Following exposure to inescapable shock, subsequent escape performance is disrupted if the task is one in which animals receive forced exposure to shock for several seconds before escape is possible. The extent of the deficit is directly related to the severity of the initial stress and the duration of escape delay used during test. Treatment with a tyrosine hydroxylase inhibitor, α-methyl-p-tyrosine (α-MpT), a dopamine-β-hydroxylase inhibitor, FLA-63, or dopamine antagonists, haloperidol, and pimozide, mimicked the effects of inescapable shock in the different escape paradigms. The effects of haloperidol were antagonized by treatment with scopolamine. As observed in the case of inescapable shock, prior escape training abated the disruptive effects of the drug treatments. Finally, decreasing or blocking catecholamine activity or increasing cholinergic activity exacerbated the effect of a moderate amount of inescapable shock on subsequent escape performance. These treatments also induced reductions in shock-elicited activity. Conversely, treatment with a catecholamine stimulant, l-dopa, or a cholinergic blocker, scopolamine, anatagonized the reduction in shock-elicited activity and the escape deficits engendered by prior inescapable shock. It was hypothesized that both DA and NE, as well as ACh, are involved in the escape deficit observed after inescapable shock, and that these transmitters mediate the interference by their influence on response initiation and maintenance, rather than on associative or cognitive processes. © 1979 Springer-Verlag.
