Deletion of Stk11 and Fos in BLA projection neurons alters their intrinsic excitability and impairs formation of long-term aversive memory

Conditioned taste aversion (CTA) is a form of one-trial learning dependent on basolateral amygdala projection neurons (BLApn), but its underlying cellular and molecular mechanisms are poorly understood. RNAseq from BLApn during learning identified changes in Stk11, a kinase with well-studied roles i...

Full description

Saved in:
Bibliographic Details
Published inbioRxiv
Main Authors Levitan, David, Liu, Chenghao, Jian-You, Lin, Wachutka, Joseph, Marrero-Garcia, Yasmin, Beltrame, Eduardo, Shima, Yasuyukii, Ramin Ali Marandi Ghoddousi, Yang, Tracy, Katz, Donald B, Nelson, Sacha B
Format Paper
LanguageEnglish
Published Cold Spring Harbor Cold Spring Harbor Laboratory Press 02.11.2019
Subjects
Amygdala
Clonal deletion
Cortex (gustatory)
Excitability
Kinases
Learning
Long term memory
Molecular modelling
Palatability
Taste aversion
Transcription activation
Online AccessGet full text

Cover

More Information
Summary:Conditioned taste aversion (CTA) is a form of one-trial learning dependent on basolateral amygdala projection neurons (BLApn), but its underlying cellular and molecular mechanisms are poorly understood. RNAseq from BLApn during learning identified changes in Stk11, a kinase with well-studied roles in growth, metabolism and development, but not previously implicated in learning. Deletion of Stk11 restricted to BLApn completely blocks memory when occurring prior to training, but not following it. This manipulation does not alter BLApn-dependent encoding of taste palatability in gustatory cortex, or transcriptional activation of BLApn during training. Deletion of Stk11 in BLApn also increases their intrinsic excitability. Conversely, BLApn activated by CTA to express the immediate early gene Fos had reduced excitability. BLApn knockout of Fos also increased excitability and impaired learning. These data suggest that Stk11 and Fos expression play key roles in CTA long-term memory formation, perhaps by modulating the intrinsic excitability of BLApn.
DOI:10.1101/787325