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.

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)

Because consciousness has an organizational, or functional, center, Gray supposes that there must be a corresponding physical center in the brain. He proposes further that since this center generates consciousness, ablating it would eliminate consciousness, while leaving behavior intact. But the center of consciousness is simply the product of the functional linkages among sensory input, memory, inner speech, and so on, and behavior.

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.

Neural transplantation as a recovery strategy for neuro-degenerative diseases in humans has used mainly grafting following acute denervation strategies in young adult hosts. Our work in aged mice and rats demonstrates an age-related increase in susceptibility to oxidative damage from neurotoxins, a remarkably poor recovery of C57BL/6 mice from MPTP insult with transplantation and growth factors, even at 12 months of age, and diminished plasticity of host neurons. We believe that extrapolation of data from young adult animal models to aged (...) humans without thorough investigation of transplantation and host response in aged recipients is scientifically and ethically inappropriate. (shrink)

Mealey proposes two categorical classes of sociopath, primary and secondary. I criticize this distinction on the basis that constructs of this kind have proved unrealistic in personality taxonomy and that dimensional systems capture reality much more successfully. I suggest how such a system could work in this particular context.

The reinforcement sensitivity theory proposes that neurobiological systems mediate protective and appetitive behaviours and the functioning of these systems is associated to personality traits. In this manner, the RST is a link between neuroscience, behaviour, and personality. The theory evolved to the present revised version describing three systems: fight-flight-freezing, behavioural approach/activation, and behavioural inhibition. However, the most widely available measure of the theory, the BIS/BAS scales, only investigates two systems. Using a large longitudinal community survey, we found that the BIS/BAS (...) scales can be re-structured to investigate the three systems of the theory with a BIS scale, three BAS scales, and a separate fight-flight-freezing system scale. The re-structured scales were age, sex, and longitudinally invariant, and associations with personality and mental health measures followed theoretical expectations and previously published associations. The proposed framework can be used to investigate behavioural choices influencing physical and mental health and bridge historical with contemporary research. (shrink)

Behavioral biologists have long sought to link behavioral units (e.g., aggression, depression, sociopathy) with biological units (e.g., genes, neurotransmitters, hormones, neuroanatomical loci). These units, originally contrived for descriptive purposes, often lead to misunderstandings when they are reified for purposes of causal analysis. This genetic and biochemical explanation for sociopathy reflects such problems.

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.

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.

Emotion is critical in Mealey's conceptual arguments. However, several of her assertions about the role of emotion in sociopathy are problematic. Questions are raised regarding the link between lack of anxiety and low levels of secondary emotions such as love and sympathy, the argument that sociopaths are low in anxiety but high in neuroticism, and the designation of anxiety as a secondary emotion.

There is considerable evidence that the hippocampal system contributes both to the temporary maintenance of memories and to 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 strong and persistent memories for events, including their constituent elements and the relationships among them, and a capacity to express memories flexibly across a wide range of circumstances. (shrink)

Continuing commentary raised several issues concerning our proposal that the hippocampus, parahippocampal region, and cortical association areas mediate different aspects of memory function. Recent relevant findings strengthen our argument that neocortical areas and the parahippocampal region maintain persistent encodings of specific single items and that the hippocampus mediates representations of the relations among these items. The reciprocally and closely interconnected structures that compose the hippocampal memory system work interactively to support flexible memory expression that is relevant to the natural behavior (...) of animals and to conscious recollection in humans. (shrink)

Gray's account is remarkable in its depth and scope but too little attention is paid to poor correspondences with the literature on hippocampal/subicular damage, the theta rhythm, and novelty detection. An alternative account, focusing on hippocampal involvement in organizing memories in a way that makes them accessible to conscious recollection but not in access to consciousness per se, avoids each of these limitations.

It is well established that neural grafts can exert functional effects on the host animal by a multiplicity of different mechanisms – by diffuse release of trophic molecules, neurohormones, and deficient neurotransmitters, as well as by growth and reformation of neural circuits. Our challenge is to understand how these different mechanisms complement each other.

Cholinergic-rich grafts have been shown to be effective in restoring maze-learning deficits in rats with lesions of the forebrain cholinergic projection system. However, the relevance of those studies to developing novel therapies for Alzheimer's disease is questioned.

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.

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.

We attempt to bring the concepts of pain, suffering, and anxiety into sufficient focus to make them serviceable for empirical investigation. The common-sense view that many animals experience these phenomena is supported by empirical and philosophical arguments. We conclude, first, that pain, suffering, and anxiety are different conceptually and as phenomena, and should not be conflated. Second, suffering can be the result — or perhaps take the form — of a variety of states including pain, anxiety, fear, and boredom. Third, (...) pain and nociception are not equivalent and should be carefully distinguished. Fourth, nociception can explain the behavior of insects and perhaps other invertebrates (except possibly the cephalopods). Fifth, a behavioral inhibition system associated with anxiety in humans seems to be present in mammals and most or all other vertebrates. Based on neurochemical and behavioral evidence, it seems parsimonious to claim that these animals are capable of experiencing anxious states. (shrink)

The 'non-sensory' feelings of familiarity, rightness and tip-of-the-tongue postulated in the target article all find a natural explanation within existing models, including Gray's comparator model, of the way in which top-down and bottom-up processing interact to select the contents of consciousness.

Multiple inventories claiming to assess the same explicit motive show only mediocre convergent validity. In three studies the structure, nomological net, and content coverage of multiple existing motive scales was investigated with exploratory factor analyses. The analyses revealed four approach factors and a general avoidance factor with a facet structure. New scales were developed using IRT, reflecting these underlying dimensions. In comparison to existing questionnaires, the UMS have the highest measurement precision and provide short and ultra-short scales. In a fourth (...) study, the UMS demonstrated incremental validity over existing motive scales with respect to several outcome criteria. (shrink)

Hysteria has been the subject of controversy for many years, with theorists arguing about whether it is best explained by a hidden organic cause or by malingering and deception. However, it has been shown that hysterical paralysis cannot be explained in any of these terms. With the recent development of cognitive psychiatry, one may understand psychiatric and organic delusions within the same conceptual framework. Here I contrast hysterical conversion with anosognosia. They are indeed remarkably similar, though the content of their (...) respective delusions is the opposite. In hysterical paralysis, patients are not aware of their preserved ability, whereas in anosognosia for hemiplegia, patients are not aware of their disability. Four main explanations have been provided to account for anosognosia: metacognitive, attentional, motor, and motivational views. I will apply each of these accounts to hysterical paralysis and show that, at each level, hysterical conversion is the reverse of anosognosia. I will suggest that hysterical paralysis results from the interaction between attentional somatosensory amplification and affective inhibition of action. (shrink)