Premium
Training‐induced changes in the expression of GABA A ‐associated genes in the amygdala after the acquisition and extinction of Pavlovian fear
Author(s) -
Heldt Scott A.,
Ressler Kerry J.
Publication year - 2007
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2007.05970.x
Subject(s) - gabaergic , gabaa receptor , amygdala , neuroscience , biology , extinction (optical mineralogy) , basolateral amygdala , psychology , glutamate decarboxylase , receptor , inhibitory postsynaptic potential , genetics , biochemistry , enzyme , paleontology
Previous work suggests the γ‐aminobutyric acid (GABA)ergic system may be dynamically regulated during emotional learning. In the current study we examined training‐induced changes in the expression of GABA A ‐related genes and the binding of GABA receptor radioligands in the amygdala after the acquisition and extinction of Pavlovian fear. Using in situ hybridization, we examined the expression pattern changes of mRNAs for GABAergic markers in the lateral, basolateral and central subdivisions of the amygdala in C57Bl/6J mice. These markers included GABA‐synthesizing enzymes (GAD67 and GAD65), major GABA A receptor subunits (α1, α2, α3, α5, β2 and γ2) and the expression of mRNAs that are involved in a variety of GABA‐related intracellular processes, including GABA transporter‐1 (GAT1), GABA A receptor‐associated protein and the GABA A clustering protein, gephyrin. With fear conditioning, we found decreased mRNA levels of α1, α5 and GAD67, as well as deceased benzodiazepine binding in the amygdala. Fear extinction induced an increase in mRNA levels of α2, β2, GAD67 and gephyrin, as well as a decrease in GAT1. Together, these findings indicate that the acquisition of fear induced a downregulation of mRNA markers related to a decrease in amygdala GABAergic function, whereas the acquisition of fear extinction produced an upregulation of GABAergic markers related to enhanced GABAergic transmission.