Trace fear conditioning involves hippocampal α 5 GABA A receptors
Open accessAbstract
The heterogeneity of gamma-aminobutyric acid type A (GABA(A)) receptors contributes to the diversity of neuronal inhibition in the regulation of information processing. Although most GABA(A) receptors are located synaptically, the small population of alpha5GABA(A) receptors is largely expressed extrasynaptically. To clarify the role of the alpha5GABA(A) receptors in the control of behavior, a histidine-to-arginine point mutation was introduced in position 105 of the murine alpha5 subunit gene, which rendered the alpha5GABA(A) receptors diazepam-insensitive. Apart from an incomplete muscle relaxing effect, neither the sedative, anticonvulsant, nor anxiolytic-like activity of diazepam was impaired in alpha5(H105R) mice. However, in hippocampal pyramidal cells, the point mutation resulted in a selective reduction of alpha5GABA(A) receptors, which altered the drug-independent behavior. In line with the role of the hippocampus in certain forms of associative learning, trace fear conditioning, but not delay conditioning or contextual conditioning, was facilitated in the mutant mice. Trace fear conditioning differs from delay conditioning in that the conditioned and unconditioned stimulus are separated by a time interval. Thus, the largely extrasynaptic alpha5GABA(A) receptors in hippocampal pyramidal cells are implicated as control elements of the temporal association of threat cues in trace fear conditioning.
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α5GABAARs have been implicated most consistently in memory, with knockdown, knockout, or pharmacological suppression of α5GABAARs leading to improvements in learning and memory.
“α5GABAARs, which are expressed most intensively in the hippocampus and deep layers of cortex, have been implicated most consistently in memory, with knockdown, knockout, or pharmacological suppression of α5GABAARs leading to improvements in learning and memory [56-61].”
From An emerging circuit pharmacology of GABAA receptors (2018) · cites this paper as [56]
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- Authors
- Crestani, F., Keist, R., Fritschy, J.-M., Benke, D., Vogt, K., Prut, L., Blüthmann, H., Möhler, H., & Rudolph, U.
- Affiliations
- F. Hoffmann-La Roche AG (CH)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2002-06-25
- Volume
- 99
- Issue
- 13
- Pages
- 8980-8985
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC124409
- OpenAlex
- W2143086898
- Cited by
- 528
- References
- 33
- Citations by year
- 2026: 9 · 2025: 11 · 2024: 7 · 2023: 8 · 2022: 13 · 2021: 14 · 2020: 16 · 2019: 17 · 2018: 21 · 2017: 18 · 2016: 21 · 2015: 20 · 2014: 30 · 2013: 17 · 2012: 24
- FWCI
- 11.29
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- alpha5 GABA-A receptor, extrasynaptic GABAA receptors, trace fear conditioning, hippocampus, hippocampal pyramidal neurons, associative learning, delay conditioning, contextual conditioning, anxiolytic effects
- MeSH terms
- Animals, Behavior, Animal, Conditioning, Classical, Fear, Hippocampus, Immunohistochemistry, Receptors, GABA-A, Point Mutation, Long-Term Potentiation, Mice, In Vitro Techniques
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