Abstract
Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism. We examined the effects of acute and chronic treatment with haloperidol on parkin mRNA expression in the rat brain by reverse transcription-polymerase chain reaction. Acute haloperidol treatment (2 mg/kg) increased parkin mRNA levels in the striatum and nucleus accumbens but not in the medial prefrontal cortex and substantia nigra. Four-week-treatment with haloperidol decanoate (25 mg eq/kg) produced a significant increase in parkin mRNA levels in the striatum without affecting to those in the medial prefrontal cortex, nucleus accumbens and substantia nigra. These results suggest that Parkin may be involved in the haloperidol-induced synaptic plasticity, since Parkin regulates the turnover of the synaptic protein, CDCrel-1.
MeSH terms
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Animals
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Brain / drug effects*
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Brain / metabolism
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Brain / physiopathology
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Brain Chemistry / drug effects*
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Brain Chemistry / genetics
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Cell Cycle Proteins*
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Dopamine Antagonists / pharmacology*
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Drug Administration Schedule
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Gene Expression Regulation / drug effects
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Gene Expression Regulation / physiology
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Haloperidol / pharmacology*
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Ligases / genetics*
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Male
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Neostriatum / drug effects
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Neostriatum / metabolism
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Nerve Tissue Proteins / metabolism
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Neuronal Plasticity / drug effects
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Neuronal Plasticity / physiology
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Nucleus Accumbens / drug effects
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Nucleus Accumbens / metabolism
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Parkinsonian Disorders / genetics
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Parkinsonian Disorders / metabolism*
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Parkinsonian Disorders / physiopathology
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RNA, Messenger / drug effects*
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RNA, Messenger / metabolism
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Rats
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Rats, Wistar
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Septins
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Substantia Nigra / drug effects
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Substantia Nigra / metabolism
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Substantia Nigra / physiopathology
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Ubiquitin-Protein Ligases*
Substances
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Cell Cycle Proteins
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Dopamine Antagonists
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Nerve Tissue Proteins
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RNA, Messenger
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Ubiquitin-Protein Ligases
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parkin protein
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Septin5 protein, rat
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Septins
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Ligases
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Haloperidol