Shock stress protects mice against amphetamine-induced dopaminergic toxicity.
Shock stress protects mice against amphetamine-induced dopaminergic toxicity.
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休克应激可保护小鼠免受安非他明诱导的多巴胺能毒性。
DOI：
10.1016/j.brainres.2006.03.020
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发表时间：
2006
期刊：
影响因子：
--
通讯作者：
Wagner,GeorgeC
中科院分区：
文献类型：
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作者：
Carlson,KirstenM;Wagner,GeorgeC
研究了尾电击（10次，2.0 mA/0.15 s电击）对成年雄性BALB/c小鼠安非他明诱导的多巴胺能毒性的影响。单次电击15分钟后，小鼠接受安非他明（50 mg/kg）或生理盐水：休克/生理盐水；NoShock /生理盐水;冲击/安非他命;没有休克/安非他命。安非他明导致无电击/安非他明组60%的多巴胺耗损。尾部电击提供了神经保护，防止安非他明引起的多巴胺耗竭，这种效果可能与应激反应有关。
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.