Sanyoung Niu, Che-Hui Kuo, Yehua Gan, Etsuko Nishikawa, Tetsushi Sadakata,
Hisashi Ichikawa and Naomasa Miki*
Department of Pharmacology, Osaka University Medical School, 2-2 Yamadaoka,
Suita, Osaka 565-0871, Japan
*Corresponding author.ﾊﾊFAX:+81-6-6879-3529
E-mail: nmiki@pharma1.med.osaka-u.ac.jp
Abstract: Calmodulin (CaM) is a principal multifunctional mediator
of Ca2+ signaling in cells. It is reported that morphine increases
CaM contents in mouse brain. However, the precise mechanism of CaM induction
by morphine is unknown. We investigated the changes of CaM by opioid receptor
stimulation in mRNA and protein levels. Expression of CaM was increased
in dose- and time-dependent manners by morphine with RT-PCR assay in PC12
cells, and naloxone inhibited the effect of morphine. The expression was
also increased with DAMGO (m-opioid agonist),
but not by DPDPE (d) and U50488 (k).
Northern blot analysis revealed that the CaMIII gene was responsive to morphine
or DAMGO. CaM protein increased by DAMGO were distributed in both soluble
and membranous fractions in the cells. Taken together, the data suggest
that morphine induces the expression of CaMIII gene through m-opioid
receptor stimulation.
Keywords: Calmodulin III, m-Opioid receptor,
Gene expression, Morphine
Copyrightｩ The Japanese Pharmacological Society 2000
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