinephrine, dopamine, and serotonin. A major element in determining the neurochemical changes is the organism's ability to cope with the aversive stimuli through behavioral means. Aversive experiences give rise to behavioral attempts to cope with the stressor, coupled with increased utilization and synthesis of brain amines to contend with environmental demands. When behavioral coping is possible, neurochemical systems are not overly taxed, and behavioral pathology will not ensue. However, when there can be no behavioral control over the stressful stimuli, or when the aversive experience is perceived as uncontrollable, increased emphasis is placed on coping through endogenous neurochemical mechanisms. Amine utilization increases appreciably and may exceed synthesis, resulting in a net reduction of amine stores, which in turn promotes or exacerbates affective disorder. The processes governing the depletions may be subject to sensitization or conditioning, such that exposure to traumatic experiences may have long-term repercussions when the organism subsequently encounters related stressful stimuli. With continued uncontrollable stimulation, adaptation occurs in the form of increased activity of synthetic enzymes, and levels of amines approach basal values. It is suggested that either the initial amine depletion provoked by aversive experiences or a dysfunction of the adaptive processes, resulting in persistent amine depletion, contributes to behavioral depression. Aside from the contribution of behavioral coping, several organismic, experiential, and environmental variables will influence the effects of aversive experiences on neurochemical activity, and may thus influence vulnerability to depression.

418 citations


Journal ArticleDOI
TL;DR: A metatheoretical view of representation is developed and Objections to the use of this concept in explanations of animal behavior, based on the claim that it is indeterminate and on behaviorist considerations of parsimony can be answered.
Abstract: A representation is a remnant of previous experience that allows that experience to affect later behavior. This paper develops a metatheoretical view of representation and applies it to issues concerning representation in animals. To describe a representational system one must specify the following: the domain or range of situations in the represented world to which the system applies; the content or set of features encoded and preserved by the system; the code or transformational rules relating features of the representation to the corresponding features of the represented world; the medium, or the representation's physical instantiation; and the dynamics, or how the system changes with time. In part because of the behaviorist assumption that the hypothetical, covert changes occurring in an organism during learning correspond to the overt physical changes that are observed, issues of representation in animal behavior have been largely ignored as irrelevant or misleading. However, it can be inferred that representations, acting as models of environmental regularities, operate at many levels of behavioral functioning, both cognitive and noncognitive. Objections to the use of this concept in explanations of animal behavior, based on the claim that it is indeterminate and on behaviorist considerations of parsimony, can be answered. Animal representations may be specialized in terms of tasks and species. Data from tasks involving spatial memory, delayed matching-to-sample, and sequence learning suggest some foundations for a general theory of animal representations.

407 citations


Journal ArticleDOI
TL;DR: In this paper, the authors suggest that play is a distinctive behavioural category whose adaptive significance calls for explanation, and that play primarily affords juveniles practice toward the exercise of later skills.
Abstract: In this paper I suggest that play is a distinctive behavioural category whose adaptive significance calls for explanation. Play primarily affords juveniles practice toward the exercise of later skills. Its benefits exceed its costs when sufficient practice would otherwise be unlikely or unsafe, as is particularly true with physical skills and socially competitive ones. Manipulative play with objects is a byproduct of increased intelligence, specifically selected for only in a few advanced primates, notably the chimpanzee.The adaptiveness of play in pongid evolution is traced through the probable changes in selective pressures that occurred in hominid evolution. It is argued that fantasy was an emergent property in hominids, made possible by symbolic intelligence and language, and serving to make play complex enough to continue to provide useful practice for increasingly complex later skills.The advent of organised instruction and education has meant that play's unplanned, intrinisic goal-setting could be replaced by extrinsic goal-setting in the systematic development of particular skills. However, the need to ensure adequate motivation has continued to give play educational value. In addition, its capacity to enhance innovative behaviour seems to be a residual function of play which has acquired a new cultural importance.

374 citations


Journal ArticleDOI

264 citations


Journal ArticleDOI
TL;DR: In this paper, several popular hypotheses about what, precisely, is wrong with schizophrenic speech and language have been evaluated, ranging from assertions that schizophrenics have peculiar word association hierarchies to the notion that schizophrenia is suffering from an intermittent form of aphasia.
Abstract: Among the many peculiarities of schizophrenics perhaps the most obvious is their tendency to say odd things. Indeed, for most clinicians, the hallmark of schizophrenia is “thought disorder” (which is usually defined tautologically as incoherent speech). Decades of clinical observations, experimental research, and linguistic analyses have produced many hypotheses about what, precisely, is wrong with schizophrenic speech and language. These hypotheses range from assertions that schizophrenics have peculiar word association hierarchies to the notion that schizophrenics are suffering from an intermittent form of aphasia. In this article, several popular hypotheses (and the observations on which they are based) are critically assessed. Work in the area turns out to be flawed by errors in experimental method, faulty observations, tautological reasoning, and theoretical models that ignore the complexities of both speech and language. This does not mean that schizophrenics are indistinguishable from nonschizophrenics. They are clearly deviant in many situations. Their problem, however, appears to be in processing information and in selective attention, not in language itself.

210 citations


Journal ArticleDOI
TL;DR: The model has implications for the study of parallels between appetitive and aversive motivation, sign tracking in aversive conditioning, and orientation of flight responses, and evidence that some avoidance responses are much more easily learned than others.
Abstract: A motivational system approach to avoidance behavior is presented. According to this approach, a motivational state increases the probability of relevant response patterns and establishes the appropriate or “ideal” consummatory stimuli as positive reinforcers. In the case of feeding motivation, for example, hungry rats are likely to explore and gnaw, and to learn to persist in activities correlated with the reception of consummatory stimuli produced by ingestion of palatable substances. In the case of defense motivation, fearful rats are likely to flee or freeze, and to learn to persist in activities correlated with consummatory stimuli produced by flight from a dangerous place. Defense system activation is distinct from alarm reactions. The latter prepare the animal for probable noxious events, involve relatively intense negative affect and extinguish rapidly in situations where the noxious event no longer occurs. In contrast, defense system activation potentiates innate and modified defense reactions, thus preparing the animal for possible, but not necessarily probable, noxious events; it involves little or no negative affect and extinguishes very slowly when the noxious event no longer occurs. With these assumptions and the resulting model we attempt to resolve several long-standing problems in avoidance learning, including the low correlation between negative affect and avoidance performance, differential rates of extinction for avoidance performance and conditioned emotional responses, and evidence that some avoidance responses are much more easily learned than others. In addition, the model has implications for the study of parallels between appetitive and aversive motivation, sign tracking in aversive conditioning, and orientation of flight responses. Historical antecedents and alternative approaches are discussed.

Journal ArticleDOI
TL;DR: The Author's Formula as discussed by the authors is a set of rules that authors can use to increase the likelihood and speed of acceptance of their manuscripts, such as not picking an important problem, not challenging existing beliefs, not obtaining surprising results, not using simple methods, not providing full disclosure, and not writing clearly.
Abstract: Recently I completed a review of the empirical research on scientific journals (Armstrong 1982). This review provided evidence for an “author’s formula,” a set of rules that authors can use to increase the likelihood and speed of acceptance of their manuscripts. Authors should: (1) not pick an important problem, (2) not challenge existing beliefs, (3) not obtain surprising results, (4) not use simple methods, (5) not provide full disclosure, and (6) not write clearly. Peters & Ceci (PC 1980), they broke most of the rules.



Journal ArticleDOI
TL;DR: The world graph model is offered as a representation of relationships among situations the animal has encountered and may encounter again, and algorithms for how the information encoded in the world graph may be used by the animal in determining its behavior are offered.
Abstract: We argue that a map is meaningless unless we have a process for using it. Thus, in this paper, we not only offer the world graph as a representation of relationships among situations the animal has encountered and may encounter again, but we also offer algorithms for how the information encoded in the world graph may be used by the animal in determining its behavior. Each node of the graph encodes a recognizable situation in the animal's world, but a given place may well be encoded in a number of different nodes. Nodes not only require algorithms for the recognition of the situation; they store information about drive reduction associated with the encoded situation. We note that the use of graphs as a basis for exploring some search space is well known in artificial intelligence (AI), but we stress the importance of the animal's exploration of its environment for growing the graph, as distinct from the mathematically described potential nodes frequent in AI search spaces. To explore a number of hypotheses about the way information in the world graph is used to guide the animal's movement, we recall a number of classical experiments on maze exploration by animals, and use them to argue for the nonlocal hypothesis (selection of a path does not depend only upon information about the immediate environment of the animal) and the competing nodes hypothesis (more than one drive may enter into the determination of the animal's behavior at any time). An important feature of the model is that it yields exploration and latent learning without the introduction of an exploratory drive. We also note that the performance exhibited by the model appears to be state-dependent when the animal operates under high drive levels. The drive-interaction matrix is offered as a subject for future research.We complement the presentation of the world graph model, its drive dynamics, and how these are constrained by experiments on maze behavior, with a brief analysis of maps in the brain. We distinguish egocentric maps–which we relate to the many visual systems–from allocentric maps. We offer a somewhat unconventional view of short-term and long-term memory. We examine cooperative computation in somatotopically organized networks, relating this to visually guided behavior in the frog, and to the interaction of colliculus and cortex in the control of eye movements. We examine, but do not advocate, the hypothesis that the hippocampus is a cognitive map. We do stress that if it is a cognitive map, it must be seen as a chart of the local neighborhood, rather than the whole atlas; and we note that the cognitive map hypothesis would lead one to expect the region to exhibit activation of place cells before the animal leaves the previous place.

Journal ArticleDOI
TL;DR: The process of gene-culture coevolution is characterized, in which culture is shaped by biological imperatives while biological traits are simultaneously altered by genetic evolution in response to cultural history.
Abstract: Despite its importance, the linkage between genetic and cultural evolution has until now been little explored. An understanding of this linkage is needed to extend evolutionary theory so that it can deal for the first time with the phenomena of mind and human social history. We characterize the process of gene-culture coevolution, in which culture is shaped by biological imperatives while biological traits are simultaneously altered by genetic evolution in response to cultural history. A case is made from both theory and evidence that genetic and cultural evolution are inseverable, and that the human mind has tended to evolve so as to bias individuals toward certain patterns of cognition and choice rather than others. With the aid of mathematical models we trace the coevolutionary circuit: The genes prescribe structure in developmental pathways that lay down endocrine and neural systems, imposing regularities in the development of cognition and behavior; these regularities (loosely labeled “epigenetic rules”) translate upward into holistic patterns of culture, which can be predicted in the form of probability density distributions (ethnographic curves); natural selection acts within human history to favor certain epigenetic rules over others; and the selection alters the frequencies of the underlying genes. The effects of genetic and cultural changes reverberate throughout the circuit and are consequently tested with the passage of each life cycle. In addition to modeling gene-culture coevolution, we apply methods from island biogeography and information theory to examine the cultural capacity of the genes, the factors determining the magnitude of cultural diversity, and the possible reasons for the uniqueness of the human achievement.



Journal ArticleDOI
TL;DR: In this article, the authors focus on the implicit assumptions behind the question posed by Stein; if nothing else they hope to heighten sensi tivity to some of the issues involved and (perhaps) to force the neuroscientist to consider his/her epistemology.
Abstract: When we are confronted with a living system, whose design is mysterious and whose optimizations are obscure, it is no easy task--as Professor Stein reminds us--to arrive at an answer to the question he has posed in this paper. Stein's target article is an important contribution for two main reasons. The first, which we shall mention only in passing, is that it is likely to provide much debate on what the controlled variables might be; moreover, it will force those who find this a burning issue to put their cards on the table. The second, and we feel more important reason, is that the paper poses a question--\"What muscle variable(s) does the nervous system control. .. ?\"--whose very nature raises questions about the strategies neuroscience uses to investigate problems of control and coordination of movement. In our commentary we will focus on some of the (not so) implicit assumptions behind the question posed by Stein; if nothing else we hope to heighten sensi tivity to some of the issues involved and (perhaps) to force the neuroscientist to consider his/her epistemology.





Journal ArticleDOI
TL;DR: Panksepp and Biven as discussed by the authors described a taxonomy of the primary-process affective network in mammals, which includes the seeking, rage, fear, lust, care, grief, and play network.
Abstract: Jaak Panksepp and Lucy Biven (2012) New York: W.W. Norton & Company, Inc. ix + 547 pp. There have been several attempts to theorize about the origin of the brain and its modular functions by drawing upon the microevolutionary processes and their distal impact on macroevolution. Most of these attempts have focused on explaining the emergence and the expansion of the phylogenetically recent neopallium and its functions in behavioral and cognitive systems (Geary, 2005; McNally et al., 2012). In contrast, there has been little attempt to characterize the evolutionary basis of human emotionsVa collection of systems with activity grounded in the phylogenetically ancient allocortex. Cognitive information processing is behaviorally and functionally distinct from affective processingVwhereas the former involves the neocortical encoding of information gleaned from the environment through the senses, the latter originates from subcortical structures in the form of ‘‘diffuse global states’’ that may be cognitively processed into higher emotions. Panksepp and Biven have now published a text that delves with great detail into the neural architecture of the human emotional life, with particular focus on its ancestral origins. This is a worthwhile endeavor, with implications for preclinical and clinical models of aberrant emotional behavior and regulation. In summary, Panksepp and Biven’s model is as follows. The emotional ‘‘brainmind’’ system is adaptive for providing humans and other living entities for which this structure has evolved intrinsic and evaluative information about their progress in the quest for survival. Whereas positive emotions are indicative of the experience of situations that are positively correlated with survival, negative emotions may be outcomes of the evaluation of situations that negatively correlate with survival. These ‘‘raw’’ emotions are ‘‘ancestral memories’’ that have been phylogenetically important for survival and, as such, have been genetically coded to be inborn capacities. The bulk of the text focuses on their essential nature as primary-process instinctual emotionsVthe most basic, primordial affective processes. Primary-process emotions are most important (or influential) in infants and other mammals. Here, these generate fixed (instinctual) behavioral responses and emotional arousal to a specific set or finite number of precipitating events. Although primary-process emotions initially control higher brain cognitive activities, with normal development, the higher cognitive abilities rooted in the neocortex come to control primary-process emotions. In Panksepp and Biven’s organization of the levels of emotional control, primary-process emotional networks regulate secondary-process emotions. Secondary-process emotions are unintentional learning and memory mechanisms grounded in the basal ganglia that include simple classical conditioning, instrumental and operant learning, and behavioral and emotional habits. During the course of development, these learning-memory mechanisms create object relations and contingencies that become linked to tertiary affects and neocortical awareness functions. Tertiary processes include emotional ruminations, evaluations, and thoughts that influence free will and intentions to act. Panksepp and Biven describewith illustrations the taxonomy of the primary-process affective network in mammals. This network comprises at least seven emotional systems, homologous across mammalian species, with neurobiology grounded in subneocortical structures. These include the seeking, rage, fear, lust, care, grief, and play network systemsVthe most important being the seeking system. It is clear from the text that one of its goals was to underscore the continuity that exists between humans and other mammals in the neural archeology and experience of emotions. The authors do this by emphasizing commonalities across species in emotional action patterns, learning and memory, and neural circuits, but this is balanced with a discussion of species-specific differences. The book is a collaboration of a neuroscientist and a clinician; as such, although the basic neurobiology of ‘‘normal’’ and ‘‘aberrant’’ affective systems is often in view, Panksepp and Biven give extensive treatment to issues relevant to clinicians such as substance addiction (e.g., pp. 192, 326, 361, 384), aggression (pp. 157Y158, 164Y 167), mood disorders (e.g., pp. 326Y337, 335Y 339, 457Y461, 479Y483), anxiety disorders (e.g., pp. 176Y191, 469Y474), schizophrenia (e.g., pp. 108Y110, 300, 441), psychological well-being (pp. 418Y420), and psychotherapy (pp. 425Y474). Clinicians involved in the treatment of posttraumatic stress disorder may find the authors’ favorable treatment of eye movement desensitization and reprocessing (EMDR) slightly one sided (pp. 468Y474) for an intervention that remains questionable in the view of many psychologists with regard to its theoretical foundations (e.g., Herbert et al., 2000). Although EMDR’s therapeutic benefits are not in question, it has been argued that it simply capitalizes on prolonged exposure, much like several other treatments of anxiety disorders, and that its characteristic eye movements to facilitate accelerated processing are pseudoscientific claims. The authors venture an explanation of the benefits of eye movementsVeye movements have neural circuits in the superior colliculi, which lie near the dorsal region of the periaqueductal gray (the negative affective regions of the periaqueductal gray). Eye movements may diffuse negative emotions by inhibiting neural networks that may contribute to negative emotions. The authors also venture the possibility that traumatic memories undergo modification (or recontextualization) during EMDR at a primary-process affective level, such that by the time the memories are reintegrated and reconsolidated into memory banks, these have been diffused of negative emotion. The authors acknowledge that there is no current neuroscientific evidence for this putative mechanism of action; however, some testable predictions that prove or disprove their hypothesis would have been welcome. Our own interest in Panksepp and Biven’s view of the archaeology of emotions draws from clinical and research interest in the phenomenology and treatment of schizophrenia and other psychotic disorders. As noted by the authors, dopamine hyperactivity in the seeking system, particularly at D2 receptors, is implicated in psychosis. Although part of the same core abnormality, this cause-effect is more direct in frank hallucinations rather than strongly held delusional beliefs, which require disturbance in error-dependent updating of beliefs and inferences characterized by deviant Bayesian inferences, prediction error signaling, and jumping-to-conclusions as espoused by information processing models (Fletcher and Frith, 2009). Antipsychotic treatments operate by blocking dopamine activity at receptor sites but also have the unfortunate consequence of decreasing an individual’s natural seeking tendencies. This generally contributes to a constellation of behaviors that mimic negative symptoms in schizophrenia. One puzzling aspect of schizophrenia is the diminished expression of positive or negative emotions (i.e., restricted emotional range) and blunted affect in a subset of patients with schizophrenia with prominent, idiopathic negative symptoms (Kirkpatrick et al., 2001; Suslow et al., 2003) and increased negative emotionality in patients with nondeficit schizophrenia. Positive symptoms are less crucial to a deficit classification, although comparisons between patients with deficit and nondeficit schizophrenia suggest comparable degrees of severity in positive symptoms (Cohen et al., 2010; Galderisi et al., 2002). Panksepp andBiven’smodelwould seem less successful at explaining co-occurring or idiopathic negative symptoms in some people with schizophrenia given that symptoms of anhedonia, avolition, asociality, and affective flattening appear inconsistent with an overactive seeking system. There has also been some suggestion that anticipatory but not consummatory pleasure deficits may be more robust in people with schizophrenia (e.g., Gard et al., 2007), which appears to run counter to an overactive seeking system. Similarly, whereas manic/hypomanic hyperactivation, cyclothymia, behavioral dysregulation, rapid cycling, and mixed episodes in BOOK REVIEW




Journal ArticleDOI
TL;DR: It is suggested that many asymmetries appear to be under the influence of a left-right maturational gradient, which often seems to favor earlier or more rapid development on the left than on the right, and that the phenomenon of equipotentiality should be unidirectional.
Abstract: of the original article, Part I: In this paper, we consider human handedness and cerebral lateralization in a general biological context, and attempt to arrive at some conclusions common to the growth of human laterality and of other structural asymmetries. We suggest that many asymmetries appear to be under the influence of a left-right maturational gradient, which often seems to favor earlier or more rapid development on the left than on the right. If the leading side is damaged or restricted, this gradient may be reversed so that growth occurs with the opposite polarity. A mechanism of this sort appears to underlie the phenomenon of situs inversus viscertim et cordis, and the same principle may help explain the equipotentiality of the two sides of the human brain with respect to the representation of language in the early years of life. However we must also suppose that the leading side normally exerts an inhibitory influence on the lagging side, for otherwise one would expect language ultimately to develop in both halves of the brain. Examples of an inhibitory influence of this kind can also be found in other biological asymmetries; for instance, in the crab Alpheus heterochelis, one claw is normally greatly enlarged relative to the other, but if the larger claw is removed the smaller one is apparently released from its inhibitory influence and grows larger. Although this account does not deny that the right hemisphere of humans may be the more specialized for certain functions, it does attribute a leading or dominant role to the left hemisphere (at least in most individuals). We suggest that so-called right-hemisphere functions are essentially acquired by default, due to the left hemisphere's prior involvement with speech and skilled motor acts; we note, for instance, that these right-hemisphere functions include rather elementary perceptual processes. But perhaps the more critical prediction from our account is that the phenomenon of equipotentiality should be unidirectional: the right (lagging) hemisphere should be more disposed to take over left-hemisphere functions following early lesions than is the left (leading) hemisphere to take over right-hemisphere functions. We note preliminary evidence that this may be so. THE BEHAVIORAL AND BRAIN SCIENCES (5) 2 261 Continuing Commentary Abstract of the original article, Part II: This paper focuses on the inheritance of human handedness and cerebral lateralization within the more general context of structural biological asymmetries. The morphogenesis of asymmetrical structures, such as the heart in vertebrates, depends upon a complex interaction between information coded in the cytoplasm and in the genes, but the polarity of asymmetry seems to depend on the cytoplasmic rather than the genetic code. Indeed it is extremely difficult to find clear-cut examples in which the direction of an asymmetry is under genetic control. As one possible case, there is some evidence that the direction, clockwise or counterclockwise, of rotation of the abdomen in certain mutant strains of Drosophila is controlled by a particular gene locus, although there appears to be some degree of confusion on this point. By contrast, it is much easier to find examples in which the degree but not the direction of asymmetry is under genetic control. For instance, there is a mutant strain of mice in which half of the animals display situs inversus of the viscera. The proportion has remained at one half despite many years of inbreeding, suggesting that the mutant allele effectively cancels the normal situs and allows the asymmetry to be specified in random fashion.of the original article, Part II: This paper focuses on the inheritance of human handedness and cerebral lateralization within the more general context of structural biological asymmetries. The morphogenesis of asymmetrical structures, such as the heart in vertebrates, depends upon a complex interaction between information coded in the cytoplasm and in the genes, but the polarity of asymmetry seems to depend on the cytoplasmic rather than the genetic code. Indeed it is extremely difficult to find clear-cut examples in which the direction of an asymmetry is under genetic control. As one possible case, there is some evidence that the direction, clockwise or counterclockwise, of rotation of the abdomen in certain mutant strains of Drosophila is controlled by a particular gene locus, although there appears to be some degree of confusion on this point. By contrast, it is much easier to find examples in which the degree but not the direction of asymmetry is under genetic control. For instance, there is a mutant strain of mice in which half of the animals display situs inversus of the viscera. The proportion has remained at one half despite many years of inbreeding, suggesting that the mutant allele effectively cancels the normal situs and allows the asymmetry to be specified in random fashion. This last example is particularly interesting because it suggests a mechanism comparable to that proposed by Annett to account for the distribution of handedness in the human population. She argued, in effect, that there is a \"right shift\" factor among the majority of the population, but that among a minority who lack this factor handedness is determined at random. If it is supposed that cerebral lateralization is also determined at random among this recessive minority, the model can be extended to provide a reasonable fit to the data on the correlation between handedness and cerebral lateralization. However this genetic model (or any other) still fails to account for the near-binomial distribution of handedness among twins and among nontwin siblings. We suggest that right-handedness and left-cerebral dominance for language are manifestations of an underlying gradient which is probably coded in the cytoplasm rather than in the genes. We leave open the question of whether departures from this pattern are due to a recessive gene which effectively cancels the asymmetry, to environmental influences, or to both genetic and cytoplasmic factors. Flatfishes and the inheritance of asymmetries