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Impaired preprodynorphin, but not preproenkephalin, mRNA induction in the striatum of mGluR1 mutant mice in response to acute administration of the full dopamine D 1 agonist SKF‐82958
Author(s) -
Mao Limin,
Conquet François,
Wang John Q.
Publication year - 2002
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.10061
Subject(s) - striatum , metabotropic glutamate receptor 1 , agonist , dopamine , endocrinology , medicine , basal ganglia , chemistry , neuropeptide , glutamate receptor , metabotropic glutamate receptor , biology , receptor , pharmacology , central nervous system , biochemistry
Metabotropic glutamate receptor 1 (mGluR1) is highly expressed in striatonigral projection neurons of rat striatum. To define the role of mGluR1 in the regulation of striatal gene expression, the responsiveness of the three neuropeptide gene expression to a single injection of the dopamine D 1 agonist SKF‐82958 was compared between mGluR1 mutant and wild‐type control mice. We found that acute injection of SKF‐82958 increased preprodynorphin (PPD), substance P (SP), and preproenkephalin (PPE) mRNAs in the dorsal and ventral striatum of mutant and wild‐type mice in a dose‐dependent manner (0.125, 0.5, and 2 mg/kg, i.p.) as revealed by quantitative in situ hybridization. However, the induction of PPD mRNA in both the dorsal and ventral striatum of mGluR1 −/− mice was significantly less than that of wild‐type +/+ mice in response to the two higher doses of SKF‐82958. In contrast to PPD, SP and PPE in the dorsal and ventral striatum of mGluR1 mutant mice were elevated to a similar level as that of wild‐type mice. There were no differences in basal levels and distribution patterns of all three mRNAs between the two genotypes of mice treated with saline. These results indicate that mGluR1 selectively participates in striatonigral PPD induction in response to D 1 receptor stimulation. Synapse 44:86–93, 2002. © 2002 Wiley‐Liss, Inc.