Nicotine-induced conditioned taste aversions are enhanced in rats with lesions of the area postrema.

Lesions, which destroy the area postrema and damage the adjacent nucleus of the solitary tract, attenuate or abolish conditioned taste aversions (CTA) induced by a variety of pharmacological agents. In the present experiment 2 groups of male rats received lesions of the area postrema and 2 groups were given sham lesions. One lesioned group and one sham-lesioned group were twice conditioned with 30-min access to a novel 0.15% saccharin solution followed by injection of nicotine (1 mg/kg, IP). The other 2 groups were similarly conditioned with saccharin followed by saline injections. In subsequent two-bottle choice tests (saccharin vs. water), the saline-injected rats exhibited strong preferences for saccharin, the sham-lesioned rats injected with nicotine showed a weak but significant (p less than 0.05) aversion to saccharin, and the area postrema-lesioned rats injected with nicotine displayed a significantly (p less than 0.05) stronger CTA than the drug-injected sham-lesioned animals. In Phase 2 all rats were given novel chocolate metrecal (30 min) followed by injection of scopolamine HCl (1 mg/kg, IP). The area postrema-lesioned rats showed significant (p less than 0.01) preference for the chocolate taste relative to the aversions shown by the sham-lesioned animals. Thus, area postrema lesions attenuated a scopolamine-induced CTA, but enhanced a nicotine-induced aversion. These results suggest that nicotine and scopolamine act at different neural sites in producing CTAs.