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Motor deficit and impairment of synaptic plasticity in mice lacking mGluR1

Nature volume 372, pages 237–243 (1994)Cite this article

Abstract

Metabotropic glutamate receptor 1 (mGluRl) is a member of a large family of G-protein-coupled glutamate receptors, the physiological functions of which are largely unknown. Mice deficient in mGluRl have severe motor coordination and spatial learning deficits. They have no gross anatomical or basic electrophysiological abnormalities in either the cerebellum or hippocampus, but they show impaired cerebellar long-term depression and hippocampal mossy fibre long-term potentiation. mGluRl-deficient mice should therefore be valuable models for studying synaptic plasticity.

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Author information

Author notes

  1. Zafar I. Bashir & Graham L. Collingridge

    Present address: Department of Anatomy, University of Bristol, Bristol, BS8 1TD, UK

  2. Ceri H. Davies

    Present address: Department of Pharmacology, The University of Edinburgh, Edinburgh, EH8 9JZ, UK

  3. Karin Franz-Bacon

    Present address: DNAX Research Institute, Palo Alto, CA, 94304, USA

Affiliations

  1. Glaxo Institute for Molecular Biology, 1228, Plan-Les-Ouates/Geneva, Switzerland

    François Conquet & Karin Franz-Bacon

  2. Department of Pharmacology, Glaxo Research Laboratories, 37100, Verona, Italy

    Francesco Ferraguti, Fabio Bordi, Angelo Reggiani & Valerie Matarese

  3. Département de Neurobiologie, CNRS and Université Paris-Sud, Orsay, Cedex 91405, France

    Hervé Daniel, Françoise Condé & Francis Crépel

  4. Department of Pharmacology, The University of Birmingham, Birmingham, B15 2TT, UK

    Zafar I. Bashir, Ceri H. Davies & Graham L. Collingridge

Authors
  1. François Conquet
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  2. Zafar I. Bashir
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  3. Ceri H. Davies
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  5. Francesco Ferraguti
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  6. Fabio Bordi
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  7. Karin Franz-Bacon
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  8. Angelo Reggiani
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  11. Graham L. Collingridge
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  12. Francis Crépel
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Cite this article

Conquet, F., Bashir, Z., Davies, C. et al. Motor deficit and impairment of synaptic plasticity in mice lacking mGluR1. Nature 372, 237–243 (1994). https://doi.org/10.1038/372237a0

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