Opioids potentiate transmitter release from SK-N-SH human neuroblastoma cells by modulating N-type calcium channels

Opioids induce dual (inhibitory and excitatory) regulation of depolarization-evoked [ 3H]dopamine release in SK-N-SH cells through either μ or δ receptors. The potentiation of dopamine release by opioid agonists is mediated by N-type voltage-dependent calcium channels and does not involve G i/G o pr...

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Bibliographic Details
Published in:Brain research 1997-08, Vol.764 (1), p.277-282
Main Authors: Keren, O, Gafni, M, Sarne, Y
Format: Article
Language:English
Subjects:
Brain Neoplasms - metabolism
Calcium channel
Calcium Channel Blockers - pharmacology
Calcium Channels - drug effects
Calcium Channels - metabolism
Dopamine
Dopamine - metabolism
GTP-Binding Proteins - metabolism
Humans
Levorphanol - pharmacology
Morphine - pharmacology
Narcotics - pharmacology
Neuroblastoma
Neuroblastoma - metabolism
Neurotransmitter Agents - metabolism
Opioid Peptides - pharmacology
Opioid receptor
Pertussis toxin
Transmitter release
Tumor Cells, Cultured
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Summary:Opioids induce dual (inhibitory and excitatory) regulation of depolarization-evoked [ 3H]dopamine release in SK-N-SH cells through either μ or δ receptors. The potentiation of dopamine release by opioid agonists is mediated by N-type voltage-dependent calcium channels and does not involve G i/G o proteins. Removal of the excitatory opioid effect by blockade with ω-conotoxin, an N-channel antagonist, reveals the inhibitiory effect of opioids on release, thus suggesting that both modulatory effects of opioids are exerted in parallel.
ISSN:0006-8993
1872-6240
DOI:10.1016/S0006-8993(97)00599-4