μ and δ opioids but not κ opioid inhibit voltage-activated Ba2+ currents in neuronal F-11 cell

Seung Yeol Nah, Anja Unteutsch, James R. Bunzow, Sean P. Cook, Daniel W. Beacham, David K. Grandy

    Research output: Contribution to journalArticlepeer-review

    11 Scopus citations

    Abstract

    Whole-cell patch-clamp recordings were used to study Ba2+ currents through voltage-dependent Ca2+ channels in dorsal root ganglion X mouse neuroblastoma hybrid (F-11) cells. Opioid agonists selective for either μ (Tyr-D-Ala-Gly-Mephe-Gly-ol; DAMGO) or (Tyr-D-Pen-Gly-Phe-D-Pen-OH; DPDPE) receptors inhibited high-threshold Ba2+ currents. The inhibition was reversible, naloxone-sensitive, and dose-dependent. The inhibitory effects of both DAMGO and DPDPE were blocked by pretreatment of the cells with pertussis toxin (PTX) as well as by brief exposure to the sulfhydryl alkylating agent, N-ethylmaleimide (NEM). The N-type Ca2+ channel antagonist ω-conotoxin GVIA (ω-CTX GVIA) irreversibly inhibited high threshold Ba2+ currents by 66% and blocked the inhibitory effect of DAMGO or DPDPE. In contrast, the L- type Ca2+ channel blocker nifedipine inhibited high threshold Ba2+ currents by 15% and failed to block the inhibitory effect of DAMGO or DPDPE. These results demonstrate that μ and δ opioid receptors are negatively coupled to N-type Ca2+ channels via PTX- and NEM-sensitive GTP-binding proteins in F-11 cells.

    Original languageEnglish (US)
    Pages (from-to)66-71
    Number of pages6
    JournalBrain research
    Volume766
    Issue number1-2
    DOIs
    StatePublished - Aug 22 1997

    Keywords

    • F-11 cell
    • High threshold Ba current
    • N-type Ca channel
    • μ and δ opioid receptor

    ASJC Scopus subject areas

    • General Neuroscience
    • Molecular Biology
    • Clinical Neurology
    • Developmental Biology

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