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 mu or delta receptors. The potentiation of dopamine release by opioid agonists is mediated by N-type voltage-dependent calcium channels and does not involve Gi/Go proteins. Removal of the excitatory opioid effect by blockade with omega-conotoxin, an N-channel antagonist, reveals the inhibitory effect of opioids on release, thus suggesting that both modulatory effects of opioids are exerted in parallel.
Keren
O
O
Department of Physiology and Pharmacology, Sackler School of Medicine, Tel-Aviv University, Israel.
Gafni
M
M
Sarne
Y
Y
D001932:Brain Neoplasms / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism; D019204:GTP-Binding Proteins / Q000378:metabolism; D006801:Humans; D007981:Levorphanol / Q000494:pharmacology; D009020:Morphine / Q000494:pharmacology; D009294:Narcotics / Q000494:pharmacology; D009447:Neuroblastoma / Q000378:metabolism*; D018377:Neurotransmitter Agents / Q000378:metabolism*; D018847:Opioid Peptides / Q000494:pharmacology*; D014407:Tumor Cells, Cultured
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D009294:Narcotics; D018377:Neurotransmitter Agents; D018847:Opioid Peptides; D007981:Levorphanol; D009020:Morphine; D019204:GTP-Binding Proteins; D004298:Dopamine