Abstract
Conditioned taste aversion (CTA) is a form of one-trial learning dependent on basolateral amygdala projection neurons (BLApn). Its underlying cellular and molecular mechanisms remain poorly understood. RNAseq from BLApn identified changes in multiple candidate learning-related transcripts including the expected immediate early gene Fos and Stk11, a master kinase of the AMP-related kinase pathway with important roles in growth, metabolism and development, but not previously implicated in learning. Deletion of Stk11 in BLApn blocked memory prior to training, but not following it and increased neuronal excitability. Conversely, BLApn had reduced excitability following CTA. BLApn knockout of a second learning-related gene, Fos, also increased excitability and impaired learning. Independently increasing BLApn excitability chemogenetically during CTA also impaired memory. STK11 and C-FOS activation were independent of one another. These data suggest key roles for Stk11 and Fos in CTA long-term memory formation, dependent at least partly through convergent action on BLApn intrinsic excitability.
Highlights
Conditioned Taste Aversion (CTA) is a form of long-lasting aversive memory induced by a single pairing of exposure to an initially palatable taste with gastric malaise (Bures et al, 1998)
RNA-seq from sorted neurons, we found that expression of the kinase Stk11, known as LKB1, is altered following learning in basolateral amygdala (BLA) projection neurons (BLApn), but not in excitatory or inhibitory neurons within the GC
CTA training consisted of 30 min of access to 0.5% saccharin followed by an intraperitoneal injection of 0.15M LiCl, 2% body weight; (Figure 1-figure supplement 1)
Summary
Conditioned Taste Aversion (CTA) is a form of long-lasting aversive memory induced by a single pairing of exposure to an initially palatable taste with gastric malaise (Bures et al, 1998). Disrupting neuronal activity within the BLA blocks the formation and retrieval of CTA memory (Yasoshima et al, 2000; Ferreira et al, 2005; Garcia-Delatorre et al, 2014; Molero-Chamizo, et al, 2017). This may reflect the fact that BLA projection neurons (BLApn) provide the principal output pathway from the amygdala to forebrain structures including the gustatory cortex and the central amygdala (Duvarci and Pare, 2014). Enabling it to distribute taste valance information to these regions (Piette et al, 2012; Samuelsen et al, 2012) Consistent with this view, BLA neurons change their activity and their functional connectivity with their down-stream targets during CTA learning (Grossman et al, 2008). Whether the BLA is a site of cellular and molecular plasticity during CTA learning, as opposed to merely gating plasticity in other structures, is not known
Sign-in/Register to view highlights & summary 
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call