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Cited by 170Neuroscience and Neuropharmacology ResearchNeural dynamics and brain functionReceptor Mechanisms and Signaling

Different transmitter transients underlie presynaptic cell type specificity of GABA A,slow and GABA A,fast

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Szabadics, János, Tamás, Gábor, Soltesz, Ivan·2007·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.0707204104PMC PMC1964542
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Abstract

Phasic (synaptic) and tonic (extrasynaptic) inhibition represent the two most fundamental forms of GABA(A) receptor-mediated transmission. Inhibitory postsynaptic currents (IPSCs) generated by GABA(A) receptors are typically extremely rapid synaptic events that do not last beyond a few milliseconds. Although unusually slow GABA(A) IPSCs, lasting for tens of milliseconds, have been observed in recordings of spontaneous events, their origin and mechanisms are not known. We show that neocortical GABA(A,slow) IPSCs originate from a specialized interneuron called neurogliaform cells. Compared with classical GABA(A,fast) IPSCs evoked by basket cells, single spikes in neurogliaform cells evoke extraordinarily prolonged GABA(A) responses that display tight regulation by transporters, low peak GABA concentration, unusual benzodiazepine modulation, and spillover. These results reveal a form of GABA(A) receptor mediated communication by a dedicated cell type that produces slow ionotropic responses with properties intermediate between phasic and tonic inhibition.

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Crossref · 10.1073/pnas.0707204104

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  • These features combined with the dense local ramification of NGFC axons are considered to underlie the ability of NGFCs to mediate volume transmission leading to slow dual component (GABAAR- and GABABR-mediated) inhibition at virtually any postsynaptic element within their dense axonal plexus.

    “These features combined with the dense local ramification of NGFC axons are considered to underlie the ability of NGFCs to mediate volume transmission leading to slow dual component (GABAAR- and GABABR-mediated) inhibition at virtually any postsynaptic element within their dense axonal plexus (550, 926, 927, 1074, 1086).”

    From Hippocampal GABAergic Inhibitory Interneurons (2017) · cites this paper as [1074]

  • While neocortical NGFCs can be found throughout all layers, they are particularly enriched in supragranular layers and form a major constituent cell population in L1.

    “While neocortical NGFCs can be found throughout all layers, they are particularly enriched in supragranular layers and form a major constituent cell population in L1 (564, 858, 1017, 1074, 1086, 1134).”

    From Hippocampal GABAergic Inhibitory Interneurons (2017) · cites this paper as [1074]

  • In contrast to the rapid and synchronous IPSCs produced by PVBCs, transmission from NGFCs generates long-lasting IPSCs resulting from prolonged GABA transients that arise from the unusual synaptic architecture where bouton density is high but close apposition to specialized postsynaptic densities is low.

    “Of particular interest, in contrast to the rapid and synchronous IPSCs produced by PVBCs, transmission from NGFCs generates long-lasting IPSCs resulting from prolonged GABA transients (550, 1074, 1086) that arise from the unusual synaptic architecture where bouton density is high but close apposition to specialized postsynaptic densities is low (550, 751, 858, 1074) (FIGURE 13C).”

    From Hippocampal GABAergic Inhibitory Interneurons (2017) · cites this paper as [1074]

  • Electrophysiological recordings from pairs of NGFCs demonstrate a marked functional connectivity with each other.

    “Electrophysiological recordings from pairs of NGFCs demonstrate a marked functional connectivity with each other (48, 550, 926, 1074).”

    From Hippocampal GABAergic Inhibitory Interneurons (2017) · cites this paper as [1074]

  • These remarkably slow kinetics are not fully attributable to dendritic filtering, asynchronous release, spillover, nor the properties of the GABAARs themselves but are primarily due to the spatiotemporal profile of GABA release from this interneuron subtype.

    “These remarkably slow kinetics are not fully attributable to dendritic filtering, asynchronous release, spillover, nor the properties of the GABAARs themselves (however, see Refs. 483, 1264) but are primarily due to the spatiotemporal profile of GABA release from this interneuron subtype (see sect. IVL) (167, 550, 870, 1074).”

    From Hippocampal GABAergic Inhibitory Interneurons (2017) · cites this paper as [1074]

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Authors
Szabadics, J., Tamás, G., & Soltesz, I.
Affiliations
  • University of California, Irvine (US)
  • University of Szeged (HU)
  • *Department of Anatomy and Neurobiology, University of California, 193 Irvine Hall, Irvine, CA 92697; and
ORCID
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
2007-09-11
Volume
104
Issue
37
Pages
14831-14836
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.0707204104
PMC
PMC1964542
OpenAlex
W2004000308
Cited by
170
References
49
Citations by year
2026: 5 · 2025: 6 · 2024: 5 · 2023: 2 · 2022: 2 · 2021: 9 · 2020: 8 · 2019: 3 · 2018: 9 · 2017: 6 · 2016: 7 · 2015: 6 · 2014: 14 · 2013: 9 · 2012: 8
FWCI
7.41
Type
journal article
Language
en
Open access
Locations
  • Proceedings of the National Academy of Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Wellcome Trust
  • National Institute of Neurological Disorders and Stroke (R29NS035915, R01NS035915, NS-35915, R37NS035915)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Keywords
GABAA receptor, tonic inhibition, extrasynaptic inhibition, phasic inhibition, neurogliaform cells, basket cells, inhibitory postsynaptic currents, benzodiazepine modulation, GABA transporters, neocortex, interneurons, presynaptic neurotransmitter release
MeSH terms
Zolpidem, Action Potentials, Animals, Interneurons, Kainic Acid, Kinetics, Models, Neurological, Neural Inhibition, Pyridines, Receptors, GABA-A, Synapses, N-Methylaspartate, Rats, Wistar, Presynaptic Terminals, Patch-Clamp Techniques, GABA Agonists, Neocortex, Rats

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