This chapter aims to draw attention to a number of researchable issues in the neuropsychology of anxiety. Progress in the study of the biological basis of anxiety has been critically dependent on availability of drugs that, clinically, reduce human anxiety. The antianxiety drugs counteract the behavioral effects of three classes of stimuli: stimuli associated with punishment, stimuli associated with the omission of expected reward, and novel stimuli. The more indirect, behavioral approach to the problem suggests that such a critical site of antianxiety drug action is likely to lie in the limbic system. There is abundant evidence that two major classes of antianxiety drugs, the benzodiazepines and the barbiturates, both enhance gamma-aminobutyric acid (GABA)-ergic inhibition; similar observations have been made with ethanol. The increased noradrenergic input may be due to reduced locus coeruleus auto-receptor-mediated inhibition, or to reduced GABAergic presynaptic inhibition of noradrenaline release, or to both; and it may be combined with decreased GABA-ergic control of intrinsic hippocampal neurons.