CATECHOLAMINE DEPLETION IN MICE UPON RE-EXPOSURE TO STRESS - MEDIATION OF THE ESCAPE DEFICITS PRODUCED BY INESCAPABLE SHOCK

Reports 9 experiments with 372 male Swiss-Webster mice in which, immediately following exposure to 60 inescapable shocks, Ss had significantly reduced hypothalamic norepinephrine (NE). Within 24 hrs NE levels returned to control values. Reexposure to as few as 10 shocks 24 hrs after initial stress exposure resulted in significant decline of NE. At this interval after shock, escape performance was severely disrupted, with a large proportion of Ss exhibiting numerous failures to escape shock. Increasing brain dopamine (DA) and NE by levodopa treatment prior to shock prevented the escape deficits. Conversely, pairing 5 inescapable shocks with NE depletion by FLA-63, or both DA and NE depletion by alpha-methylparatyrosine, disrupted escape performance 24 hrs later. Residual drug effects, state dependence, or sustained amine turnover could not account for the behavioral changes. Data are discussed in terms of catecholamine mediation of escape performance through variations in response maintenance abilities. It is suggested that long-term effects of inescapable shock may be due to sensitization effects or conditioned amine depletion. (28 ref) (PsycINFO Database Record (c) 2006 APA, all rights reserved). © 1979 American Psychological Association.