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-aden ine dinucleotide phosphate (NADPH)-diaphorase activity, generates nitr ic oxide (NO) which is an important bioregulatory molecule in the nerv ous, immune, and cardiovascular systems. NOS is linked to nonadrenergi c non-cholinergic (NANC) neuronal pathways and modulation of the N-met hyl-D-aspartate receptors, yet its modification by ethanol has been li ttle explored. A possible modification by chronic ethanol administrati on of activity and/or localization of NADPH-diaphorase (NO-synrhase) i n rat brain may thus provide the pathogenic basis of alcohol-induced b rain injury. When female Wistar rats were treated chronically with eth anol for 50 days, the NADPH-diaphorase staining of granular neurons an d neurons located in the molecular layer of the cerebral correx was si gnificantly reduced. Chronic ethanol consumption led to a significant reduction in NP,DPH-diaphorase staining in the superficial layers of t he superior colliculus. The number of NADPH-diaphorase-positive neuron s was significantly reduced (P < 0.001) in the stratum zonale and stra tum griseum superficiale (by 42.3-65.6% of control values). This could alter synaptic processes in the highly organized structures involved in oculomotor and somatic motor coordination and thus contribute to th e motor disturbances which are associated with alcohol abuse.