CONDITIONED TASTE-AVERSIONS IN RATS AFTER INTRACEREBRAL ADMINISTRATION OF NICOTINE

Previous studies suggested that the conditioned taste aversion (CTA) p roduced by nicotine was of central origin. The aims of the present wor k were to identify neural substrates that mediate nicotine-induced CTA , and to examine the relationship between the CTA and locomotor depres sant effects of nicotine. After two conditioning trials with 0.1 or 0. 4 mg/kg nicotine (s.c.), significant CTA was apparent. In contrast, CT A was absent when nicotine (4 or 32 mu g) was administered into a late ral ventricle or when nicotine(4 mu g) was administered into the fourt h ventricle, but decreases in locomotor activity were apparent during the conditioning phase. Nicotine (8 mu g) produced CTA when administer ed bilaterally into the nucleus accumbens. This finding was confirmed in a second experiment, but was not found in rats pretreated with the nicotine antagonist mecamylamine (2 mg/kg s.c). Bilateral administrati on of nicotine into the striatum, ventral tegmental area, dorsal hippo campus or the mesopontine tegmentum failed to produce CTA, and adminis tration of nicotine into the interpeduncular nucleus produced CTA in o ne of two experiments only. It was concluded that the aversive effects produced by systemically administered nicotine may be mediated in par t through nicotinic receptors located in the nucleus accumbens. The lo comotor depression associated with intraventricular administration of nicotine could be dissociated from the aversive effect as measured by the CTA procedure.