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      Expression of the metabotropic glutamate receptor mGluR1 alpha and the ionotropic glutamate receptor GluR1 in the brain during the postnatal development of normal mouse and in the cerebellum from mutant mice.

      1 , , ,
      Journal of neuroscience research
      Wiley

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          Abstract

          Expression of the metabotropic glutamate receptor type 1 alpha (mGluR1 alpha) and the non-N-methyl-D-aspartate (NMDA) ionotropic glutamate receptor type 1 (GluR1) in mouse brain was investigated using the antibodies raised against the synthetic peptides corresponding to their C-terminal amino acid sequences. Both receptor proteins are glycosylated predominantly in an asparagine-linked manner, and are abundant in post-synaptic membranes. We showed that mGluR1 alpha and GluR1 expression within the first 3 postnatal weeks undergoes dramatic changes in time and space, i.e., in the hippocampus and cerebellum. These spatio-temporal expression patterns appear to be correlated with the postnatal ontogenesis and establishment of the glutamatergic neurotransmission system in the hippocampus and cerebellum, cell migration, dendritic and axonal growth, spine formation, and synaptogenesis. In the adult cerebellum, mGluR1 alpha is intensely expressed in Purkinje neurons and GluR1 in Bergmann glial cells. Both receptors are expressed to a fair degree in weaver mutant cerebellum despite granule cell degeneration. However, the intrinsic expression levels of both mGluR1 alpha and GluR1 are markedly reduced in the cerebellum of the Purkinje cell-deficient and underdeveloped mutant mice, Purkinje-cell-degeneration, Lurcher, and staggerer, suggesting that GluR1 expression in Bergmann glia cells may be correlated with the sustained interaction with adjacent Purkinje neurons.

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          Author and article information

          Journal
          J. Neurosci. Res.
          Journal of neuroscience research
          Wiley
          0360-4012
          0360-4012
          Sep 01 1993
          : 36
          : 1
          Affiliations
          [1 ] Department of Molecular Neurobiology, University of Tokyo, Japan.
          Article
          10.1002/jnr.490360104
          8230318
          551ef924-3cef-40c8-b166-63a41fa1c6cd
          History

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