A series of experiments assessed the potential role of acetylcholine (ACh) in the escape interference produced by inescapable shock. Treatment with the anticholinesterase, physostigmine, succesfully mimicked the effects of inescapable shock. That is, the drug disrupted performance when escape was prevented for 6 s on any given trial, thereby necessitating sustained active responding. When escape was possible upon shock onset, the drug treatment did not influence performance. The centrally acting anticholinergic scopolamine hydrobromide antagonized the effects of physostigmine, and when administered prior to escape testing antagonized the disruptive effects of previously administered inescapable shock. In contrast, the peripherally acting agent scopolamine methylbromide did not influence the effects of these treatments, suggesting that the effects of physostigmine and inescapable shock involved central ACh changes. Scopolamine hydrobromide administered prior to inescapable shock did not prevent the escape interference from subsequently appearing, but this effect could not be attributed to state dependence. It was argued that the interference of escape following uncontrollable stress was due to nonassociative motor deficits. Alterations of the escape deficits by scopolamine were due to elimination of the motor disruption.

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Department of Psychology

Anisman, H, Glazier, S.J. (Stephen J.), & Sklar, L.S. (Lawrence S.). (1981). Cholinergic influences on escape deficits produced by uncontrollable stress. Psychopharmacologia, 74(1), 81–87. doi:10.1007/BF00431762