There is an accumulation of evidence indicating that induction of the
calcium-independent isoform of nitric oxide synthase (iNOS) in glial c
ells can contribute to nitric oxide-mediated neural-cell damage. Eluci
dation of iNOS inducing signals and mechanisms regulating its augmenta
tion and suppression may have implications for our understanding of ba
sic processes underlying some forms of central nervous system disease.