Ethanol intake is increased by injection of galanin in the paraventricular nucleus and reduced by a galanin antagonist.

Ethanol intake stimulates expression of galanin in several hypothalamic sites, including the paraventricular nucleus. Because injection of galanin in the paraventricular nucleus induces eating, we hypothesized that galanin might also affect ethanol intake. Rats were given ad libitum access to 4% ethanol for 4 weeks and assigned to one of two groups according to levels of ethanol consumption: high levels (>1.5 g/ kg/day) or low levels (<1.0 g/kg/day). In Experiment 1, galanin (1.0 nmol) or Ringer's solution was injected unilaterally into the paraventricular nucleus, with food and water absent during the first 4 h. Galanin significantly increased ethanol intake only in rats that drank high levels of ethanol. In Experiment 2, injection of galanin (0.5 and 1.0 nmol) in the paraventricular nucleus dose-dependently increased ethanol intake with food and water available. The higher dose was also effective in eliciting ethanol intake when tested with food and water absent. In Experiment 3, a test of receptor specificity was provided by injecting rats with the galanin antagonist M-40 (0.5 nmol) or Ringer's solution. Injection of M-40 in the paraventricular nucleus significantly decreased ethanol consumption. In Experiment 4, an anatomic control, with galanin injected 2 mm dorsal to the paraventricular nucleus in the same animals, caused no change in ethanol intake. In conclusion, injection of galanin in the paraventricular nucleus, at a dose known to induce feeding, acted by means of a galanin receptor to potentiate intake of 4% ethanol, even with food and water available as alternate sources of calories and fluid, respectively. Because ethanol can increase expression of galanin mRNA in the paraventricular nucleus, this could set the stage for a positive feedback loop between galanin and ethanol intake.