Pharmacological evidence on the specialization of CNS mechanisms responsible for motor act inhibition by aversive events.
Our use of selected pharmacological agents has now extended the range of treatment-behaviour interactions previously studied by other (e.g., lesion) approaches in the search for appropriate models of behaviour organization and underlying physiological mechanisms. The case of muscarinic blockers has special interest, because the drugs induce only one type of primary change. At present, it appears difficult to reconcile the evidence in favour of a motor (perseverative) deficit with other evidence favouring an impairment of sensory processes. However, critical experiments using several go-no go avoidance tasks show that the two deficits may be inseparable. The complex profile of cue-dependent disinhibitory effects of antimuscarinics suggests that separate sensori-motor mechanisms are employed for response suppression not simply as a function of cue type, response type, or response-reinforcement relation but as a joint function of all these factors. Sedative-tranquillizing agents with so-called anti-conflict properties add still another dimension to the problem of motor act inhibition. These agents are maximally effective in disrupting response withholding when both reward and punishment follow the emission of a particular response, less consistently effective in tests with CS paired with non-contingent shock (CER), and mostly ineffective in those go-no go avoidance tasks which show a very high sensitivity to muscarinic blockade.
D000818:Animals; D014151:Anti-Anxiety Agents / Q000494:pharmacology; D001362:Avoidance Learning / Q000187:drug effects; D001522:Behavior, Animal / Q000187:drug effects*; D001921:Brain / Q000187:drug effects* / Q000502:physiology; D003213:Conditioning, Psychological / Q000187:drug effects; D010276:Parasympatholytics / Q000494:pharmacology*
D014151:Anti-Anxiety Agents; D010276:Parasympatholytics