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.

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.