• synapse;
  • interneuron;
  • cerebellar cortex;
  • GABAergic

Background Ethanol-related synaptic loss, Purkinje neuron dendritic regression, and parallel fiber degeneration have been reported in the molecular layer of the adult cerebellar cortex. The known plasticity of the cerebellar cortex suggests that this region may respond to ethanol-related losses by compensatory remodeling of cerebellar circuitry. Stellate and basket interneurons may play an essential role in the remodeling process. Little is known about ethanol-related effects on cerebellar interneurons or on the GABAergic synapses that they form despite the fact that ethanol-related alterations in these components may contribute to the sensitivity of the cerebellum to ethanol. The paucity of data on GABAergic synapses extends to other synaptic components as well including synaptophysin, a glycoprotein component of synaptic vesicles and a synaptic marker.

Methods Thirty 12-month-old F 344 rats were divided into ethanol-fed, pair-fed, and chow-fed groups (10/group). Ethanol rats were treated for 40 weeks with a liquid diet in which 35% of the calories were derived from ethanol. At the end of treatment, rats were perfused, and tissue processed for quantitative immunohistochemistry of GABA and synaptophysin labels.

Results Levels of GABA within inhibitory synapses formed by stellate and basket neurons and levels of synaptophysin were not altered by long-term ethanol treatment.

Conclusions Stable levels of GABA within GABAergic basket and stellate interneuron synapses suggest that interneurons in the molecular layer of the cerebellar cortex may not play a major role in remodeling of cerebellar circuitry following long-term ethanol consumption. The lack of ethanol-related alterations in synaptophysin levels reported here suggests that synaptic vesicles may be relatively insensitive to ethanol and that known ethanol-related effects on synapse number are due to other mechanisms.