No abstract

The effects of inescapable shock on subsequent T-maze water escape and position discrimination performance were evaluated in seven experiments. Escapable shock did not disrupt water escape performance; however, escape performance was retarded 24 hr after inescapable shock. These deficits were not apparent if escape was possible upon stress inception; however, pronounced deficits were noted if sustained active responding was necessitated by briefly (3-5 sec) preventing escape. When water escape testing was conducted in relatively warm water (20 degrees C), the disruptive effects of preshock were not apparent. In colder water (15 degrees C), which increases the motor difficulty of the task, the disruptive effects of preshock were noted. When the motor difficulty of the task was increased further, by testing mice in 10 degrees C water, or when the associative difficulty was increased by using a vigorous reversal learning task, the differences between the preshocked and nonpreshocked groups were obviated. Exposure to inescapable shock did not disrupt position discrimination performance regardless of the motor difficulties of the task. Similarly, deficits of discrimination performance were not apparant in mice exposed to inescapable shock even when the associative difficulty of the task was increased by removing intramaze cues or by testing animals in a position discrimination reversal task. It is concluded that inescapable shock results in deficits of response maintenance but probably has a minor, if any, influence on cognitive/associative processes.

Following exposure to inescapable shock, mice exhibit deficits of escape performance, which are progressively more pronounced as training continues. Comparable effects were produced by DA and NE depletion by alpha-MpT and reserpine, NE depletion by FLA-63, and DA receptor blockade through haloperidol. Treatment with PCPA or 5-HTP did not influence performance. The disruptive effects of reserpine and alpha-MpT, as well as haloperidol and FLA-63, were additive. Unexpectedly, mice that received both reserpine and FLA-63 exhibited escape latencies that were significantly lower than those of mice that received either treatment alone. Consistent with the view that increased DA synthesis in the reserpine plus FLA-63 condition prevented the escape interference, L-DOPA antagonized the effects of both alpha-MpT and FLA-63. The results suggest that DA and NE act in a serial fashion to produce the escape deficits. Moreover, although both newly synthesized and previously stored amines contribute to the interference, the short latency responses seen during initial test trials could not be ascribed to previously stored amines.

No abstract

The effects of inescapable shock on subsequent escape performance and shock-elicited activity were examined in six lines of mice selectively bred for differences in general locomotor activity. The line differences in locomotor activity were found to be unrelated to the differences observed on shock-elicited activity. However, escape performance following exposure to inescapable shock was predictable from the levels of shock-elicited activity. Those lines that displayed the greatest decline in motor activity during shock likewise displayed the most pronounced escape deficits. The line differences in escape performance induced by inescapable shock could be mimicked by treatment with a tyrosine hydroxylase inhibitor, a-methyl-p -tyrosine. As predicted, the lines that displayed the least interference after tyrosine hydroxylase inhibition exhibited the smallest reduction in levels of catecholamines. The effects on escape performance following inescapable shock are interpreted in terms of the role of response maintenance deficits produced by catecholamine depletion.