Reduced perisomatic inhibition, increased excitatory transmission, and impaired long-term potentiation in mice deficient for the extracellular matrix glycoprotein tenascin-R
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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, Vol. 17, No. 1, 01.2001, p. 226-40.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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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 -