Abstract
Lesions of the area postrema (AP) block many of the behavioral and physiological effects of lithium chloride (LiCl) in rats, including formation of conditioned taste aversions (CTAs). Systemic administration of LiCl induces c-Fos immunoreactivity in several brain regions, including the AP, nucleus of the solitary tract (NTS), lateral parabrachial nucleus (latPBN), supraoptic nucleus (SON), paraventricular nucleus (PVN), and central nucleus of the amygdala (CeA). To determine which of these brain regions may be activated in parallel with the acquisition of LiCl-induced CTAs, we disrupted CTA learning in rats by ablating the AP and then quantified c-Fos-positive cells in these brain regions in sham- and AP-lesioned rats 1 h following LiCl or saline injection. Significant c-Fos induction after LiCl was observed in the CeA and SON of AP-lesioned rats, demonstrating activation independent of an intact AP. LiCl-induced c-Fos was significantly attenuated in the NTS, latPBN, PVN and CeA of AP-lesioned rats, suggesting that these regions are dependent on AP activation. Almost all of the lesioned rats showed some damage to the subpostremal NTS, and some rats also had damage to the dorsal motor nucleus of the vagus; this collateral damage in the brainstem may have contributed to the deficits in c-Fos response. Because c-Fos induction in several regions was correlated with magnitude of CTA acquisition, these regions are implicated in the central mediation of lithium effects during CTA learning.