The precise relationship between the autonomic nervous system and emotion has been a topic of intense debate and research throughout the history of modern psychology. The present article considers some of the more influential theoretical frameworks that continue to drive contemporary research on the relationship between emotion and physiological processes. In particular, we highlight the multiple routes through which somatovisceral afference influences emotion and how this relates to the topic of emotion-specific patterns of autonomic nervous system activity.

There is considerable evidence that the hippocampal system contributes both to (1) the temporary maintenance of memories and to (2) the processing of a particular type of memory representation. The findings on amnesia suggest that these two distinguishing features of hippocampal memory processing are orthogonal. Together with anatomical and physiological data, the neuropsychological findings support a model of cortico-hippocampal interactions in which the temporal and representational properties of hippocampal memory processing are mediated separately. We propose that neocortical association areas maintain (...) shortterm memories for specific items and events prior to hippocampal processing as well as providing the final repositories of long-term memory. The parahippocampal region supports intermediate-term storage of individual items, and the hippocampal formation itself mediates an organization of memories according to relevant relationships among items. Hippocampal-cortical interactions produce (i) strong and persistent memories for events, including their constituent elements and the relationships among them, and (ii) a capacity to express memories flexibly across a wide range of circumstances. (shrink)

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 in animals. From such psychopharmacologi-cal experiments the concept of a “behavioural inhibition system” 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, the Papez circuit, the prefrontal cortex, and ascending monoaminergic and cholinergic pathways which innervate these forebrain structures. Analysis of the functions of this system 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. (shrink)

A comparative method of studying the biological bases of personality compares human trait dimensions with likely animal models in terms of genetic determination and common biological correlates. The approach is applied to the trait of sensation seeking, which is defined on the human level by a questionnaire, reports of experience, and observations of behavior, and on the animal level by general activity, behavior in novel situations, and certain types of naturalistic behavior in animal colonies. Moderately high genetic determination has been (...) found for human sensation seeking, and marked strain differences in rodents have been found in open-field behavior that may be related to basic differences in brain neurochemistry. Agonistic and sociable behaviors in both animals and humans and the trait measure of sensation seeking in humans have been related to certain common biological correlates such as gonadal hormones, monoamine oxidase (MAO), and augmenting of the cortical evoked potential.The monoamine systems in the rodent brain are involved in general activity, exploratory behavior, emotionality, socialization, dominance, sexual and consummately behaviors, and intracranial self-stimulation. Preliminary studies have related norepinephrine and enzymes involved in its production and degradation to human sensation seeking. A model is suggested that relates mood, behavioral activity, sociability, and clinical states to activity of the central catecholamine neurotransmitters and to neuroregulators and other transmitters that act in opposite ways on behavior or stabilize activity in the arousal systems. Stimulation and behavioral activity act on the catecholamine systems in a brain–behavior feedback loop. At optimal levels of catecholamine systems activity (CSA) mood is positive and activity and sociability are adaptive. At very low or very high levels of CSA mood is dysphoric, activity is restricted or stereotyped, and the organism is unsocial or aggressively antisocial. Novelty, in the absence of threat, may be rewarding through activation of noradrenergic neurons. (shrink)

Animal research suggests that central serotonergic neurons are involved in behavioral suppression, particularly anxiety-related inhibition. The hypothesis linking decreased serotonin transmission to reduced anxiety as the mechanism in the anxiolytic activity of benzodiazepines conflicts with most clinical observations. Serotonin antagonists show no marked capacity to alleviate anxiety. On the other hand, clinical signs of reduced serotonergic transmission (low 5-HIAA levels in the cerebrospinal fluid) are frequently associated with aggressiveness, suicide attempts, and increased anxiety. The target article attempts to reconcile such (...) human and animal findings by investigating whether anxiety reduction or increased impulsivity is more Likely to account for animal behavioral changes associated with decreased serotonergic transmission. The effects of manipulating central serotonin in experimental anxiety paradigms in animals (punishment, extinction, novelty) are reviewed and compared with the effects of antianxiety drugs. Anxiety seems neither necessary nor sufficient to induce control by serotonergic neurons on behavior. Further evidence suggests that behavioral effects of anxiolytics thought to be mediated by decreases in anxiety are not caused by the ability of these drugs to reduce serotonin transmission. Blockade of serotonin transmission, especially at the level of the substantia nigra, results in a shift of behavior toward facilitation of responding. This behavioral shift is particularly marked when there is competition between acting and restraining response tendencies and when obstacles prevent the immediate attainment of an anticipated reward. It is proposed that serotonergic neurons are involved not only in behavioral arousal but also in enabling the organism to arrange or tolerate delay before acting. Decreases in serotonin transmission seem to be associated with the increased performance of behaviors that are usually suppressed, though not necessarily because of the alleviation of anxiety, which might contribute to the suppression. (shrink)

To explore the mechanism of sensation correlations between EP component amplitude and signal detection indices were studied. The time of sensation coincided with the peak latency of those EP components that showed a correlation with both indices. The components presumably reflected information synthesis in projection cortical neurons. A mechanism providing the synthesis process is proposed.

Gray's integration of the different levels of description and explanation in his theory is problematic: The introduction of consciousness into his theorising consists of the mind-brain identity assumption, which tells us nothing new. There need not be correlations between levels of description. Gray's account does not extend beyond “brute” correlation. Integration must be achieved in a principled, mutually constraining way.

The commentary argues that we cannot be sure that human consciousness has survival value and that in order to understand the origins and, perhaps, the function of consciousness, we should examine the behavioural and neural precursors to consciousness in nonhumans. An example is given of research on the role of context in decisions regarding fleeing from probable predators in the Mongolian gerbil.

Gray has expanded his account of schizophrenia to explain consciousness as well. His theory explains neither phenomenon adequately because he treats individual minds in isolation. The primary function of consciousness is to permit high level interactions with other conscious beings. The key symptoms of schizophrenia reflect a failure of this mechanism.

Evidence abounds of a close relation between ingestive and affective processes in rats and in humans. Emotional distress alters food intake and body weight; conversely, alterations in eating and weight influence emotional health. Thorough experimental analysis of the ingestion-affect relation may clarify the mechanisms of anxiety and depression. A strategy is proposed for examination of environmental and dispositional determinants of ingestive processes, emotionality, and responses to stress.

The psychological mechanisms implicated in psychopathy do not limit their activity to those behaviors that support a cheater strategy in social games. They result in a number of other clearly maladaptive behaviors that do not directly involve other individuals. Thus, any gains that might arise from the use of a cheater strategy in social situations are probably lost elsewhere.

As more criminals are imprisoned, other individuals change their behavior to replace them, as predicted by the theory of strategic behavior. The physiological correlates of sociopathy suggest that research in cognitive neuroscience can lead toward a solution. Promising pathways include building upon current knowledge of self-deceit, the independence of positive and negative emotions, the lateralization of risk and caution, and the conditions promoting prosocial behavior.

It is often presumed that effects of neural tissue transplants are due to release of neurotransmitter. In many cases, however, effects attributed to transplants may be related to phenomena such as trophic effects mediated by glial cells or even tissue reactions to injury. Any conclusion regarding causation of graft effects must be based on the control groups or other comparisons used. In human clinical studies, for example, comparing the same subject before and after transplantation allows for many interpretations of the (...) causes of clinical changes. (shrink)

Although Mealey's account provides several interesting hypotheses, her integration across disparate samples renders the value of her explanation for psychopathy ambiguous. Recent evidence on Psychopathy Checklist-identified samples (Hare, 1991) suggests primary emotional and cognitive deficits inconsistent with her model. Whereas high-anxious psychopaths display interpersonal deficits consistent with Mealey's hypotheses, low-anxious psychopaths' deficits appear more sensitive to situational parameters than predicted.

Strengths of Mealey's target article are its implementation of results from game-theoretic analyses and its potential links with other formal developments. In recent dynamic decision/choice models, reduced salience of avoidance tendencies, said to typify primary sociopaths, has quantifiable consequences for response latencies and choices. Also, formal models of stress effects on information processing predict selected effects of hypoarousability.

If sociopathy is a biological adaptation, it probably evolved in small social groups in which individuals lacked the social mobility required for a con-man strategy to work. On the other hand, conflicts between groups may have provided a large niche for sociopathy throughout human history.

This commentary extends arousal theory to suggest an explanation for the well-established inverse correlation between church attendance and involvement in crime. In addition, the results of two surveys of social scientists are reviewed to reveal just how little impact the biosocial/sociobiological perspective has had thus far on social science.

Mealey distinguishes two types of sociopathy: (1) or obligate, and (2) or facultative. Either sociopathy evolved twice, or one form is derived from the other, e.g., through: (1) genetic assimilation generating polymorphism in the relative strength of biases favoring the development of otherwise facultative strategies, or (2) independently heritable but strategically relevant characteristics biasing the optimal selection of facultative strategies.

Although serotonin, testosterone, and genes contribute to sociopathy, the relationships are probably indirect and subject to modifiers (e.g., present only under certain conditions of rearing and temperament). Age at menarche may be a marker variable as well as a causal factor. Since the genders differ in all four areas, sex differences in sociopathy represent a very complex interaction of these factors.

Recent studies lend support to the two-pathway model of the evolution of sociopathy with evidence that: 1) psychopathy (primary sociopathy) is a discrete type and 2) in general, sociopaths have relatively high levels of reproductive success. Hare's Psychopathy Checklist may provide a start for the revision of terminology that will be necessary to distinguish between primary and secondary trajectories.

Questions are raised about several issues discussed by Mealey: (1) the nature of the distinction between primary and secondary sociopaths, (2) some difficulties with a general arousal theory of criminality, and (3) the possible role of countervailing forces in the development of sociopathy. An important area that calls for attention is the patterning of different specific emotions in the lives of sociopaths as compared to other groups.

Grafts of embryonic neural tissue into the brains of adult patients are currently being used to treat Parkinson's disease and are under serious consideration as therapy for a variety of other degenerative and traumatic disorders. This target article evaluates the use of transplants to promote recovery from brain injury and highlights the kinds of questions and problems that must be addressed before this form of therapy is routinely applied. It has been argued that neural transplantation can promote functional recovery through (...) the replacement of damaged nerve cells, the reestablishment of specific nerve pathways lost as a result of injury, the release of specific neurotransmitters, or the production of factors that promote neuronal growth. The latter two mechanisms, which need not rely on anatomical connections to the host brain, are open to examination for nonsurgical, less intrusive therapeutic use. Certain subjective judgments used to select patients who will receive grafts and in assessment of the outcome of graft therapy make it difficult to evaluate the procedure. In addition, little long-term assessment of transplant efficacy and effect has been done in nonhuman primates. Carefully controlled human studies, with multiple testing paradigms, are also needed to establish the efficacy of transplant therapy. (shrink)