Food intake of rats depleted of dopamine as neonates is impaired by inhibition of catecholamine biosynthesis

Abstract

The food intake of rats depleted of brain dopamine (DA) as neonates was markedly reduced by doses of the catecholamine synthesis inhibitor, α-methyl- p-tyrosine (AMT), that had little effect on control animals. In contrast, rats depleted of DA as neonates were subsensitive to doses of the DA antagonist, haloperidol, that greatly inhibited food intake in controls. Unexpectedly, low doses of haloperidol potentiated the effects of AMT in both control and DA-depleted animals. These results suggest that activity within residual DA neurons may remain important for the expression of ingestive behavior in rats depleted of DA as neonates although the precise mechanisms may differ from those operating in normal animals