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

J. Szabadics, G. Tamás, Ivan Soltesz

Research output: Contribution to journalArticle

101 Citations (Scopus)

Abstract

Phasic (synaptic) and tonic (extrasynaptic) inhibition represent the two most fundamental forms of GABAA receptor-mediated transmission. Inhibitory postsynaptic currents (IPSCs) generated by GABAA receptors are typically extremely rapid synaptic events that do not last beyond a few milliseconds. Although unusually slow GABAA 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 GABAA,fast IPSCs evoked by basket cells, single spikes in neurogliaform cells evoke extraordinarily prolonged GABAA responses that display tight regulation by transporters, low peak GABA concentration, unusual benzodiazepine modulation, and spillover. These results reveal a form of GABAA receptor mediated communication by a dedicated cell type that produces slow ionotropic responses with properties intermediate between phasic and tonic inhibition.

Original languageEnglish
Pages (from-to)14831-14836
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume104
Issue number37
DOIs
Publication statusPublished - Sep 11 2007

Fingerprint

Inhibitory Postsynaptic Potentials
GABA-A Receptors
gamma-Aminobutyric Acid
Interneurons
Benzodiazepines

Keywords

  • Inhibition
  • Neocortex
  • Neurogliaform cell

ASJC Scopus subject areas

  • Genetics
  • General

Cite this

@article{2a2f9f4e4d4548c7b3c5aa32b2aa302a,
title = "Different transmitter transients underlie presynaptic cell type specificity of GABAA,slow and GABAA,fast",
abstract = "Phasic (synaptic) and tonic (extrasynaptic) inhibition represent the two most fundamental forms of GABAA receptor-mediated transmission. Inhibitory postsynaptic currents (IPSCs) generated by GABAA receptors are typically extremely rapid synaptic events that do not last beyond a few milliseconds. Although unusually slow GABAA 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 GABAA,fast IPSCs evoked by basket cells, single spikes in neurogliaform cells evoke extraordinarily prolonged GABAA responses that display tight regulation by transporters, low peak GABA concentration, unusual benzodiazepine modulation, and spillover. These results reveal a form of GABAA receptor mediated communication by a dedicated cell type that produces slow ionotropic responses with properties intermediate between phasic and tonic inhibition.",
keywords = "Inhibition, Neocortex, Neurogliaform cell",
author = "J. Szabadics and G. Tam{\'a}s and Ivan Soltesz",
year = "2007",
month = "9",
day = "11",
doi = "10.1073/pnas.0707204104",
language = "English",
volume = "104",
pages = "14831--14836",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
issn = "0027-8424",
number = "37",

}

TY - JOUR

T1 - Different transmitter transients underlie presynaptic cell type specificity of GABAA,slow and GABAA,fast

AU - Szabadics, J.

AU - Tamás, G.

AU - Soltesz, Ivan

PY - 2007/9/11

Y1 - 2007/9/11

N2 - Phasic (synaptic) and tonic (extrasynaptic) inhibition represent the two most fundamental forms of GABAA receptor-mediated transmission. Inhibitory postsynaptic currents (IPSCs) generated by GABAA receptors are typically extremely rapid synaptic events that do not last beyond a few milliseconds. Although unusually slow GABAA 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 GABAA,fast IPSCs evoked by basket cells, single spikes in neurogliaform cells evoke extraordinarily prolonged GABAA responses that display tight regulation by transporters, low peak GABA concentration, unusual benzodiazepine modulation, and spillover. These results reveal a form of GABAA receptor mediated communication by a dedicated cell type that produces slow ionotropic responses with properties intermediate between phasic and tonic inhibition.

AB - Phasic (synaptic) and tonic (extrasynaptic) inhibition represent the two most fundamental forms of GABAA receptor-mediated transmission. Inhibitory postsynaptic currents (IPSCs) generated by GABAA receptors are typically extremely rapid synaptic events that do not last beyond a few milliseconds. Although unusually slow GABAA 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 GABAA,fast IPSCs evoked by basket cells, single spikes in neurogliaform cells evoke extraordinarily prolonged GABAA responses that display tight regulation by transporters, low peak GABA concentration, unusual benzodiazepine modulation, and spillover. These results reveal a form of GABAA receptor mediated communication by a dedicated cell type that produces slow ionotropic responses with properties intermediate between phasic and tonic inhibition.

KW - Inhibition

KW - Neocortex

KW - Neurogliaform cell

UR - http://www.scopus.com/inward/record.url?scp=35548944940&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=35548944940&partnerID=8YFLogxK

U2 - 10.1073/pnas.0707204104

DO - 10.1073/pnas.0707204104

M3 - Article

VL - 104

SP - 14831

EP - 14836

JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

IS - 37

ER -