Abstract

Anyone trying to study the neural basis of anxiety faces a major problem: ‘anxiety’ is, at least initially, defined in terms of human self-report, but the brain can be adequately studied only in animals. A way is needed, therefore, to cross the huge gulf that divides observations on people from those on animals. The best aid to date in this endeavour is probably the one provided by the anxiolytic drugs: there may be great uncertainty about the equivalence of everything else on the two sides, animal and human, of the gulf (brain, behaviour, biochemistry, etc.), but at least one can be sure that the compound administered (e.g., a benzodiazepine) is identical. Starting from this premiss, and taking into account a large body of psychopharmacological data on both human (Rickels, 1978) and animal (Gray, 1977) subjects, Gray (1982) has developed a general theory of both the psychology of anxiety and the neural structures that mediate this state. At the behavioural level, this theory postulates the existence of a ‘behavioural inhibition system’ (BIS) (Fig. 2.1), activity that constitutes anxiety; at the neural level, the theory further postulates that the BIS depends upon the integrated activity of a number of structures, principally in the limbic system, but including also ascending monoaminergic pathways and neocortical areas closely linked to the limbic system (Fig. 2.2); and, finally, at the cognitive level, the theory postulates that the BIS discharges the information-processing functions of a comparator, as illustrated in Fig. 2.3.

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