Document Detail


Sensitized increase of period gene expression in the mouse caudate/putamen caused by repeated injection of methamphetamine.
MedLine Citation:
PMID:  11259635     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Methamphetamine (MAP) causes the sensitization phenomena not only in MAP-induced locomotor activity, dopamine release, and Fos expression, but also in MAP-induced circadian rhythm. Cocaine-induced sensitization is reportedly impaired in Drosophila melanogaster mutant for the Period (Per) gene. Thus, sensitization may be related to induction of the Per gene. A rapid induction of mPer1 and/or mPer2 in the suprachiasmatic nucleus after light exposure is believed to be necessary for light-induced behavioral phase shifting. Although the caudate/putamen (CPu) expresses mPer1 and/or mPer2 mRNA, the function of these genes in this nucleus has not yet been elucidated. Therefore, we examined whether MAP affects the expression of mPer1 and/or mPer2 mRNA in the mouse CPu. Injection of MAP augmented the expression of mPer1 but not mPer2 or mPer3 in the CPu, and this MAP-induced increase in mPer1 expression lasted for 2 h. Also, the MAP-induced increase of mPer1 mRNA was strongly antagonized by pretreatment with a dopamine D1 receptor and N-methyl-D-aspartate (NMDA) receptor antagonist, but not by a D2 receptor antagonist. Interestingly, application of either the D1 or the D2 agonist alone did not cause mPer1 expression. The present results demonstrate that activation of both NMDA and D1 receptors is necessary to produce MAP-induced mPer1 expression in the CPu. Repeated injection of MAP caused a sensitization in not only the locomotor activity but also mPer1 expression in the CPu without affecting the level of mPer2, mPer3, or mTim mRNA. Thus, these results suggest that MAP-induced mPer1 gene expression may be related to the mechanism for MAP-induced sensitization in the mouse.
Authors:
T Nikaido; M Akiyama; T Moriya; S Shibata
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Molecular pharmacology     Volume:  59     ISSN:  0026-895X     ISO Abbreviation:  Mol. Pharmacol.     Publication Date:  2001 Apr 
Date Detail:
Created Date:  2001-03-22     Completed Date:  2001-04-19     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0035623     Medline TA:  Mol Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  894-900     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Brain Science, School of Human Sciences, Waseda University, Tokorozawa, Saitama, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Brain / drug effects,  metabolism
Caudate Nucleus / drug effects,  metabolism*
Cell Cycle Proteins
Dopamine Antagonists / pharmacology
Dose-Response Relationship, Drug
Drug Administration Schedule
Excitatory Amino Acid Antagonists / pharmacology
Gene Expression / drug effects*
Injections
Male
Methamphetamine / administration & dosage*
Mice
Motor Activity / drug effects
Nuclear Proteins / genetics,  metabolism*
Period Circadian Proteins
Putamen / drug effects,  metabolism*
RNA, Messenger / metabolism
Receptors, Dopamine D1 / agonists,  antagonists & inhibitors
Receptors, Dopamine D2 / agonists,  antagonists & inhibitors
Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors
Transcription Factors
Chemical
Reg. No./Substance:
0/Cell Cycle Proteins; 0/Dopamine Antagonists; 0/Excitatory Amino Acid Antagonists; 0/Nuclear Proteins; 0/PER1 protein, human; 0/Per1 protein, mouse; 0/Per2 protein, mouse; 0/Period Circadian Proteins; 0/RNA, Messenger; 0/Receptors, Dopamine D1; 0/Receptors, Dopamine D2; 0/Receptors, N-Methyl-D-Aspartate; 0/Transcription Factors; 537-46-2/Methamphetamine

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