A potential role for nitric oxide in alcohol-induced changes in brain
function is discussed. Chronic alcohol exposure may lead to excitotoxi
city partially due to increased levels of nitric oxide (NO). Excessive
NO has been linked to cytotoxicity in neurons, glia and myelin. Cytok
ines produced in response to cell injury may trigger increased product
ion of NO. These events may be involved in alcohol-induced brain damag
e. Formation of NO has recently been linked to increased preference fo
r and tolerance to alcohol. A hypothesis for prevention and treatment
of alcohol-induced brain damage, and craving and alcohol intake by alc
oholics is proposed.