DECREASED EXPERIMENTAL ANXIETY AND VOLUNTARY ETHANOL-CONSUMPTION IN RATS FOLLOWING CENTRAL BUT NOT BASOLATERAL AMYGDALA LESIONS

A long-debated 'tension reduction' hypothesis postulates anti-anxiety effects to be important for ethanol reward, and states that elevated a nxiety levels might predispose for ethanol consumption and addiction. Human data are contradictory, possibly due to heterogeneity of patient samples. In rats, baseline levels of experimental anxiety have been r eported to correlate with voluntary ethanol consumption. Here, we addr essed the possibility that mechanisms underlying experimental anxiety might be causally related to regulation of voluntary ethanol intake. R ats were bilaterally lesioned in central amygdala using microinjection s of ibotenic acid. This resulted in a robust release of punished drin king in a modified Vogel conflict test, an effect typically seen with anxiety reducing drugs. This effect was specific, as unpunished drinki ng was unaffected by the lesion. On the elevated plus-maze, central am ygdala lesions did not affect behaviour under baseline conditions, but attenuated the anxiogenic effect of restraint stress. Measures of loc omotor activity were not affected. Voluntary ethanol consumption was e xamined in a two-bottle, free choice paradigm. Ethanol intake was mark edly decreased in the lesion group. Total fluid intake was not affecte d. Basolateral amygdala lesions, which did not affect conflict behavio ur, also left ethanol intake unaffected. These results are consistent with previous reports of an important role for central amygdala in anx iety related behaviours, and suggest that cell bodies located in centr al amygdala might be important in this context. Further, our results s upport a relation between experimental anxiety and voluntary ethanol c onsumption.