Hypothalamic sites sensitive to morphine and naloxone: Effects on feeding behavior

Abstract

Three experiments investigated the feeding response of brain cannulated rats to hypothalamic injection of norepinephrine (NE), the opiate agonist morphine sulfate (MO) and the opiate antagonist naloxone (NAL). Morphine elicited feeding in a dose-dependent manner when injected into the paraventricular nucleus (PVN) of satiated rats, at doses of 0.78 to 100 nmoles, with a threshold dose of 1.56 nmoles. Naloxone, at doses of 3.13 to 200 nmoles, was injected into the PVN of food-deprived rats and was found to produce a dose-dependent suppression of feeding (threshold dose of 6.25 nmoles). Animals with brain cannulas aimed at the PVN, the perifornical hypothalamus (PFH), the dorsomedial (DMN) and ventromedial (VNM) nuclei were compared for their sensitivity to the feeding stimulatory effects of NE and MO (except in the DMN) and the feeding suppressive effects of NAL. Consistent with earlier reports, the PVN-cannulated animals exhibited a reliable increase in feeding after NE injection; the VMN cannula yielded a small feeding response, whereas the DMN and PFH were insensitive to NE. Morphine, in contrast, strongly stimulated eating after administration into PFH, as well as the PVN, apparently dissociating the NE and MO eating responses. The VMN, however, was generally unresponsive to both MO and NE. With regard to NAL's suppressive effect on feeding, the PVN and PFH, which were sensitive to MO, also exhibited responsiveness to opiate antagonism suggesting the existence in these areas of opiate receptors that modulate feeding. This contrasts with the DMN, where NAL had no effect on feeding and the VMN, where NAL was sensitive in the absence of MO responsiveness. These mapping studies suggest that the opiate receptors affecting eating behavior are mowst dense within the PVN and PFH but are either less dense or have variable responsiveness within the DMN and VMN.