PortalPublikationenReduced perisomatic inhibition, increased excitatory transmi...

Reduced perisomatic inhibition, increased excitatory transmission, and impaired long-term potentiation in mice deficient for the extracellular matrix glycoprotein tenascin-R

Standard

Reduced perisomatic inhibition, increased excitatory transmission, and impaired long-term potentiation in mice deficient for the extracellular matrix glycoprotein tenascin-R. / Saghatelyan, A K; Dityatev, A; Schmidt, S; Schuster, T; Bartsch, U; Schachner, M.

in: MOL CELL NEUROSCI, Jahrgang 17, Nr. 1, 01.2001, S. 226-40.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Saghatelyan, AK, Dityatev, A, Schmidt, S, Schuster, T, Bartsch, U & Schachner, M 2001, 'Reduced perisomatic inhibition, increased excitatory transmission, and impaired long-term potentiation in mice deficient for the extracellular matrix glycoprotein tenascin-R', MOL CELL NEUROSCI, Jg. 17, Nr. 1, S. 226-40. https://doi.org/10.1006/mcne.2000.0922

APA

Saghatelyan, A. K., Dityatev, A., Schmidt, S., Schuster, T., Bartsch, U., & Schachner, M. (2001). Reduced perisomatic inhibition, increased excitatory transmission, and impaired long-term potentiation in mice deficient for the extracellular matrix glycoprotein tenascin-R. MOL CELL NEUROSCI, 17(1), 226-40. https://doi.org/10.1006/mcne.2000.0922

Vancouver

Saghatelyan AK, Dityatev A, Schmidt S, Schuster T, Bartsch U, Schachner M. Reduced perisomatic inhibition, increased excitatory transmission, and impaired long-term potentiation in mice deficient for the extracellular matrix glycoprotein tenascin-R. MOL CELL NEUROSCI. 2001 Jan;17(1):226-40. https://doi.org/10.1006/mcne.2000.0922

Bibtex

@article{8bcaf02f52d345499ea407ff0794e3c8,
title = "Reduced perisomatic inhibition, increased excitatory transmission, and impaired long-term potentiation in mice deficient for the extracellular matrix glycoprotein tenascin-R",
abstract = "The role of the extracellular matrix molecule tenascin-R (TN-R) in regulation of synaptic transmission and plasticity in the CA1 region of the hippocampus was studied using mice deficient in expression of this molecule. The mutant mice showed normal NMDA-receptor-mediated currents but an impaired NMDA-receptor-dependent form of long-term potentiation (LTP) as compared to wild-type littermates. Reduced LTP in mutants was accompanied by increased basal excitatory synaptic transmission in synapses formed on CA1 pyramidal neurons. A possible mechanism for increased excitatory synaptic transmission in mutants could involve modulation of inhibition, since TN-R and its associated carbohydrate HNK-1 decorate perisomatic interneurons. Indeed, the amplitudes of unitary perisomatic inhibitory currents were smaller in mutants compared to wild-type mice. Thus, our data show that a deficit in TN-R results in reduction of perisomatic inhibition and, as a consequence, in an increase of excitatory synaptic transmission in CA1 to the levels close to saturation, impeding further expression of LTP.",
keywords = "Animals, Antigens, CD57, Glycoproteins, Hippocampus, In Vitro Techniques, Interneurons, Long-Term Potentiation, Mice, Mice, Mutant Strains, Neural Inhibition, Neuronal Plasticity, Patch-Clamp Techniques, Pyramidal Cells, Receptors, AMPA, Receptors, GABA-A, Receptors, N-Methyl-D-Aspartate, Synaptic Transmission, Tenascin, Journal Article, Research Support, Non-U.S. Gov't",
author = "Saghatelyan, {A K} and A Dityatev and S Schmidt and T Schuster and U Bartsch and M Schachner",
year = "2001",
month = jan,
doi = "10.1006/mcne.2000.0922",
language = "English",
volume = "17",
pages = "226--40",
journal = "MOL CELL NEUROSCI",
issn = "1044-7431",
publisher = "Academic Press Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - Reduced perisomatic inhibition, increased excitatory transmission, and impaired long-term potentiation in mice deficient for the extracellular matrix glycoprotein tenascin-R

AU - Saghatelyan, A K

AU - Dityatev, A

AU - Schmidt, S

AU - Schuster, T

AU - Bartsch, U

AU - Schachner, M

PY - 2001/1

Y1 - 2001/1

N2 - The role of the extracellular matrix molecule tenascin-R (TN-R) in regulation of synaptic transmission and plasticity in the CA1 region of the hippocampus was studied using mice deficient in expression of this molecule. The mutant mice showed normal NMDA-receptor-mediated currents but an impaired NMDA-receptor-dependent form of long-term potentiation (LTP) as compared to wild-type littermates. Reduced LTP in mutants was accompanied by increased basal excitatory synaptic transmission in synapses formed on CA1 pyramidal neurons. A possible mechanism for increased excitatory synaptic transmission in mutants could involve modulation of inhibition, since TN-R and its associated carbohydrate HNK-1 decorate perisomatic interneurons. Indeed, the amplitudes of unitary perisomatic inhibitory currents were smaller in mutants compared to wild-type mice. Thus, our data show that a deficit in TN-R results in reduction of perisomatic inhibition and, as a consequence, in an increase of excitatory synaptic transmission in CA1 to the levels close to saturation, impeding further expression of LTP.

AB - The role of the extracellular matrix molecule tenascin-R (TN-R) in regulation of synaptic transmission and plasticity in the CA1 region of the hippocampus was studied using mice deficient in expression of this molecule. The mutant mice showed normal NMDA-receptor-mediated currents but an impaired NMDA-receptor-dependent form of long-term potentiation (LTP) as compared to wild-type littermates. Reduced LTP in mutants was accompanied by increased basal excitatory synaptic transmission in synapses formed on CA1 pyramidal neurons. A possible mechanism for increased excitatory synaptic transmission in mutants could involve modulation of inhibition, since TN-R and its associated carbohydrate HNK-1 decorate perisomatic interneurons. Indeed, the amplitudes of unitary perisomatic inhibitory currents were smaller in mutants compared to wild-type mice. Thus, our data show that a deficit in TN-R results in reduction of perisomatic inhibition and, as a consequence, in an increase of excitatory synaptic transmission in CA1 to the levels close to saturation, impeding further expression of LTP.

KW - Animals

KW - Antigens, CD57

KW - Glycoproteins

KW - Hippocampus

KW - In Vitro Techniques

KW - Interneurons

KW - Long-Term Potentiation

KW - Mice

KW - Mice, Mutant Strains

KW - Neural Inhibition

KW - Neuronal Plasticity

KW - Patch-Clamp Techniques

KW - Pyramidal Cells

KW - Receptors, AMPA

KW - Receptors, GABA-A

KW - Receptors, N-Methyl-D-Aspartate

KW - Synaptic Transmission

KW - Tenascin

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1006/mcne.2000.0922

DO - 10.1006/mcne.2000.0922

M3 - SCORING: Journal article

C2 - 11161481

VL - 17

SP - 226

EP - 240

JO - MOL CELL NEUROSCI

JF - MOL CELL NEUROSCI

SN - 1044-7431

IS - 1

ER -