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Training‐induced changes in the expression of GABAA‐associated genes in the amygdala after the acquisition and extinction of Pavlovian fear

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Heldt, Scott A., Ressler, Kerry J.·2007·European Journal of Neuroscience

Abstract

Previous work suggests the gamma-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 (alpha1, alpha2, alpha3, alpha5, beta2 and gamma2) 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 alpha1, alpha5 and GAD67, as well as deceased benzodiazepine binding in the amygdala. Fear extinction induced an increase in mRNA levels of alpha2, beta2, 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.

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Crossref · 10.1111/j.1460-9568.2007.05970.x

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  • Following acquisition of fear conditioning, α1GABAAR expression in the BLA is reduced.

    “Following acquisition of fear conditioning, α1GABAAR expression in the BLA is reduced ([24]), possibly enhancing the acquisition of subsequent fear-conditioning experiences.”

    From An emerging circuit pharmacology of GABAA receptors (2018) · cites this paper as [24]

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Authors
Heldt, S. A., & Ressler, K. J.
Affiliations
Emory University (US)
Venue
European Journal of Neuroscience
Publisher
Wiley
Published
2007-12
Volume
26
Issue
12
Pages
3631-3644
ISSN
  • 0953-816X (ISSN-L)
  • 1460-9568
OpenAlex
W1959821071
Cited by
125
References
113
Citations by year
2026: 1 · 2025: 4 · 2024: 1 · 2023: 3 · 2022: 3 · 2021: 7 · 2020: 1 · 2019: 6 · 2018: 4 · 2017: 7 · 2016: 7 · 2015: 11 · 2014: 17 · 2013: 6 · 2012: 11
FWCI
3.50
Type
journal article
Language
en
Open access
Locations
  • European Journal of Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Alliance for Research on Schizophrenia and Depression
  • National Institute of Mental Health (F32MH073389)
  • National Institute on Drug Abuse (R01DA019624, DA-019624)
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords
GABAA receptor, amygdala, fear conditioning, fear extinction, GABAergic system, gene expression, GAD67, GAD65, GABA receptor subunits, gephyrin, GABA transporter 1, benzodiazepine binding, emotional learning, lateral amygdala, basolateral amygdala, central amygdala
MeSH terms
Amygdala, Animals, Carrier Proteins, Conditioning, Classical, Extinction, Psychological, Fear, Glutamate Decarboxylase, Male, Membrane Proteins, Mice, Inbred C57BL, Receptors, GABA-A, Retention, Psychology, RNA, Messenger, Reflex, Startle, Tissue Distribution, Biomarkers, Gene Expression, In Situ Hybridization, Protein Isoforms, GABA Plasma Membrane Transport Proteins, Mice

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