POSSIBLE INVOLVEMENT OF TYPE 1 INOSITOL 1,4,5-TRISPHOSPHATE RECEPTORS UP-REGULATED BY DOPAMINE D1 AND D2 RECEPTORS IN MOUSE NUCLEUS ACCUMBENS NEURONS IN THE DEVELOPMENT OF METHAMPHETAMINE-INDUCED PLACE PREFERENCE
被引:16
作者:
Kurokawa, K.
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Kawasaki Med Sch, Dept Pharmacol, Kurashiki, Okayama 7010192, JapanKawasaki Med Sch, Dept Pharmacol, Kurashiki, Okayama 7010192, Japan
Kurokawa, K.
[1
]
Mizuno, K.
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Kawasaki Med Sch, Dept Pharmacol, Kurashiki, Okayama 7010192, JapanKawasaki Med Sch, Dept Pharmacol, Kurashiki, Okayama 7010192, Japan
Mizuno, K.
[1
]
Ohkuma, S.
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Kawasaki Med Sch, Dept Pharmacol, Kurashiki, Okayama 7010192, JapanKawasaki Med Sch, Dept Pharmacol, Kurashiki, Okayama 7010192, Japan
Ohkuma, S.
[1
]
机构:
[1] Kawasaki Med Sch, Dept Pharmacol, Kurashiki, Okayama 7010192, Japan
Little is known about regulatory mechanisms of type 1 inositol-1,4,5-triphosphate receptor (IP3R-1) expression in conditioned place preference by methamphetamine (METH), though significant enhancement of IP3R-1 expression in the mouse frontal cortex and limbic forebrain by intermittent administration of cocaine is reported. The present study investigated the role and regulation of IP3R-1 in mice with METH-induced place preference. Injection of IP3R antagonists with different chemical structures, 2-aminophenoxyethane-borate and xestospongin C, into the mouse nucleus accumbens (NAcc) dose-dependently inhibited METH-induced place preference. The levels of IP3R-1 protein in the NAcc of METH-conditioned mice significantly increased, which was completely abolished by microinjection of SCH23390 and raclopride, selective dopamine D1-like and D2-like receptor (D1 and D2DR) antagonists respectively, into the mouse NAcc. Immunohistochemical assessment revealed co-localization of immunoreactivity for IP3R-1 and those for D1 and D2DRs in the NAcc. These findings suggest that IP3R-1 could be involved in the development of METH-induced place preference and that D1 and D2DRs in the NAcc of mice showing METH-induced place preference play possible regulatory roles in IP3R-1 expression. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.