Role of the Gustatory Thalamus and Medial Amygdala in Taste Learning

Taste neophobia and conditioned taste aversion (CTA) are feeding system defense mechanisms involved in taste learning. Taste neophobia limits the ingestion of novel, potentially poisonous, foods. If feeding is followed by signs of poisoning, then, a CTA is acquired, which renders the food disgusting thereby preventing repeated self-poisoning. The current studies sought to improve the understanding of the role of the gustatory thalamus (GT) and medial amygdala (MeA) in taste neophobia and CTA. In rats, I used intracranial infusions of GABA agonists (i.e., baclofen and muscimol) to examine the effects of inactivating the GT or MeA on taste neophobia (Experiment 1A and 2A, respectively). Then I examined whether inactivation of the GT (Experiment 1B) or MeA (Experiment 2B) can induce a CTA. In Experiment 3, I used a chemogenetic approach to examine the effect of exciting (via hM3D[Gq]) or inhibiting (via hM4D[Gi]) neurons in the MeA on the expression of taste neophobia. In Experiment 1A, inactivating GT neurons with GABA agonists increased intake of a novel tastant (0.5% saccharin), indicating that neuronal excitation in the GT is critical for the normal expression of taste neophobia. Inactivating MeA neurons with GABA agonists (Experiment 2A) had no significant effect on novel taste consumption (0.5% saccharin). In both Experiment 1B and 2B, infusing GABA agonists after the presentation of a novel taste (0.0001 M quinine) suppressed tastant intake during subsequent encounters. Therefore, infusion of GABA agonists into either the GT or MeA can act as an aversive stimulus. In Experiment 3, chemogenetic excitation did not influence the consumption of the novel tastant, but did seem to attenuate the habituation of taste neophobia on subsequent trials. Conversely, inhibition of MeA neurons suppressed both intake and palatability (i.e., initial lick rate and lick cluster size) of a novel tastant (0.15% saccharin) without influencing subsequent performance. So, inhibiting MeA neurons with chemogenetics (Experiment 3), but not GABA agonists (Experiment 2A), enhanced taste neophobia, a behavioral effect that has not previously been observed consequent to a neural manipulation. Thus, some form of inhibitory signaling in the MeA might be involved in the expression of taste neophobia.