The effect of ethanol withdrawal, after chronic administration, on the electrophysiological properties of antidromically identified mesoaccumbens dopaminergic neurons was studied in two groups of rats with relative controls (withdrawal from chronic saline). The first group was anesthetized with chloral hydrate whereas the second was immobilized with D-tubocurarine. In chloral hydrate anesthetized rats, a significant reduction in the number of spontaneously active dopamine neurons was observed as compared with chronic saline withdrawn controls. In contrast, in ethanol-withdrawn D-tubocurarine treated rats, the number of spontaneously active dopamine neurons, as measured by the cells/track index, was found not different than chronic saline withdrawn controls. Further, intravenous administration of apomorphine, did not reverse the reduced cells/track index in chloral-hydrate anesthetized rats but consistently inhibited dopaminergic firing. Apomorphine-induced inhibition of firing was significantly more pronounced in ethanol withdrawn chloral-hydrate anesthetized rats. Firing rate and firing pattern were found decreased during ethanol withdrawal irrespective of experimental conditions. The results do not support the possibility that dopaminergic neurons of the mesoaccumbens pathway might be affected by depolarization inactivation during ethanol withdrawal. Rather, they confirm a reduction of neuronal activity already reported by previous studies. The reduced cells/track index observed in chloral hydrate anesthetized rats during ethanol withdrawal awaits an alternative explanation to the depolarization inactivation mechanism.
Ethanol withdrawal does not induce a reduction in the number of spontaneously active dopaminergic-neurons in the mesolimbic system
PISTIS, MARCO;
1995-01-01
Abstract
The effect of ethanol withdrawal, after chronic administration, on the electrophysiological properties of antidromically identified mesoaccumbens dopaminergic neurons was studied in two groups of rats with relative controls (withdrawal from chronic saline). The first group was anesthetized with chloral hydrate whereas the second was immobilized with D-tubocurarine. In chloral hydrate anesthetized rats, a significant reduction in the number of spontaneously active dopamine neurons was observed as compared with chronic saline withdrawn controls. In contrast, in ethanol-withdrawn D-tubocurarine treated rats, the number of spontaneously active dopamine neurons, as measured by the cells/track index, was found not different than chronic saline withdrawn controls. Further, intravenous administration of apomorphine, did not reverse the reduced cells/track index in chloral-hydrate anesthetized rats but consistently inhibited dopaminergic firing. Apomorphine-induced inhibition of firing was significantly more pronounced in ethanol withdrawn chloral-hydrate anesthetized rats. Firing rate and firing pattern were found decreased during ethanol withdrawal irrespective of experimental conditions. The results do not support the possibility that dopaminergic neurons of the mesoaccumbens pathway might be affected by depolarization inactivation during ethanol withdrawal. Rather, they confirm a reduction of neuronal activity already reported by previous studies. The reduced cells/track index observed in chloral hydrate anesthetized rats during ethanol withdrawal awaits an alternative explanation to the depolarization inactivation mechanism.
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