Neuroprotective effects of thiamine-megadoses after long-term ethanol application in the rat brain. A structural investigation of hippocampal CA1 pyramidal and cerebellar Purkinje neurons

J Hirnforsch. 1996;37(3):377-87.


Using the Golgi-impregnation technique we could document that twenty weeks of ethanol consumption induce significant elongation of dendritic spines of rat cerebellar Purkinje cells, and as demonstrated for the first time in the present study, of hippocampal pyramidal neurons. Spine hypertrophy might be the result of compensative growth of spines in search of new synaptic contacts due to neuronal cell loss caused by the prolonged ethanol intake. In contrast, this neuromorphological alteration could not be detected in the alcohol group fed at the same time with a high dose of thiamine (119 mg/100 g food) = thiaminemegadose). As thiamine participates in a number of enzymatic reactions primarily concerned with carbohydrate metabolism, it may be concluded that megadoses of thiamine are able to support neuronal energy metabolism, which was initially impaired by ethanol-induced thiamine deficiency. Therefore, a megavitamintherapy in association with chronic alcohol intake could be able to attenuate or prevent ethanol-induced damages in rat central nervous system.

MeSH terms

  • Animals
  • Brain / drug effects*
  • Ethanol / toxicity*
  • Hippocampus / drug effects*
  • Hippocampus / ultrastructure
  • Male
  • Microscopy, Electron
  • Neuroprotective Agents / pharmacology*
  • Pyramidal Cells / drug effects*
  • Pyramidal Cells / ultrastructure
  • Rats
  • Rats, Wistar
  • Thiamine / pharmacology*


  • Neuroprotective Agents
  • Ethanol
  • Thiamine