Ethanol-related Increases in Degenerating Bodies in the Purkinje Neuron Dendrites of Aging Rats

摘要: Chronic ethanol consumption in aging rats results regression of Purkinje neuron (PN) dendritic arbors ([Pentney, 1995 Measurements pathlengths provide evidence that ethanol-induced lengthening terminal segments may result from regression. Alcohol Alcohol. 30, 87-96]), loss synapses (Dlugos and Pentney, 1997), dilation the smooth endoplasmic reticulum (SER), formation degenerating bodies within PN dendrites ([Dlugos, C.A., 2006a. Ethanol-Related Smooth Endoplasmic Reticulum Dilation Dendrites Aging Rats. Alcohol., Clin. Exp. Res. 883-891,Dlugos, 2006b. degeneration ethanol-fed female rats. Cerebellum. 5, 155-162]). SER be a predictor Ethanol-induced effects on mitochondria involved as cooperate with to maintain calcium homeostasis. The purpose this study was determine whether body number mitochondrial density structure are altered by chronic treatment dendrites. Male, Fischer 344 rats, 12 months age, were fed an or pair-fed liquid diet, rat chow for period 10, 20, 40 weeks (15 rats/treatment; 45 rats/treatment duration). Ethanol-fed received 35% their calories ethanol. At end treatment, all animals euthanized, perfused, tissue prepared electron microscopy. densities mitochondria, areas, distance between measured. Results showed there ethanol-related increase compared controls at weeks. alterations absent. Correlation present those previous studies suggest formed membrane reabsorption during whose function has been compromised dilation.