T. Zima et al., THE INFLUENCE OF CHRONIC MODERATE ETHANOL ADMINISTRATION ON NADPH-DIAPHORASE (NITRIC-OXIDE SYNTHASE) ACTIVITY IN RAT-BRAIN, Alcohol and alcoholism, 33(4), 1998, pp. 341-346
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.