Abstract
Rats with unilateral dopamine denervation exhibit turning behaviour in response to the selective D1 agonist SKF 38393 only after a previous exposure to dopamine agonists. We demonstrate here that this 'priming' phenomenon is related to both an increased expression of the pre-existing AP-1 complex and the occurrence of novel AP-1 complexes which are formed by FosB- and JunD-related proteins. While the former protein is expressed as a consequence of the dopamine denervation, the latter is related to the first exposure to a dopamine agonist. Pre-treatment with MK-801, an antagonist for glutamatergic receptors, prevents both the priming development and the AP-1 compositional changes. Rotational behaviour induced by SKF 38393 closely correlates with the presence of the priming AP-1 complexes, regardless of the capability of the D1 agonist to induce the immediate-early gene cFos.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine / pharmacology*
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Animals
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Benserazide / pharmacology*
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Cell Nucleus / metabolism
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Corpus Striatum / drug effects
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Corpus Striatum / metabolism*
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Denervation
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Dizocilpine Maleate / pharmacology
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Gene Expression Regulation / drug effects*
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Levodopa / pharmacology*
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Male
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Motor Activity / drug effects
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Motor Activity / physiology*
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Neurons / drug effects
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Neurons / metabolism*
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Oxidopamine
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Proto-Oncogene Proteins c-fos / biosynthesis*
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Proto-Oncogene Proteins c-jun / biosynthesis*
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Rats
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Rats, Sprague-Dawley
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Rotation
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Stereotyped Behavior / drug effects
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Transcription Factor AP-1 / metabolism*
Substances
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Proto-Oncogene Proteins c-fos
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Proto-Oncogene Proteins c-jun
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Transcription Factor AP-1
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Levodopa
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2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine
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Dizocilpine Maleate
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Benserazide
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Oxidopamine