Ethanol-related increases in degenerating bodies in the Purkinje neuron dendrites of aging rats

Brain Res. 2008 Jul 24;1221:98-107. doi: 10.1016/j.brainres.2008.05.015. Epub 2008 May 16.

Abstract

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

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Aging / pathology*
  • Alcohol-Induced Disorders, Nervous System / chemically induced
  • Alcohol-Induced Disorders, Nervous System / pathology*
  • Alcohol-Induced Disorders, Nervous System / physiopathology
  • Animals
  • Central Nervous System Depressants / toxicity
  • Cerebellar Cortex / drug effects
  • Cerebellar Cortex / pathology
  • Cerebellar Cortex / physiopathology
  • Cerebellar Diseases / chemically induced
  • Cerebellar Diseases / pathology
  • Cerebellar Diseases / physiopathology
  • Dendrites / drug effects*
  • Dendrites / pathology
  • Disease Models, Animal
  • Endoplasmic Reticulum, Smooth / drug effects
  • Endoplasmic Reticulum, Smooth / pathology
  • Ethanol / toxicity*
  • Male
  • Microscopy, Electron, Transmission
  • Mitochondria / drug effects
  • Mitochondria / pathology
  • Nerve Degeneration / chemically induced*
  • Nerve Degeneration / pathology
  • Nerve Degeneration / physiopathology
  • Purkinje Cells / drug effects*
  • Purkinje Cells / pathology
  • Rats
  • Rats, Inbred F344

Substances

  • Central Nervous System Depressants
  • Ethanol