Abstract
Nociceptin is a non-opioid peptide that modulates pain response. One of mechanism underlying its analgesic action is the inhibition of voltage-dependent calcium current (ICa), similar to that of opioids. We investigated the molecular mechanism by which nociceptin inhibits Ica using sensory neurons and a heterologous expression system. Ica inhibition by nociceptin was voltage-dependent, exhibited the slowing of activation kinetics and prepulse facilitation, and was blocked by N-ethylmaleimide, indicating the involvement of Gi/Go protein. ICa inhibition by nociceptin was primarily mediated through binding to its own receptor, ORL-1, but not through affecting other μ-opioid receptors. Thus, our results strongly demonstrate that heterologous cross-talk between ORL1 and μOR is not involved in the ICa inhibition by nociceptin.
Original language | English |
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Pages (from-to) | 2205-2209 |
Number of pages | 5 |
Journal | Neuroreport |
Volume | 15 |
Issue number | 14 |
DOIs | |
Publication status | Published - 2004 Oct 5 |
Keywords
- Calcium currents
- DAMGO
- Nociceptin
- ORL-1
- Trigeminal ganglion neurons
- μOR
ASJC Scopus subject areas
- Neuroscience(all)