Abstract
Associative learning is driven by survival incentives that naturally dispose animals towards risk avoidance and reward seeking in the natural world. In the case of conditioned taste aversion (CTA), animals learn to avoid a palatable taste stimulus after associating it with gastric malaise. In a previous study, an activity-dependent immediate early gene, Fos, and a gene encoding the master kinase for metabolic control, serine/threonine kinase 11 (Stk11), were identified as key regulators for long-term memory formation. Deletion of either Fos or Stk11 in basolateral amygdala projection neurons (BLApn) prevent CTA acquisition yet increase neuronal intrinsic excitability, and the mechanistic connection between enhanced intrinsic excitability and learning impairment is unclear. Recent studies show that the anterior BLA consists of functionally divergent subpopulations of projection neurons that drive motivationally opposing behaviors. In order to further understand the subtype-specific molecular mechanisms of learning and motivation, we used a multiplex labeling system to investigate whether CTA would induce differential transcriptional changes of Fos and Stk11 in different BLApn subpopulations. Results show that Fos mRNA fold change significantly increases in negative valence subpopulations and significantly decreases in positive valence subpopulations after CTA training. On the other hand, expression of Stk11 and Mark2 underwent a global reduction across subpopulations after CTA training. Overall, these findings suggest that cell type-specific expression of Fos and experience-dependent expression of Stk11 takes place during CTA acquisition. These results suggest that Fos and Stk11 pathways are likely activated by different components of gustatory learning, and the means by which both pathways independently regulate learning and memory is yet to be determined.