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休克应激可保护小鼠免受苯丙胺诱导的多巴胺能毒性。

Shock stress protects mice against amphetamine-induced dopaminergic toxicity.

作者信息

Carlson Kirsten M, Wagner George C

机构信息

Department of Psychology, Busch Campus, Rutgers University, New Brunswick, NJ 08854, USA.

出版信息

Brain Res. 2006 May 4;1087(1):186-9. doi: 10.1016/j.brainres.2006.03.020. Epub 2006 Apr 13.

Abstract

The effect of tail shock (ten, 2.0 mA/0.15 s shocks) on amphetamine-induced dopaminergic toxicity in adult, male BALB/c mice was assessed. Fifteen minutes following a single shock session, mice received amphetamine (50-mg/kg) or saline as follows: Shock/Saline; NoShock/Saline; Shock/Amphetamine; No Shock/Amphetamine. Amphetamine caused a 60% dopamine depletion in the No Shock/Amphetamine group. Tail shock provided neuroprotection against amphetamine-induced dopamine depletion, an effect likely related to the stress response.

摘要

评估了尾部电击(十次,2.0毫安/0.15秒电击)对成年雄性BALB/c小鼠中苯丙胺诱导的多巴胺能毒性的影响。在单次电击 session 后15分钟,小鼠接受如下苯丙胺(50毫克/千克)或生理盐水:电击/生理盐水;无电击/生理盐水;电击/苯丙胺;无电击/苯丙胺。在无电击/苯丙胺组中,苯丙胺导致多巴胺耗竭60%。尾部电击对苯丙胺诱导的多巴胺耗竭具有神经保护作用,这种作用可能与应激反应有关。

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