CATECHOLAMINE DEPLETION IN MICE UPON RE-EXPOSURE TO STRESS - MEDIATION OF THE ESCAPE DEFICITS PRODUCED BY INESCAPABLE SHOCK
CATECHOLAMINE DEPLETION IN MICE UPON RE-EXPOSURE TO STRESS - MEDIATION OF THE ESCAPE DEFICITS PRODUCED BY INESCAPABLE SHOCK
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DOI：
10.1037/h0077603
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发表时间：
1979-01-01
期刊：
影响因子：
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通讯作者：
SKLAR, LS
中科院分区：
文献类型：
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作者：
ANISMAN, H;SKLAR, LS
在暴露于60次不可避免的电击后，Swiss-Webster小鼠的下丘脑去甲肾上腺素（NE）显著降低。24小时内NE水平恢复到控制值。在初次应激暴露24小时后再暴露10次电击会导致下丘脑NE显著下降。在不可避免的电击后的这段时间内，小鼠的逃脱能力受到严重破坏，大部分小鼠表现出多次失败的逃脱电击。不可避免性休克前左旋多巴治疗增加脑多巴胺（DA）和NE，可防止逃避缺陷。相反，将5次不可避免的冲击与FLA-63的NE消耗或DA和α的NE消耗配对。-甲基-对酪氨酸，24 h后破坏逃逸性能。残留药物效应、状态依赖或持续胺转换不能解释观察到的行为改变。探讨了儿茶酚胺通过反应维持能力的变化对逃避行为的调节作用。不可避免的休克的长期影响可能是由于致敏效应或条件胺耗竭。
Immediately following exposure to 60 inescapable shocks, Swiss-Webster mice had significantly reduced hypothalamic norepinephrine (NE). Within 24 h NE levels returned to control values. Reexposure to as few as 10 shocks 24 h after initial stress exposure resulted in a significant decline of hypothalamic NE. At this interval after inescapable shock, escape performance was severely disrupted, with a large proportion of mice exhibiting numerous failures to escape shock. Increasing brain dopamine (DA) and NE by L-dopa treatment prior to inescapable shock prevented the escape deficits. Conversely, pairing 5 inescapable shocks with NE depletion by FLA-63, or both DA and NE depletion by .alpha.-methyl-p-tyrosine, disrupted escape performance 24 h later. Residual drug effects, state dependence or sustained amine turnover could not account for the behavioral changes observed. Catecholamine mediation of escape performance through variations in response maintenance abilities was discussed. The long-term effects of inescapable shock may be due to sensitization effects or conditioned amine depletion.