Nitric oxide and L-arginine have mixed effects on mammalian feeding in condition of a high motivation to feed

Feeding inhibition caused by satiation in rats is partially mediated by the unconventional neurotransmitter nitric oxide (NO). Thus, in satiated rats blocking NO production increases feeding, and treatment with the NO precursor t-arginine or with an NO donor reduces feeding beyond that caused by satiation. Do NO and t-arginine also inhibit feeding when feeding motivation is high? When feeding motivation in satiated animals was hedonically increased by offering a highly attractive food, blocking NO production reduced the quantity eaten, rather than increasing it, indicating that hedonic aspects of food are partially mediated by NO. Increasing NO via an NO donor or t-arginine did not further increase the quantity eaten, indicating a ceiling effect. The NO donor, but not t-arginine, also decreased some motivation-dependent parameters of feeding. When feeding motivation was increased by hunger, quantities of food eaten were unaffected by an NO donor, blocker or precursor, with only the blocker of NO production affecting feeding patterning. We also examined effects on feeding of dissolving t-arginine in drinking water over 3 weeks. Chronic t-arginine administration had different effects during the first and in subsequent weeks, increasing feeding at first, but not later. The data indicate that NO has complex, state dependent effects on both the quantity of food eaten, and on patterns of feeding, probably reflecting different sites and mechanisms of action in the nervous system.

Automated summary

Nitric oxide (NO) has complex, state-dependent effects on both the quantity of food eaten and on patterns of feeding in rats, mediating feeding inhibition caused by satiation through unconventional pathways.