Effects of acute exposure to stress on subsequent aggression and locomotion performance.
Avoidance-escape deficits following certain highly stressful conditions result from changes in activity of noradrenergic or other monoaminergic neural systems. A "motor activation deficit" has been used to explain these stress-induced neurochemical changes. The present experiment showed that exposure to a stressor decreased aggression and produced deficits in locomotor performance similar to those observed after inescapable stressor conditions in the "motor activation deficit" studies and earlier "learned helplessness" studies in that (a) the animals recovered with the passage of time, (b) the decrease in aggression and locomotion was larger under conditions of inescapable as opposed to escapable shock, and (c) plasma corticosterone was higher following inescapable shock than after escapable shock. Thus, while the findings obtained are not a variance with the "motor activation deficit" hypothesis, they suggest that other mechanisms might be postulated as well to account for certain deficits in emotional behavior following inescapable stress.
D000374:Aggression / Q000502:physiology; D000818:Animals; D001362:Avoidance Learning; D003216:Conditioning, Operant; D003345:Corticosterone / Q000097:blood; D004597:Electroshock; D006801:Humans; D008297:Male; D051379:Mice; D009043:Motor Activity; D013315:Stress, Psychological / Q000502:physiology; D013997:Time Factors
D003345:Corticosterone