INTERACTION OF THE HYPOTHALAMIC PARAVENTRICULAR NUCLEUS AND CENTRAL NUCLEUS OF THE AMYGDALA IN NALOXONE BLOCKADE OF NEUROPEPTIDE GAMMA-INDUCED FEEDING REVEALED BY C-FOS EXPRESSION

Neuropeptide Y (NPY) is a powerful inducer of food intake with a key s ite of action in the paraventricular nucleus (PVN) of the hypothalamus . An effective method for inhibiting the effects of NPY is pretreatmen t with the opioid antagonists naloxone or naltrexone. In the present s tudy, we used immunohistochemistry for cFos as a marker of neuronal ac tivity to map the effects of PVN-injected NPY and blockade of these ef fects by peripheral injection of naloxone. Injection of NPY into the P VN resulted in an increase in food intake that was blocked by peripher al administration of naloxone. PVN NPY also resulted in increased cFos immunoreactivity (cFos-IR) in the PVN independent of food intake, and although peripheral naloxone inhibited NPY-induced feeding, it did no t alter cFos-IR in the PVN. cFos-IR in the central nucleus of the amyg dala (CNA) increased in response to both NPY and naloxone. Furthermore , the response to NPY and naloxone was additive, suggesting that perip heral naloxone and PVN NPY activate different neuronal populations in the CNA. Three other brain regions, the nucleus of the solitary tract, the ventrolateral medulla, and the supraoptic nucleus, all showed inc reases in cFos-IR in this study, but these changes came only as a resu lt of increased food intake after PVN-injected NPY. The current data s uggest that the CNA is a site important for the integration of the NPY and opioid systems.