Premium
Differential expression of mGluR5 metabotropic glutamate receptor mRNA by rat striatal neurons
Author(s) -
Testa Claudia M.,
Standaert David G.,
Landwehrmeyer G. Bernhard,
Penney John B.,
Young Anne B.
Publication year - 1995
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.903540207
Subject(s) - metabotropic glutamate receptor 5 , biology , neuroscience , metabotropic glutamate receptor , glutamate receptor , metabotropic glutamate receptor 1 , metabotropic glutamate receptor 7 , striatum , metabotropic glutamate receptor 6 , medium spiny neuron , cholinergic , metabotropic glutamate receptor 3 , cholinergic neuron , in situ hybridization , microbiology and biotechnology , receptor , gene expression , dopamine , biochemistry , gene
Metabotropic glutamate receptors (mGluRs) mediate the effects of glutamate neurotransmission on intracellular second messenger systems. Among the seven distinct mGluR receptor isoforms currently identified, the mGluR5 isoform is expressed particularly prominently in the striatum, where it may contribute to neuronal plasticity, motor behaviors, and excitotoxic injury. mGluR5 mRNA expression in striatal enkephalinergic, somatostatinergic, and cholinergic neurons was examined using double label in situ hybridization techniques. mGluR5 expression is abundant in a large number of medium‐sized striatal cells but is absent in a significant minority of neurons. Double label in situ hybridization with 35 S‐dATP‐ and digoxygenin‐dUTP‐tailed oligonucleotide probes demonstrated that mGluR5 message is highly expressed by enkephalinergic striatal neurons but is not detectable in cholinergic or somatostatin interneurons. In addition, some nonenkephalin, presumably substance P, neurons were also strongly labeled for mGluR5. The differential expression of mGluR5 in striatal projection neurons vs. interneurons may contribute to the selective vulnerability of these neurons to disease processes. © 1995 Wiley‐Liss, Inc.