A nitric oxide synthase inhibitor reduces hyperphagia induced in rats by the 5-HT(1A) receptor agonist, 8-OH-DPAT, independently of hypothalamic serotonin metabolism.

In rats, a nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME) inhibited the hyperphagia induced by the 5-hydroxytryptamine (5-HT)(1A) autoreceptor agonist, 8-hydroxy-2-di-n-(propylamino)tetralin (8-OH-DPAT). 8-OH-DPAT reduced 5-HT metabolism in the hypothalamus, and this was not blocked by pretreatment with L-NAME. L-NAME also did not affect basal hypothalamic 5-HT metabolism or reverse the decreases in 5-HT synthesis in hypothalamus. These results suggest that the hypophagic effects of L-NAME, which inhibits NO formation, are independent of 5-HT metabolism in the hypothalamus.