THE INFLUENCE OF CHRONIC MODERATE ETHANOL ADMINISTRATION ON NADPH-DIAPHORASE (NITRIC OXIDE SYNTHASE) ACTIVITY IN RAT BRAIN

Nitric oxide synthase (NOS), the enzyme with reduced nicotinamide-adeninedinucleoude phosphate (NADPH)-diaphorase activity, generatesnitric oxide (NO) which is an important bioregulatory moleculein the nervous, immune, and cardiovascular systems. NOS is linkedto non-adrenergic non-cholinergic (NANC) neuronal pathways andmodulation of the N-methyl-D-aspartate receptors, yet its modificationby ethanol has been little explored. A possible modificationby chronic ethanol administration of activity and*or localizationof NADPH-diaphorase (NO-synthase) in rat brain may thus providethe pathogenic basis of alcohol-induced brain injury. When femaleWistar rats were treated chronically with ethanol for 50 days,the NADPH-diaphorase staining of granular neurons and neuronslocated in the molecular layer of the cerebral cortex was significantlyreduced. Chronic ethanol consumption led to a significant reductionin NADPH-diaphorase staining in the superficial layers of thesuperior colliculus. The number of NADPH-diaphorase-positiveneurons was significantly reduced (P < 0.001) in the stratumzonale and stratum griseum superficiale (by 42 3–65 6%of control values). This could alter synaptic processes in thehighly organized structures involved in oculomotor and somaticmotor coordination and thus contribute to the motor disturbanceswhich are associated with alcohol abuse.