PHARMACOLOGICAL ANALYSIS OF PROCESSES UNDERLYING DIFFERENTIAL RESPONDING - REVIEW AND FURTHER EXPERIMENTS WITH SCOPOLAMINE, AMPHETAMINE, LYSERGIC-ACID DIETHYLAMIDE (LSD-25), CHLORDIAZEPOXIDE, PHYSOSTIGMINE, AND CHLORPROMAZINE

Enhancements of locomotor responses to no go signals can occur after scopolamine and amphetamine, both with an extinction and with a passive avoidance contingency during compounds made up of the active avoidance signal and of a stimulus from a different modality. Complex interactions between treatments, cues and response-reinforcement relations can lead to marked differences between amphetamine and scopolamine hyperresponding in unsignaled portions of the schedules. A moderate LSD-25 disinhibition can take place in conditioned inhibition tasks, but not when the no go compound signals a passive avoidance contingency. A moderate disinhibition occurs also after chlordiazepoxide treatments. The physostigmine facilitation of differential responding does not depend on the particular response-reinforcement contingency in no go trials. The chlorpromazine depression of active responding is a nonselective one, and is not accompanied by any increase of low baseline responses. The LSD-25 disinhibition depends on response-reinforcement relations in no go trials, and not on task difficulty per se, which suggests that the mechanisms underlying response withholding with an extinction and with a passive avoidance contingency, respectively, are at least in part separated from each other, even when stimulus factors appear to make comparable contributions to the overall variance with different response-reinforcement relations (Frontali and Bignami, 1974). The scopolamine syndrome consists of high order interactions between treatment, sensory and response factors given a particular reinforcement background, while response-reinforcement relations have importance mainly for compensation phenomena that allow elimination of adverse consequences at the reinforcement level. The definition of the amphetamine syndrome oscillates between a genuine motor bias (when responses of the preparatory type are used in alimentary tasks, or highly prepared motor responses are used in defensive tasks) and a genuine stimulation of reinforcement mechanisms (when other types of outputs are used, often allowing a facilitation of differential responding). Highly tentative alternative models are required to account for the benzodiazepine syndrome, since at least part of it cannot be ascribed to an attenuation of punishment suppression, nor to a reduction of fear. The most parsimonious explanation of the chlorpromazine syndrome is an overall psychomotor depression.