EFFECTS OF LONG DURATIONS OF ETHANOL TREATMENT DURING AGING ON DENDRITIC PLASTICITY IN FISCHER 344 RATS

Twelve-month-old Fischer 344 rats were fed a liquid diet containing 35% ethanol until they were 18 or 24 months old. Pair-fed and chow-fed control rats were matched to each ethanol-fed rat for concurrent treatment. Cerebellar Purkinje cell networks were measured in half of the rats at the end of the ethanol treatment and in the remaining rats after a subsequent 2-month recovery period. Chronic ethanol consumption resulted in significant elongation of terminal segments in the networks, and the unpaired terminal segments were the predominant sites of this growth. An increase in the duration of ethanol consumption from 24 to 48 weeks caused significantly greater segment elongation in the ethanol-fed rats in spite of the fact that circulating blood levels of ethanol declined markedly with the increased duration of treatment. During the same period of time, a pattern of terminal segment regression followed by terminal segment regrowth characterized age-induced changes in these networks. Thus the effects of long-term ethanol consumption were distinct from effects of concurrent aging processes in the Purkinje cell networks. There were significant interactions between the diets and the longer duration of treatment, such that as segments elongated in the ethanol-fed rats, they shortened in the pair-fed rats, and between the diets and the recovery period, such that as segments elongated during recovery in the pair-fed rats, they shortened in the ethanol-fed rats. These results demonstrated a direct relationship between the duration of chronic ethanol consumption during aging and the extent of dendritic elongation in surviving dendritic networks, supporting the current interpretation that the dendritic growth described here represents a compensatory response to damage of the neuropil in the Purkinje cell microenvironment.