SIGNIFICANCE OF ADRENAL CORTICOSTEROID SECRETION FOR THE FOOD RESTRICTION-INDUCED ENHANCEMENT OF ALCOHOL-DRINKING IN THE RAT

1994a, b, c). For example, Fahlke et al. (1995) found that adrenalectomized (ADX) rats exposed to a constant corticosterone signal over the course of several weeks doubled their daily ethanol intake. This finding raises the possibility that the increased alcohol consumption that can be observed during stress (Pohorecky 1981; Higley et al. 1991; Sayette 1993) is partly mediated by enhanced levels of corticosterone. We have tested this hypothesis by monitoring alcohol intake in rats subjected to the stress of food restriction (FR). This procedure increases circulating corticosterone concentrations (Broocks et al. 1990; Burlet et al. 1992; Garcia-Belenguer et al. 1993; Mitev et al. 1993). It also facilitates alcohol intake (e.g. Richter and Campbell 1940; Lester and Freed 1972; Mardones 1972; Meisch and Thompson 1972, 1974; Roehrs and Samson 1981; Linseman and Harding 1989), although this effect is not always found (Linseman 1989). The first experiment of this study confirmed that FR increases ethanol drinking in our strain of rats. In the second experiment, ethanol intake of FR animals was recorded when corticosterone secretion was prevented by prior ADX. In the third experiment, FR rats were treated with cyanoketone, an enzyme inhibitor that blocks stress-induced, but not basal, corticosterone secretion (Akana et al. 1983). The results of these experiments collectively suggest that corticosterone contributes significantly to the FR-induced facilitation of alcohol drinking.