Impaired long-term potentiation induction in dentate gyrus of calretinin-deficient mice

Calretinin (Cr) is a Ca(2+) binding protein present in various populations of neurons distributed in the central and peripheral nervous systems. We have generated Cr-deficient (Cr(−/−)) mice by gene targeting and have investigated the associated phenotype. Cr(−/−) mice were viable, and a large numbe...

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Prif Awduron: Schurmans, Stéphane, Schiffmann, Serge N., Gurden, Hirac, Lemaire, Martine, Lipp, Hans-Peter, Schwam, Valérie, Pochet, Roland, Imperato, Assunta, Böhme, Georg Andrees, Parmentier, Marc
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Cyhoeddwyd: The National Academy of Sciences of the USA 1997
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Biological Sciences
Mynediad Ar-lein:https://ncbi.nlm.nih.gov/pmc/articles/PMC23377/
https://ncbi.nlm.nih.gov/pubmed/9294225
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spelling pubmed-233772005-04-12 Impaired long-term potentiation induction in dentate gyrus of calretinin-deficient mice Schurmans, Stéphane Schiffmann, Serge N. Gurden, Hirac Lemaire, Martine Lipp, Hans-Peter Schwam, Valérie Pochet, Roland Imperato, Assunta Böhme, Georg Andrees Parmentier, Marc Proc Natl Acad Sci U S A Biological Sciences Calretinin (Cr) is a Ca(2+) binding protein present in various populations of neurons distributed in the central and peripheral nervous systems. We have generated Cr-deficient (Cr(−/−)) mice by gene targeting and have investigated the associated phenotype. Cr(−/−) mice were viable, and a large number of morphological, biochemical, and behavioral parameters were found unaffected. In the normal mouse hippocampus, Cr is expressed in a widely distributed subset of GABAergic interneurons and in hilar mossy cells of the dentate gyrus. Because both types of cells are part of local pathways innervating dentate granule cells and/or pyramidal neurons, we have explored in Cr(−/−) mice the synaptic transmission between the perforant pathway and granule cells and at the Schaffer commissural input to CA1 pyramidal neurons. Cr(−/−) mice showed no alteration in basal synaptic transmission, but long-term potentiation (LTP) was impaired in the dentate gyrus. Normal LTP could be restored in the presence of the GABA(A) receptor antagonist bicuculline, suggesting that in Cr(−/−) dentate gyrus an excess of γ-aminobutyric acid (GABA) release interferes with LTP induction. Synaptic transmission and LTP were normal in CA1 area, which contains only few Cr-positive GABAergic interneurons. Cr(−/−) mice performed normally in spatial memory task. These results suggest that expression of Cr contributes to the control of synaptic plasticity in mouse dentate gyrus by indirectly regulating the activity of GABAergic interneurons, and that Cr(−/−) mice represent a useful tool to understand the role of dentate LTP in learning and memory. The National Academy of Sciences of the USA 1997-09-16 /pmc/articles/PMC23377/ /pubmed/9294225 Text en Copyright © 1997, The National Academy of Sciences of the USA
institution US National Library of Medicine
collection PubMed Central
language en
format Article
topic Biological Sciences
spellingShingle Biological Sciences
Schurmans, Stéphane
Schiffmann, Serge N.
Gurden, Hirac
Lemaire, Martine
Lipp, Hans-Peter
Schwam, Valérie
Pochet, Roland
Imperato, Assunta
Böhme, Georg Andrees
Parmentier, Marc
Impaired long-term potentiation induction in dentate gyrus of calretinin-deficient mice
description Calretinin (Cr) is a Ca(2+) binding protein present in various populations of neurons distributed in the central and peripheral nervous systems. We have generated Cr-deficient (Cr(−/−)) mice by gene targeting and have investigated the associated phenotype. Cr(−/−) mice were viable, and a large number of morphological, biochemical, and behavioral parameters were found unaffected. In the normal mouse hippocampus, Cr is expressed in a widely distributed subset of GABAergic interneurons and in hilar mossy cells of the dentate gyrus. Because both types of cells are part of local pathways innervating dentate granule cells and/or pyramidal neurons, we have explored in Cr(−/−) mice the synaptic transmission between the perforant pathway and granule cells and at the Schaffer commissural input to CA1 pyramidal neurons. Cr(−/−) mice showed no alteration in basal synaptic transmission, but long-term potentiation (LTP) was impaired in the dentate gyrus. Normal LTP could be restored in the presence of the GABA(A) receptor antagonist bicuculline, suggesting that in Cr(−/−) dentate gyrus an excess of γ-aminobutyric acid (GABA) release interferes with LTP induction. Synaptic transmission and LTP were normal in CA1 area, which contains only few Cr-positive GABAergic interneurons. Cr(−/−) mice performed normally in spatial memory task. These results suggest that expression of Cr contributes to the control of synaptic plasticity in mouse dentate gyrus by indirectly regulating the activity of GABAergic interneurons, and that Cr(−/−) mice represent a useful tool to understand the role of dentate LTP in learning and memory.
author Schurmans, Stéphane
Schiffmann, Serge N.
Gurden, Hirac
Lemaire, Martine
Lipp, Hans-Peter
Schwam, Valérie
Pochet, Roland
Imperato, Assunta
Böhme, Georg Andrees
Parmentier, Marc
author_facet Schurmans, Stéphane
Schiffmann, Serge N.
Gurden, Hirac
Lemaire, Martine
Lipp, Hans-Peter
Schwam, Valérie
Pochet, Roland
Imperato, Assunta
Böhme, Georg Andrees
Parmentier, Marc
author_sort Schurmans, Stéphane
title Impaired long-term potentiation induction in dentate gyrus of calretinin-deficient mice
title_short Impaired long-term potentiation induction in dentate gyrus of calretinin-deficient mice
title_full Impaired long-term potentiation induction in dentate gyrus of calretinin-deficient mice
title_fullStr Impaired long-term potentiation induction in dentate gyrus of calretinin-deficient mice
title_full_unstemmed Impaired long-term potentiation induction in dentate gyrus of calretinin-deficient mice
title_sort impaired long-term potentiation induction in dentate gyrus of calretinin-deficient mice
publisher The National Academy of Sciences of the USA
publisher_facet The National Academy of Sciences of the USA
publishDate 1997
url https://ncbi.nlm.nih.gov/pmc/articles/PMC23377/
https://ncbi.nlm.nih.gov/pubmed/9294225
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