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Reduced GABAergic transmission and number of hippocampal perisomatic inhibitory synapses in juvenile mice deficient in the neural cell adhesion molecule L1

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Reduced GABAergic transmission and number of hippocampal perisomatic inhibitory synapses in juvenile mice deficient in the neural cell adhesion molecule L1. / Saghatelyan, Armen K; Nikonenko, Alexander G; Sun, Mu; Rolf, Bettina; Putthoff, Peggy; Kutsche, Michael; Bartsch, Udo; Dityatev, Alexander; Schachner, Melitta.

in: MOL CELL NEUROSCI, Jahrgang 26, Nr. 1, 05.2004, S. 191-203.

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

Harvard

Saghatelyan, AK, Nikonenko, AG, Sun, M, Rolf, B, Putthoff, P, Kutsche, M, Bartsch, U, Dityatev, A & Schachner, M 2004, 'Reduced GABAergic transmission and number of hippocampal perisomatic inhibitory synapses in juvenile mice deficient in the neural cell adhesion molecule L1', MOL CELL NEUROSCI, Jg. 26, Nr. 1, S. 191-203. https://doi.org/10.1016/j.mcn.2004.01.008

APA

Saghatelyan, A. K., Nikonenko, A. G., Sun, M., Rolf, B., Putthoff, P., Kutsche, M., Bartsch, U., Dityatev, A., & Schachner, M. (2004). Reduced GABAergic transmission and number of hippocampal perisomatic inhibitory synapses in juvenile mice deficient in the neural cell adhesion molecule L1. MOL CELL NEUROSCI, 26(1), 191-203. https://doi.org/10.1016/j.mcn.2004.01.008

Vancouver

Saghatelyan AK, Nikonenko AG, Sun M, Rolf B, Putthoff P, Kutsche M et al. Reduced GABAergic transmission and number of hippocampal perisomatic inhibitory synapses in juvenile mice deficient in the neural cell adhesion molecule L1. MOL CELL NEUROSCI. 2004 Mai;26(1):191-203. https://doi.org/10.1016/j.mcn.2004.01.008

Bibtex

@article{de919e3d0b0945f79101abc5b7e897a1,
title = "Reduced GABAergic transmission and number of hippocampal perisomatic inhibitory synapses in juvenile mice deficient in the neural cell adhesion molecule L1",
abstract = "Cell adhesion molecules have been implicated in neural development and hippocampal synaptic plasticity. Here, we investigated the role of the neural cell adhesion molecule L1 in regulation of basal synaptic transmission and plasticity in the CA1 area of the hippocampus of juvenile mice. We show that theta-burst stimulation (TBS) and pairing of low-frequency presynaptic stimulation with depolarization of postsynaptic CA1 pyramidal cells induced similar levels of LTP in L1-deficient and wild-type mice. The basal excitatory synaptic transmission and density of asymmetric excitatory synapses in the stratum radiatum were also normal in L1-deficient mice. Since L1 is expressed not only by principal cells but also by inhibitory interneurons, we recorded inhibitory postsynaptic currents (IPSCs) evoked in CA1 pyramidal cells by minimal stimulation of perisomatic interneurons. L1-deficient mice showed a reduction in the mean amplitude of putative unitary IPSCs, higher values of the coefficient of amplitude variation, higher number of failures in transmitter release, and a reduction in frequency but not amplitude of miniature IPSCs. The use-dependent modulation of inhibitory transmission by paired-pulse or short tetanic stimulation was, however, normal in L1-deficient mice. The physiological abnormalities correlated with a strong reduction in the density of inhibitory active zones, indicating that L1 is involved in establishing inhibitory perisomatic synapses in the hippocampus.",
keywords = "Animals, Cell Differentiation, Down-Regulation, Electric Stimulation, Gene Expression Regulation, Developmental, Hippocampus, In Vitro Techniques, Interneurons, Mice, Mice, Knockout, Microscopy, Electron, Neural Cell Adhesion Molecule L1, Neural Inhibition, Pyramidal Cells, Synapses, Synaptic Transmission, Theta Rhythm, gamma-Aminobutyric Acid, Journal Article, Research Support, Non-U.S. Gov't",
author = "Saghatelyan, {Armen K} and Nikonenko, {Alexander G} and Mu Sun and Bettina Rolf and Peggy Putthoff and Michael Kutsche and Udo Bartsch and Alexander Dityatev and Melitta Schachner",
year = "2004",
month = may,
doi = "10.1016/j.mcn.2004.01.008",
language = "English",
volume = "26",
pages = "191--203",
journal = "MOL CELL NEUROSCI",
issn = "1044-7431",
publisher = "Academic Press Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - Reduced GABAergic transmission and number of hippocampal perisomatic inhibitory synapses in juvenile mice deficient in the neural cell adhesion molecule L1

AU - Saghatelyan, Armen K

AU - Nikonenko, Alexander G

AU - Sun, Mu

AU - Rolf, Bettina

AU - Putthoff, Peggy

AU - Kutsche, Michael

AU - Bartsch, Udo

AU - Dityatev, Alexander

AU - Schachner, Melitta

PY - 2004/5

Y1 - 2004/5

N2 - Cell adhesion molecules have been implicated in neural development and hippocampal synaptic plasticity. Here, we investigated the role of the neural cell adhesion molecule L1 in regulation of basal synaptic transmission and plasticity in the CA1 area of the hippocampus of juvenile mice. We show that theta-burst stimulation (TBS) and pairing of low-frequency presynaptic stimulation with depolarization of postsynaptic CA1 pyramidal cells induced similar levels of LTP in L1-deficient and wild-type mice. The basal excitatory synaptic transmission and density of asymmetric excitatory synapses in the stratum radiatum were also normal in L1-deficient mice. Since L1 is expressed not only by principal cells but also by inhibitory interneurons, we recorded inhibitory postsynaptic currents (IPSCs) evoked in CA1 pyramidal cells by minimal stimulation of perisomatic interneurons. L1-deficient mice showed a reduction in the mean amplitude of putative unitary IPSCs, higher values of the coefficient of amplitude variation, higher number of failures in transmitter release, and a reduction in frequency but not amplitude of miniature IPSCs. The use-dependent modulation of inhibitory transmission by paired-pulse or short tetanic stimulation was, however, normal in L1-deficient mice. The physiological abnormalities correlated with a strong reduction in the density of inhibitory active zones, indicating that L1 is involved in establishing inhibitory perisomatic synapses in the hippocampus.

AB - Cell adhesion molecules have been implicated in neural development and hippocampal synaptic plasticity. Here, we investigated the role of the neural cell adhesion molecule L1 in regulation of basal synaptic transmission and plasticity in the CA1 area of the hippocampus of juvenile mice. We show that theta-burst stimulation (TBS) and pairing of low-frequency presynaptic stimulation with depolarization of postsynaptic CA1 pyramidal cells induced similar levels of LTP in L1-deficient and wild-type mice. The basal excitatory synaptic transmission and density of asymmetric excitatory synapses in the stratum radiatum were also normal in L1-deficient mice. Since L1 is expressed not only by principal cells but also by inhibitory interneurons, we recorded inhibitory postsynaptic currents (IPSCs) evoked in CA1 pyramidal cells by minimal stimulation of perisomatic interneurons. L1-deficient mice showed a reduction in the mean amplitude of putative unitary IPSCs, higher values of the coefficient of amplitude variation, higher number of failures in transmitter release, and a reduction in frequency but not amplitude of miniature IPSCs. The use-dependent modulation of inhibitory transmission by paired-pulse or short tetanic stimulation was, however, normal in L1-deficient mice. The physiological abnormalities correlated with a strong reduction in the density of inhibitory active zones, indicating that L1 is involved in establishing inhibitory perisomatic synapses in the hippocampus.

KW - Animals

KW - Cell Differentiation

KW - Down-Regulation

KW - Electric Stimulation

KW - Gene Expression Regulation, Developmental

KW - Hippocampus

KW - In Vitro Techniques

KW - Interneurons

KW - Mice

KW - Mice, Knockout

KW - Microscopy, Electron

KW - Neural Cell Adhesion Molecule L1

KW - Neural Inhibition

KW - Pyramidal Cells

KW - Synapses

KW - Synaptic Transmission

KW - Theta Rhythm

KW - gamma-Aminobutyric Acid

KW - Journal Article

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

U2 - 10.1016/j.mcn.2004.01.008

DO - 10.1016/j.mcn.2004.01.008

M3 - SCORING: Journal article

C2 - 15121190

VL - 26

SP - 191

EP - 203

JO - MOL CELL NEUROSCI

JF - MOL CELL NEUROSCI

SN - 1044-7431

IS - 1

ER -