Molecular mechanisms underlying calcium current modulation by nociceptin

Kyu Young Yeon; Mi Young Sim; Se Young Choi; Sung Joong Lee; Kyungpyo Park; Joong Soo Kim; Jong Heun Lee; Kyung Mi Lee; Seog Bae Oh

doi:10.1097/00001756-200410050-00012

Molecular mechanisms underlying calcium current modulation by nociceptin

Kyu Young Yeon, Mi Young Sim, Se Young Choi, Sung Joong Lee, Kyungpyo Park, Joong Soo Kim, Jong Heun Lee, Kyung Mi Lee, Seog Bae Oh

Department of Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

17 Citations (Scopus)

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 (I_Ca), similar to that of opioids. We investigated the molecular mechanism by which nociceptin inhibits I_ca using sensory neurons and a heterologous expression system. I_ca 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. I_Ca 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 I_Ca inhibition by nociceptin.

Original language	English
Pages (from-to)	2205-2209
Number of pages	5
Journal	Neuroreport
Volume	15
Issue number	14
DOIs	https://doi.org/10.1097/00001756-200410050-00012
Publication status	Published - 2004 Oct 5

Keywords

Calcium currents
DAMGO
Nociceptin
ORL-1
Trigeminal ganglion neurons
μOR

ASJC Scopus subject areas

Neuroscience(all)

Access to Document

10.1097/00001756-200410050-00012

Cite this

@article{c01fdf97db304443840ea18ff5980273,

title = "Molecular mechanisms underlying calcium current modulation by nociceptin",

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.",

keywords = "Calcium currents, DAMGO, Nociceptin, ORL-1, Trigeminal ganglion neurons, μOR",

author = "Yeon, {Kyu Young} and Sim, {Mi Young} and Choi, {Se Young} and Lee, {Sung Joong} and Kyungpyo Park and Kim, {Joong Soo} and Lee, {Jong Heun} and Lee, {Kyung Mi} and Oh, {Seog Bae}",

year = "2004",

month = oct,

day = "5",

doi = "10.1097/00001756-200410050-00012",

language = "English",

volume = "15",

pages = "2205--2209",

journal = "NeuroReport",

issn = "0959-4965",

publisher = "Lippincott Williams and Wilkins",

number = "14",

}

TY - JOUR

T1 - Molecular mechanisms underlying calcium current modulation by nociceptin

AU - Yeon, Kyu Young

AU - Sim, Mi Young

AU - Choi, Se Young

AU - Lee, Sung Joong

AU - Park, Kyungpyo

AU - Kim, Joong Soo

AU - Lee, Jong Heun

AU - Lee, Kyung Mi

AU - Oh, Seog Bae

PY - 2004/10/5

Y1 - 2004/10/5

N2 - 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.

AB - 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.

KW - Calcium currents

KW - DAMGO

KW - Nociceptin

KW - ORL-1

KW - Trigeminal ganglion neurons

KW - μOR

UR - http://www.scopus.com/inward/record.url?scp=6344269328&partnerID=8YFLogxK

U2 - 10.1097/00001756-200410050-00012

DO - 10.1097/00001756-200410050-00012

M3 - Article

C2 - 15371734

AN - SCOPUS:6344269328

VL - 15

SP - 2205

EP - 2209

JO - NeuroReport

JF - NeuroReport

SN - 0959-4965

IS - 14

ER -

Molecular mechanisms underlying calcium current modulation by nociceptin

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this