Chemical stimulation or glutamate injections in the nucleus of solitary tract enhance conditioned taste aversion

Abstract

Taste memory depends on motivational and post-ingestional consequences after a single taste–illness pairing. During conditioned taste aversion (CTA), the taste and visceral pathways reach the nucleus of the solitary tract (NTS), which is the first relay in the CNS and has a vital function in receiving vagal chemical stimuli and humoral signals from the area postrema that receives peripheral inputs also via vagal afferent fibers. The specific aim of the present set of experiments was to determine if the NTS is involved in the noradrenergic and glutamatergic activation of the basolateral amygdala (BLA) during CTA. Using in vivo microdialysis, we examined whether chemical NTS stimulation induces norepinephrine (NE) and/or glutamate changes in the BLA during visceral stimulation with intraperitoneal (i.p.) injections of low (0.08M) and high (0.3M) concentrations of lithium chloride (LiCl) during CTA training. The results showed that strength of CTA can be elicited by chemical NTS stimulation (Ringer's high potassium solution; 110mM KCl) and by intra-NTS microinjections of glutamate, immediately after, but not before, low LiCl i.p. injections that only induce a week aversive memory. However visceral stimulation (with low or high i.p. LiCl) did not induce significantly more NE release in the amygdala compared with the NE increment induced by NTS potassium depolarization. In contrast, high i.p. concentrations of LiCl and chemical NTS stimulation induced a modest glutamate sustained release, that it is not observed with low LiCl i.p. injections. These results indicate that the NTS mainly mediates the visceral stimulus processing by sustained releasing glutamate in the BLA, but not by directly modulating NE release in the BLA during CTA acquisition, providing new evidence that the NTS has an important function in the transmission of signals from the periphery to brain systems that process aversive memory formation.