Ethanol consumption following recovery from unilateral damage to the forelimb area of the sensorimotor cortex: reinstatement of deficits and prevention of dendritic pruning.

Unilateral injury to the forelimb-representation area of the sensorimotor cortex (FL-SMC) in adult rats results in use-dependent proliferation of dendritic processes, followed by partial pruning, of layer V pyramidal neurons of the contralateral homotopic cortex. In development, 'exuberant' growth of neurons is often followed by pruning, a process that has been associated with a glutamatergic-NMDA receptor mechanism. A related mechanism may play a role in injury-related pruning of dendrites in adults. The N-methyl-D-aspartate (NMDA) receptor antagonist MK801, administered throughout the pruning phase to adult animals with FL-SMC lesions, prevents dendritic pruning and disrupts behavioral recovery. Ethanol (ETOH) also acts as an NMDA receptor antagonist. It has been shown to reduce NMDA-active ion currents, inhibit NMDA-evoked electrophysiological responses, and decrease glutamate-binding in the hippocampus and cortex. ETOH also affects neuromorphology in the developing and adult cerebellum, hippocampus, and cortex. Ethanol's involvement with NMDA receptor function and its influence on dendritic morphology led us to examine its effect on dendritic pruning and behavioral recovery following unilateral FL-SMC lesions. Lesioned animals were exposed to moderate doses of ethanol in a liquid diet only during the period of dendritic pruning. As with MK801, ETOH prevented pruning and reinstated chronic behavioral asymmetries.