Conditioned taste aversions in rats after intracerebral administration of nicotine

Previous studies suggested that the conditioned taste aversion (CTA) produced by nicotine was of central origin. The aims of the present work were to identify neural substrates that mediate nicotine-induced CTA, and to examine the relationship between the CTA and locomotor depressant effects of nicotine. After two conditioning trials with 0.1 or 0.4mg/kg nicotine (s.c.), significant CTA was apparent. In contrast, CTA was absent when nicotine (4 or 32µg) was administered into a lateral ventricle or when nicotine (4µg) was administered into the fourth ventricle, but decreases in locomotor activity were apparent during the conditioning phase. Nicotine (8µg) produced CTA when administered 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 (2mg/kg s.c.). Bilateral administration of nicotine into the striatum, ventral tegmental area, dorsal hippocampus or the mesopontine tegmentum failed to produce CTA, and administration of nicotine into the interpeduncular nucleus produced CTA in one of two experiments only. It was concluded that the aversive effects produced by systemically administered nicotine may be mediated in part through nicotinic receptors located in the nucleus accumbens. The locomotor depression associated with intraventricular administration of nicotine could be dissociated from the aversive effect as measured by the CTA procedure.