Abstract
Conditioned taste aversion (CTA) is an evolutionarily useful association of gastric malaise with prior consumption of a taste. Communication between the gustatory cortex (GC) and basolateral amygdala (BLA) seems to play a central role in CTA acquisition. While it is the amygdala-cortical pathway that is most commonly thought of as being central to this form of learning, recently, it has been suggested that chronic chemogenetic perturbation of GC to BLA projecting neurons during exposure to a novel tastant in a CTA learning paradigm attenuates CTA acquisition. However, such perturbations of GC cell bodies likely also alter the activity of the larger GC population via lateral connections of these GC to BLA projecting neurons. Thus, the nature of the perturbation used in this previous study leaves it unclear whether communication via the GC to BLA projection itself is truly vital for CTA acquisition. My study tests this hypothesis using a more temporally and spatially precise optogenetic perturbation of specifically GC to BLA axon terminals: I inhibited the immediate, short-term (2.5-second) taste-evoked activity of bilateral GC-projecting neuron (GC-PN) terminals in BLA during exposure to a novel tastant in a CTA learning paradigm. My results suggest reduced learning in animals that underwent this optogenetic perturbation. On closer inspection, I observed a bimodal distribution of responses to the perturbation, such that some animals failed to learn, and others robustly learned the aversion. Initial post-hoc histological analysis reveals no underlying relationships between sites of virus injection in GC or optical fiber localization above BLA with learning outcome. Nonetheless, acknowledging the need for further data acquisition, I cautiously interpret these results to implicate activity of the GC to BLA projection in CTA learning.