The lateral hypothalamus, catecholamines and ethanol self-administration in rats.

Abstract

The possible involvement of the medial forebrain bundle and the lateral hypothalamus in the maintenance, regulation and control of ethanol and morphine intake in animals received a fair amount of attention over the past five years. In what we believe to be the first study of this kind, Segal, Nerobkova and Rybalkina (1969) reported that electrical stimulation of the ventro-medial hypothalamic nucleus of rats resulted in a temporary increase in ethanol consumption. Stimulation parameters were similar to those commonly used in self-stimulation experiments. This elevated intake of ethanol returned to pre-stimulation baseline after three days of stimulation sessions. In contrast with this study, Marfaing-Jallat, Larue and LeMagnen (1969) reported that lesions of the ventro-medial nucleus also resulted in an increase in the consumption of 8% ethanol solution. Martin and Myers (1972) found that rats that were reinforced for drinking ethanol with lateral hypothalamic stimulation, ingested voluminous amounts of ethanol to the point of intoxication. However, Martin and Myers reported that this electrically reinforced ethanol drinking did not have any effect on home-cage preference levels for ethanol. Thus in spite of the large amounts of ethanol consumed by these rats during the electrical stimulation sessions, they continued to prefer water over ethanol in the home cage. My colleagues and I have reported (Amit, Stern and Wise, 1970; Amit and Stern, 1971; Stern and Amit, 1972; Amit and Cohen, 1974; Corcoran and Amit, 1974) that repeated electrical stimulation of the lateral hypothalamus (LH) resulted in the development of a permanent home-cage preference for ethanol over water in rats that previously rejected these ethanol solutions when presented to them. The rats continued to prefer ethanol for as long as they were allowed to live and even when the ethanol was adulterated with high doses of quinine (0.05%). Wayner and Greenberg, (1972) confirmed these findings although they argued that the elevated ethanol preference observed in these studies was due more to the schedule of ethanol presentation and less to hypothalamic stimulation. We also reported that lesions produced in ethanol prefering rats through the electrode previously used to stimulate the LH, caused a partial reduction in ethanol intake while lesions produced contralateral to the side previously stimulated did not have any effect on ethanol drinking (Amit and Stern, 1972; Levitan, 1971). However, in subsequent tests we found it difficult to replicate this finding. In this context, it is interesting to note that Wise and James (1974) recently reported that surgical insult to the LH (such as that produced by implanting a chronic hypothalamic electrode) reduced ethanol intake in rats placed on an alternate day method of ethanol presentation. They further reported that this reduction in ethanol intake was eliminated by electrical stimulation of the LH through the implanted electrode.