Hypophagia is induced by intracerebroventricular administration of nerve growth factor.

In previous experiments examining the stimulatory effect of intracerebroventricular (icv) NGF treatment on basal forebrain choline acetyltransferase (ChAT) activity, many of the rats treated with the maximally effective dose of NGF appeared gaunt compared to the vehicle-treated control animals. The present experiments determined that icv infusion of NGF at a dose of 1.2 micrograms/day causes a significant reduction in food consumption during the entire period of treatment compared to untreated and vehicle-treated animals. Male rats infused with NGF lost an average of about 30 g of body wt during the first week after the start of infusion and did not gain appreciable weight during the second week of NGF treatment. The hypophagic effect of NGF is dose-dependent, centrally mediated, and reversible. There is no correlation between the stimulatory effect of NGF on basal forebrain ChAT and the inhibitory effect of NGF on weight gain. A therapeutic dose of NGF for Alzheimer's patients comparable to the rat dose for maximally stimulating central cholinergic neurons would approach 1 mg/day. If such therapy is applied, the potential exits for induction of hypophagia as a side effect of the NGF administration.