Lasting potentiation of inhibition is associated with an increased number of gamma-aminobutyric acid type A receptors activated during miniature inhibitory postsynaptic currents.
Open accessAbstract
Whole-cell patch-clamp recordings unveiled a substantial increase in the amplitude, but no change in the frequency, of miniature inhibitory postsynaptic currents (mIPSCs) in dentate gyrus granule cells following chronic epilepsy induced by kindling. This novel and persistent enhancement of gamma-aminobutyric acid type A (GABAA) receptor-mediated inhibition lasted for at least 48 hr following its induction. Nearly a doubling of the number of activated functional postsynaptic GABAA receptor channels during mIPSCs without any change in single-channel conductance or kinetics could be demonstrated using nonstationary fluctuation analysis. As postsynaptic GABAA receptors are likely to be pharmacologically saturated by the transmitter concentration in the cleft, incrementing the number of functional receptor channels may be the most effective means to augment inhibition in the mammalian brain.
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Functional strength of GABAergic synapses changes in proportion with the number of postsynaptic GABAARs.
“the functional strength of GABAergic synapses changes in proportion with the number of postsynaptic GABAARs4546.”
Chronic unpredictable stress may increase inhibitory synaptic transmission onto AgRP neurons partially through augmented postsynaptic sensitivity to synaptically released GABA, due either to increased function or increased number of postsynaptic GABA receptors clustered at synaptic sites.
“These data suggest that chronic unpredictable stress may increase inhibitory synaptic transmission onto AgRP neurons partially through augmented postsynaptic sensitivity to synaptically released GABA, due either to increased function or increased number of postsynaptic GABA receptors clustered at synaptic sites [63, 64].”
From Chronic unpredictable stress induces depression-related behaviors by suppressing AgRP neuron activity (2021) · cites this paper as [63]
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References 48 · Cited by 257
- Authors
- Otis, T. S., De Koninck, Y., & Mody, I.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center, Dallas 75235-9068.
- ORCID
- Otis, T S
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1994-08-02
- Volume
- 91
- Issue
- 16
- Pages
- 7698-7702
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC44469
- OpenAlex
- W2068507111
- Cited by
- 257
- References
- 48
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 3 · 2023: 3 · 2022: 3 · 2021: 3 · 2020: 4 · 2019: 4 · 2018: 6 · 2017: 8 · 2016: 13 · 2015: 7 · 2014: 4 · 2013: 3 · 2012: 5
- FWCI
- 7.37
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Medical Research Council
- National Institute of Neurological Disorders and Stroke (NS27528, NS30549, R01NS027528, NS12151)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Keywords
- GABAA receptor, miniature inhibitory postsynaptic currents, kindling, chronic epilepsy, dentate gyrus granule cells, synaptic inhibition, GABAergic synapses
- MeSH terms
- Animals, Chronic Disease, Disease Models, Animal, Electric Conductivity, Epilepsy, Hippocampus, Kindling, Neurologic, Male, Receptors, GABA-A, Synapses, Rats, Wistar, Long-Term Potentiation, Rats
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