Evidence against the involvement of a noradrenergic mechanism in the release by diazepam of novelty-induced hypophagia in rats.

The involvement of noradrenergic processes in both the behavioral suppression and release of food intake induced by diazepam, was investigated using the novelty-induced inhibition of food consumption model. Clonidine (7.5-60 micrograms/kg i.p.) and another alpha 2-noradrenergic receptor agonist, guanfacine (0.25-1 mg/kg i.p.), increased the food intake of rats placed in an unfamiliar situation. The effects of clonidine (15 micrograms/kg) were antagonized by yohimbine (0.5-2 mg/kg i.p.). Clonidine (7.5 micrograms/kg) was unable to enhance the efficacy of diazepam (0.5 and 1 mg/kg i.p.) in stimulating food consumption, whereas yohimbine (0.5-2 mg/kg) did not reduce and even increased the potency of diazepam (2 mg/kg) to facilitate food intake. These findings suggest that although noradrenergic processes (and in particular alpha 2-adrenoreceptors) are involved in the hyponeophagia model they do not mediate the releasing effect exerted by benzodiazepines on novelty-induced suppression of food intake.