Chronic alcoholism in the absence of Wernicke-Korsakoff syndrome and cirrhosis does not result in the loss of serotonergic neurons from the median raphe nucleus

Metab Brain Dis. 1996 Sep;11(3):217-27. doi: 10.1007/BF02237959.

Abstract

Previous studies have identified alcohol, thiamine deficiency and liver disease as contributing to the neuropathology of alcohol-related brain damage. In order to examine the effects of alcohol toxicity and thiamine deficiency on serotonergic neurons in the median raphe nucleus (MnR), alcoholic and previously published Wernicke-Korsakoff syndrome (WKS) cases without liver disease, were compared with age-matched non-alcoholic controls. While there was no difference between the estimated number of serotonergic neurons in either controls or alcoholics without WKS (means of 63,010 +/- 8,900 and 59,560 +/- 8,010 respectively), a substantial loss of serotonergic neurons was previously found in WKS cases (mean of 19,050 +/- 13,140). Further analysis revealed a significant difference in the maximum daily alcohol consumption between these groups. However, analysis of covariance showed that the number or serotonergic neurons in the MnR did not correlate with the amount of alcohol consumed. Therefore, our results suggest that cell loss in the MnR can be attributed to thiamine deficiency rather than alcohol per se.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adult
  • Aged
  • Alcohol Amnestic Disorder / pathology
  • Alcohol Drinking
  • Alcoholism / classification
  • Alcoholism / complications
  • Alcoholism / pathology*
  • Female
  • Humans
  • Immunohistochemistry
  • Liver Cirrhosis, Alcoholic / pathology
  • Male
  • Middle Aged
  • Neurons / physiology*
  • Neurons / ultrastructure
  • Raphe Nuclei / pathology*
  • Serotonin / physiology*
  • Thiamine Deficiency / etiology
  • Thiamine Deficiency / pathology

Substances

  • Serotonin