As motor coordination impairment is a common symptom of acute and chronic alcohol intoxication, different studies have been conducted on cerebellar Purkinje cell sensitivity to ethanol since Purkinje cell firing constitutes the final integrative output of the cerebellar cortex. However, the effects of chronic ethanol ingestion on Purkinje firing and other cerebellar neurons such as Golgi cells remain unknown. Here, we studied the extracellular discharge of Purkinje and Golgi cells in four groups of non-anesthetized mice drinking ad libitum either 0%, 6%, 12% or 18% ethanol isocallorically compensated with sucrose 25% during a 3-month period. No difference in Golgi cell firing was found with respect to ethanol consumption. The only group that presented significant differences in Purkinje cell firing compared to the other groups was the 18% ethanol-drinking group. These mice presented decreased simple spike and complex spike firing and increased complex spike duration and pause. The 18% ethanol-drinking group was also the only one to present a slight but significant motor coordination impairment (evaluated by rotarod and runway) in naïve task. No motor coordination impairment was noticed in task learned before ethanol consumption. These results suggest that chronic high doses of ethanol are necessary to produce Purkinje cell firing alterations and measurable motor coordination impairment in naïve task. These alterations in Purkinje cell firing did not affect the ability to learn or to recall a motor coordination task.

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http://dx.doi.org/10.1016/j.brainres.2005.07.026DOI Listing

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