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乙醇可刺激未麻醉大鼠黑质多巴胺能神经元的放电频率。

Ethanol stimulates the firing rate of nigral dopaminergic neurons in unanesthetized rats.

作者信息

Mereu G, Fadda F, Gessa G L

出版信息

Brain Res. 1984 Jan 30;292(1):63-9. doi: 10.1016/0006-8993(84)90890-4.

DOI:10.1016/0006-8993(84)90890-4
PMID:6697212
Abstract

In unanesthetized paralyzed rats, i.v. ethanol administration (0.5-2.0 g/kg) increased (by 30-120%) the firing rate of dopaminergic (DA) neurons in the substantia nigra, pars compacta. Doses of 4.0 g/kg or higher produced an initial stimulation followed by a long-lasting inhibition of firing. On the contrary, in rats anesthetized with halothane (2.5% v/v in air) or with chloral hydrate (400 mg/kg), doses of ethanol up to 2 g/kg failed to activate DA neurons, while a dose of 4 g/kg inhibited neuronal firing without the initial stimulant response. In unanesthetized-curarized rats, the i.v. administration of either chloral hydrate (100-400 mg/kg) or pentobarbital (10-40 mg/kg) or the inhalation of halothane (0.5-2.5% v/v in air) produced a dose-dependent increase in the firing rate of DA neurons. However, the maximum increase produced by these anesthetics was less pronounced and shorter lasting than that produced by ethanol.

摘要

在未麻醉的瘫痪大鼠中,静脉注射乙醇(0.5 - 2.0 g/kg)可使黑质致密部多巴胺能(DA)神经元的放电频率增加(30% - 120%)。4.0 g/kg及以上的剂量会先产生刺激作用,随后是对放电的长期抑制。相反,在用氟烷(空气中体积分数为2.5%)或水合氯醛(400 mg/kg)麻醉的大鼠中,高达2 g/kg的乙醇剂量无法激活DA神经元,而4 g/kg的剂量会抑制神经元放电,且无初始刺激反应。在未麻醉并用箭毒处理的大鼠中,静脉注射水合氯醛(100 - 400 mg/kg)或戊巴比妥(10 - 40 mg/kg)或吸入氟烷(空气中体积分数为0.5% - 2.5%)会使DA神经元的放电频率呈剂量依赖性增加。然而,这些麻醉剂产生的最大增加幅度不如乙醇明显,且持续时间更短。

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