Abstract
Nociceptin, an endogenous agonist of the opioid receptor-like 1 (ORL 1) receptor, is implicated in a wide range of physiological functions including cardiovascular control. However, the effect of nociceptin on peripheral sympathetic ganglion neurons has not been studied. Whole-cell voltage clamp was used to study Ca 2+ currents on freshly dissociated sympathetic superior cervical ganglion neurons from juvenile rats. Nociceptin (1 μM) caused a fast inhibition of the peak currents by 69±3% in all neurons. Strong positive prepulses counteracted the inhibition of the peak current by 64% and no effect of nociceptin was observed when the cells were pre-incubated with Pertussis toxin. The inhibition was reversible and dose-dependent with an EC 50 of 508±50 pM. Blockade of N-type channels by 1 μM ω-conotoxin GVIA reduced the peak currents by 83±1% and abolished the action of nociceptin. Naloxone could not prevent the inhibition by nociceptin and [D-Ala 2, N-Me-Phe 4, Gly 5-ol] enkephalin (DAMGO) only depressed a small proportion of the current in 1/7 neurons. These data suggests that nociceptin inhibits transmitter release from sympathetic neurons by a selective blockade of N-type channels, which may be of importance for its depressive effect on the cardiovascular system.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
