Dynorphin reduces calcium-dependent action potential duration by decreasing voltage-dependent calcium conductance.
The opioid peptide dynorphin decreased somatic calcium-dependent action potential duration in a portion of mouse dorsal root ganglion (DRG) neurons without altering resting membrane potential or conductance. Dynorphin action was antagonized by naloxone. Responses of DRG neurons to dynorphin differed from responses to the opioid peptides leucine-enkephalin, which binds preferentially to delta-opiate receptors, and morphiceptin, which binds preferentially to mu-opiate receptors. Firstly, many DRG neurons responded to dynorphin but not to leucine-enkephalin or morphiceptin. Secondly, dynorphin responses, unlike leucine-enkephalin or morphiceptin responses, persisted following intracellular injection of cesium, a potassium channel blocker. We suggest that dynorphin acts at an opiate receptor distinct from mu- and delta-receptors and that this receptor is coupled to a voltage-dependent calcium channel.
D000200:Action Potentials / Q000187:drug effects*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D004399:Dynorphins; D004723:Endorphins / Q000494:pharmacology; D004743:Enkephalin, Leucine / Q000494:pharmacology; D005727:Ganglia, Spinal / Q000187:drug effects*; D007473:Ion Channels / Q000187:drug effects*; D051379:Mice; D009270:Naloxone / Q000494:pharmacology; D010446:Peptide Fragments / Q000494:pharmacology; D011957:Receptors, Opioid / Q000187:drug effects*
D004723:Endorphins; D007473:Ion Channels; D010446:Peptide Fragments; D011957:Receptors, Opioid; D009270:Naloxone; D004743:Enkephalin, Leucine; D004399:Dynorphins; C028889:morphiceptin; D002118:Calcium