The mu opioid agonist DAMGO stimulates cAMP production in SK-N-SH cells through a PLC-PKC-Ca++ pathway

Vardit Rubovitch; Mikhal Gafni; Yosef Sarne

doi:10.1016/S0169-328X(02)00656-3

The mu opioid agonist DAMGO stimulates cAMP production in SK-N-SH cells through a PLC-PKC-Ca⁺⁺ pathway

Vardit Rubovitch, Mikhal Gafni, Yosef Sarne^*

^*Corresponding author for this work

Physiology Pharmacology

Tel Aviv University

Research output: Contribution to journal › Article › peer-review

32 Scopus citations

Abstract

The μ-opioid agonist DAMGO exerts a dual activity on cAMP production in SK-N-SH neuroblastoma cells. While the classic inhibitory effect was prevented by pretreating the cells with pertussis toxin (PTX), the stimulatory activity was PTX-resistant. The stimulatory effect was abolished by the selective phospholipase C (PLC) blocker U-73122, by the selective protein kinase C (PKC) blocker chelerythrine and by the calcium-channels blockers Ni⁺⁺, Co⁺⁺ and Cd⁺⁺. Hence, it is suggested that the opioid receptor activates PLC (probably through Gq GTP-binding proteins), to mobilize PKC, that positively modulates calcium channels in the plasma membrane; the entry of Ca⁺⁺ into the cells stimulates calcium-activated adenylyl cyclases to produce cAMP.

Original language	English
Pages (from-to)	261-266
Number of pages	6
Journal	Molecular Brain Research
Volume	110
Issue number	2
DOIs	https://doi.org/10.1016/S0169-328X(02)00656-3
State	Published - 20 Feb 2003

Funding

Funders	Funder number
Israel Academy of Sciences and Humanities	184-99
Israel Science Foundation

Keywords

Adenylyl cyclase
Calcium-channels
Opioids
Pertussis toxin (PTX)
Phospholipase C (PLC)
Protein kinase C (PKC)
cAMP

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/S0169-328X(02)00656-3

Cite this

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title = "The mu opioid agonist DAMGO stimulates cAMP production in SK-N-SH cells through a PLC-PKC-Ca++ pathway",

abstract = "The μ-opioid agonist DAMGO exerts a dual activity on cAMP production in SK-N-SH neuroblastoma cells. While the classic inhibitory effect was prevented by pretreating the cells with pertussis toxin (PTX), the stimulatory activity was PTX-resistant. The stimulatory effect was abolished by the selective phospholipase C (PLC) blocker U-73122, by the selective protein kinase C (PKC) blocker chelerythrine and by the calcium-channels blockers Ni++, Co++ and Cd++. Hence, it is suggested that the opioid receptor activates PLC (probably through Gq GTP-binding proteins), to mobilize PKC, that positively modulates calcium channels in the plasma membrane; the entry of Ca++ into the cells stimulates calcium-activated adenylyl cyclases to produce cAMP.",

keywords = "Adenylyl cyclase, Calcium-channels, Opioids, Pertussis toxin (PTX), Phospholipase C (PLC), Protein kinase C (PKC), cAMP",

author = "Vardit Rubovitch and Mikhal Gafni and Yosef Sarne",

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AU - Rubovitch, Vardit

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AU - Sarne, Yosef

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