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Repeated Methamphetamine Administration Alters Expression of the NMDA Receptor Channel ɛ2 Subunit and Kinesins in the Mouse Brain
Author(s) -
YAMAMOTO HIDEKO,
IMAI KAZUHIDE,
KAMEGAYA ETSUKO,
TAKAMATSU YUKIO,
IRAGO MASASHI,
HAGINO YOKO,
KASAI SINYA,
SHIMADA KIYO,
YAMAMOTO TOSHIFUMI,
SORA ICHIRO,
KOGA HISASHI,
IKEDA KAZUTAKA
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1369.009
Subject(s) - methamphetamine , meth , nmda receptor , sensitization , glutamatergic , amphetamine , gene expression , pharmacology , protein subunit , glutamate receptor , endocrinology , medicine , receptor , neuroscience , chemistry , biology , gene , biochemistry , dopamine , monomer , organic chemistry , acrylate , polymer
Repeated amphetamine administration results in behavioral sensitization. Behavioral sensitization related to abuse and/or relapse may be associated with stable changes in gene expression. To explore the participating genes, we examined the changes in gene expression levels 24 h or 21 days (long‐term withdrawal period) after chronic methamphetamine (METH) treatment for 2 weeks. The expression of several genes related to glutamatergic neural transmission was altered, although changes in the corresponding protein expression were not always consistent with the results for mRNA expression. Of interest, in the frontal cortex of mice treated with METH for 2 weeks, protein expression levels of KIF17 and the N‐methyl‐D‐asparate (NMDA) receptor channel ɛ2 subunit (NRɛ2) were concomitantly increased. The alteration in expression of these proteins, KIF17 and NRɛ2, might be a part of the molecular basis of the behavioral sensitization to METH.