Nitric oxide synthase (NOS) activity was examined in forebrain, cerebellum and optic lobes of adult domestic fowl, having a hereditary primary generalized convulsive disorder. NOS was approximately 2-fold higher in only the forebrain of adult epileptic fowl compared to non-epileptic (carrier) hatchmates. A significant increase in NOS was also evident in forebrains of 1-day-old epileptic chicks. Ca(2+)-dependency experiments confirmed that these increments were principally due to type I NOS (NOS-I). Induction of convulsions by intermittent photic stimulation did not affect pre-existing forebrain NOS-I activity. The present data suggest that an enhanced NO signaling may ensue in selected regions of the brain as an adaptive response to hereditary epileptogenesis.
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