Increase of Calmodulin III Gene Expression by μ-Opioid Receptor Stimulation in PC12 Cells

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Author(s)

Abstract

Calmodulin (CaM) is a principal multifunctional mediator of Ca<SUP>2+</SUP> 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 (μ-opioid agonist), but not by DPDPE (δ) and U50488 (κ). 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 μ-opioid receptor stimulation.

Journal

  • The Japanese Journal of Pharmacology

    The Japanese Journal of Pharmacology 84(4), 412-417, 2000-12-01

    The Japanese Pharmacological Society

References:  38

Codes

  • NII Article ID (NAID)
    10008186655
  • NII NACSIS-CAT ID (NCID)
    AA00691188
  • Text Lang
    ENG
  • Article Type
    ART
  • ISSN
    00215198
  • NDL Article ID
    5612031
  • NDL Source Classification
    ZS51(科学技術--薬学)
  • NDL Call No.
    Z53-D199
  • Data Source
    CJP  NDL  J-STAGE 
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