Elsevier

Brain Research

Volume 292, Issue 1, 30 January 1984, Pages 63-69
Brain Research

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

https://doi.org/10.1016/0006-8993(84)90890-4Get rights and content

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 lasting than that produced by ethanol.

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    Brain sensitivity to ethanol is an important indicator of the liability for ethanol addiction, since a low level of response to the drug in humans has been related to a greater likelihood of future alcoholism (Schuckit, 1994). Even though the nigrostriatal pathway has not been involved in alcohol reward circuits, some studies have shown that ethanol increases the DAergic neurotransmission of the nigrostriatal pathway (Fadda et al., 1980; Mereu et al., 1984; Russell et al., 1988). This activation could be critical in determining brain sensitivity to ethanol, thus contributing to alcohol addiction (Yanai et al., 1995).

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