Preliminary results from the immunohistochemical examination of the br
ainstems of chronic alcoholics, suggest that alcohol may have a role i
n damage to the principal serotonergic (5HT) nuclei. This view is rein
forced by evidence from previous animal experiments which demonstrated
a reduction in 5HT neurons in the brains of alcohol-preferring rats a
nd selective neurotoxicity to 5HT neurons following 5,6-dihydroxytrypt
amine-induced increased ethanol intake. It is speculated that, like ot
her neurotoxins, alcohol or its metabolites cause degeneration of 5HT
axons and axon terminals. It is possible that if axonal damage is suff
iciently severe and chronic, the eventual consequence is cell death. T
his could be due to insufficient opportunity for repair and regrowth u
nder repeated and sustained insults of high alcohol consumption.