A blocker of nitric oxide synthase, N-G-nitro-L-arginine methyl ester, attenuates light-induced Fos protein expression in rat suprachiasmatic nucleus

Nitric oxide (NO) serves as a messenger molecule in some of the neuronal systems that use glutamate as a transmitter. Because glutamate mediates the transmission of photic signals from retinal ganglion cell axons to the suprachiasmatic nucleus (SCN) circadian pacemaker, and because pharmacological treatments which block NO production by NO synthase (NOS) inhibit light-induced pacemaker phase-resetting, it has been proposed that NO is involved in circadian light signaling in the SCN. In the present study we investigated this hypothesis by assessing in rats the effect of treatment with the NOS blocker, NG-nitro-L-arginine methyl ester (L-NAME), on light-induced expression of the transcription factor Fos, a cellular marker of light signaling in the SCN. We found that systemic administration of L-NAME (100 mg/kg) but not of the inactive analog, D-NAME, significantly attenuates light-induced expression of Fos immunoreactivity in the SCN. (C) 1997 Elsevier Science Ireland Ltd.