C-FOS GENE-EXPRESSION IS INDUCED IN A SUBPOPULATION OF STRIATAL NEURONS FOLLOWING A SINGLE ADMINISTRATION OF A DOPAMINE D1-RECEPTOR AGONISTIN ADULT RATS LESIONED WITH 6-OHDA AS NEONATES

Citation
Jj. Soghomonian et al., C-FOS GENE-EXPRESSION IS INDUCED IN A SUBPOPULATION OF STRIATAL NEURONS FOLLOWING A SINGLE ADMINISTRATION OF A DOPAMINE D1-RECEPTOR AGONISTIN ADULT RATS LESIONED WITH 6-OHDA AS NEONATES, Molecular brain research, 57(1), 1998, pp. 155-160
Citations number
21
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
0169328X
Volume
57
Issue
1
Year of publication
1998
Pages
155 - 160
Database
ISI
SICI code
0169-328X(1998)57:1<155:CGIIIA>2.0.ZU;2-9
Abstract
The effects of the dopamine D1 receptor agonist, SKF-38393, on the lev els of mRNAs encoding for the proto-oncogene c-fos and the GABA-synthe sizing enzyme glutamate decarboxylase (GAD65) were measured by in situ hybridization histochemistry in the striatum of adult rats depleted o f dopamine as neonates, c-fos mRNA levels exhibited a prominent increa se following the acute systemic administration of SKF-38393 in dopamin e-depleted but not in normal rats. Double-labeling in situ hybridizati on histochemistry using a radioactive c-Sos probe and a digoxigenin-la beled preproenkephalin (PPE) cRNA probe indicated that c-fos mRNA leve ls were increased by SKF-38393 exclusively in a subpopulation of PPE-u nlabeled neurons. Dopamine-depleted rats exhibited an increase in GAD6 5 mRNA levels relative to control rats. Acute administration of SKF-38 393 did not alter GAD65 mRNA levels in control or in dopamine-depleted rats. Our results demonstrate that an acute administration of a D1-re ceptor agonist induces c-fos but not GAD65 gene expression in a subpop ulation of presumed striato-nigral/entopeduncular neurons. They also s uggest that the D1-dependent behavioral plasticity exhibited by adult rats depleted of dopamine as neonates is not the result of an altered activation of the two subpopulations of striatal efferent neurons. (C) 1998 Elsevier Science B.V. All rights reserved.