CoChat
Sign Up
Cited by 483Neuroscience and Neuropharmacology ResearchEpilepsy research and treatmentNeural dynamics and brain function

Increased number of synaptic GABAA receptors underlies potentiation at hippocampal inhibitory synapses

Nusser, Zoltan, Hájos, Norbert, Somogyi, Peter, Mody, Istvan·1998·Nature
DOI 10.1038/25999
Open this paper in CoChat — free account

Abstract

Changes in synaptic efficacy are essential for neuronal development, learning and memory formation and for pathological states of neuronal excitability, including temporal-lobe epilepsy. At synapses, where there is a high probability of opening of postsynaptic receptors, all of which are occupied by the released transmitter, the most effective means of augmenting postsynaptic responses is to increase the number of receptors. Here we combine quantal analysis of evoked inhibitory postsynaptic currents with quantitative immunogold localization of synaptic GABA(A) receptors in hippocampal granule cells in order to clarify the basis of inhibitory synaptic plasticity induced by an experimental model of temporal-lobe epilepsy (a process known as kindling). We find that the larger amplitude (66% increase) of elementary synaptic currents (quantal size) after kindling results directly from a 75% increase in the number of GABA(A) receptors at inhibitory synapses on somata and axon initial segments. Receptor density was up by 34-40% and the synaptic junctional area was expanded by 31%. Presynaptic boutons were enlarged, which may account for the 39% decrease in the average number of released transmitter packets (quantal content). Our findings establish the postsynaptic insertion of new GABA(A) receptors and the corresponding increase in postsynaptic responses augmenting the efficacy of mammalian inhibitory synapses.

Integrity signals

Registry

Crossref · 10.1038/25999

Cites

31 of 31 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • 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 [64]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
Nusser, Z., Hájos, N., Somogyi, P., & Mody, I.
Affiliations
University of California, Los Angeles (US)
ORCID
Hájos, Norbert
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
1998-09
Volume
395
Issue
6698
Pages
172-177
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
DOI
10.1038/25999
OpenAlex
W1480770914
Cited by
483
References
31
Citations by year
2026: 5 · 2025: 10 · 2024: 8 · 2023: 5 · 2022: 10 · 2021: 10 · 2020: 14 · 2019: 9 · 2018: 8 · 2017: 10 · 2016: 15 · 2015: 22 · 2014: 13 · 2013: 7 · 2012: 8
FWCI
12.26
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (unspecified)
Locations
  • Nature (publishedVersion)
  • PubMed (publishedVersion)
  • RePEc: Research Papers in Economics (submittedVersion)
Funders
  • National Institutes of Health (5r01ns036142-03)
  • National Institute of Neurological Disorders and Stroke (NS-36142)
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 › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
Keywords
GABAA receptor, synaptic potentiation, inhibitory synapses, hippocampal granule cells, kindling, temporal lobe epilepsy, synaptic plasticity, quantal size, quantal content, receptor density, axon initial segment, inhibitory postsynaptic currents, immunogold localization
MeSH terms
Animals, Electrophysiology, Evoked Potentials, Hippocampus, Immunoenzyme Techniques, Kindling, Neurologic, Neural Inhibition, Neuronal Plasticity, Neurons, Receptors, GABA-A, Synapses, Rats, Wistar, Dentate Gyrus, Rats

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review