Antagonist-induced opiate receptor upregulation in cultures of fetal mouse spinal cord-ganglion explants

Ann Tempel, Stanley M. Crain, Edith R. Peterson, Eric J. Simon, R. Suzanne Zukin

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

Chronic exposure of fetal mouse spinal cord-ganglion explants to the opioid antagonist naloxone (10 μM, 7 days) produced a pronounced upregulation of μ opioid receptors. The antagonist action was stereospecific, as it was produced by (-)-, but not by (+)-naloxone, and was dose-dependent. Half-maximal naloxone-induced receptor upregulation occurred after two days; receptor density was maximal at 5 days. Exposure of the explant cultures to naloxone (10 μM) in the presence of the protein synthesis inhibitor, cycloheximide (1 μM; a concentration which blocks >90% protein synthesis) resulted in receptor density changes that were similar to those observed in cultures exposed to naloxone alone. This finding suggests that antagonist-induced opiate receptor upregulation does not require the synthesis of new receptor molecules.

Original languageEnglish (US)
Pages (from-to)287-291
Number of pages5
JournalBrain Research
Volume390
Issue number2
StatePublished - Mar 1986

Fingerprint

Spinal Ganglia
Opioid Receptors
Naloxone
Spinal Cord
Up-Regulation
Protein Synthesis Inhibitors
Narcotic Antagonists
Cycloheximide
Proteins

Keywords

  • naloxone
  • opiate receptor
  • receptor upregulation
  • sensory ganglion
  • spinal cord
  • tissue culture

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Neurology
  • Molecular Biology
  • Developmental Biology

Cite this

Antagonist-induced opiate receptor upregulation in cultures of fetal mouse spinal cord-ganglion explants. / Tempel, Ann; Crain, Stanley M.; Peterson, Edith R.; Simon, Eric J.; Zukin, R. Suzanne.

In: Brain Research, Vol. 390, No. 2, 03.1986, p. 287-291.

Research output: Contribution to journalArticle

Tempel, A, Crain, SM, Peterson, ER, Simon, EJ & Zukin, RS 1986, 'Antagonist-induced opiate receptor upregulation in cultures of fetal mouse spinal cord-ganglion explants', Brain Research, vol. 390, no. 2, pp. 287-291.
Tempel, Ann ; Crain, Stanley M. ; Peterson, Edith R. ; Simon, Eric J. ; Zukin, R. Suzanne. / Antagonist-induced opiate receptor upregulation in cultures of fetal mouse spinal cord-ganglion explants. In: Brain Research. 1986 ; Vol. 390, No. 2. pp. 287-291.
@article{6a2758b36e684a3796b3f67fcf551305,
title = "Antagonist-induced opiate receptor upregulation in cultures of fetal mouse spinal cord-ganglion explants",
abstract = "Chronic exposure of fetal mouse spinal cord-ganglion explants to the opioid antagonist naloxone (10 μM, 7 days) produced a pronounced upregulation of μ opioid receptors. The antagonist action was stereospecific, as it was produced by (-)-, but not by (+)-naloxone, and was dose-dependent. Half-maximal naloxone-induced receptor upregulation occurred after two days; receptor density was maximal at 5 days. Exposure of the explant cultures to naloxone (10 μM) in the presence of the protein synthesis inhibitor, cycloheximide (1 μM; a concentration which blocks >90{\%} protein synthesis) resulted in receptor density changes that were similar to those observed in cultures exposed to naloxone alone. This finding suggests that antagonist-induced opiate receptor upregulation does not require the synthesis of new receptor molecules.",
keywords = "naloxone, opiate receptor, receptor upregulation, sensory ganglion, spinal cord, tissue culture",
author = "Ann Tempel and Crain, {Stanley M.} and Peterson, {Edith R.} and Simon, {Eric J.} and Zukin, {R. Suzanne}",
year = "1986",
month = "3",
language = "English (US)",
volume = "390",
pages = "287--291",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "2",

}

TY - JOUR

T1 - Antagonist-induced opiate receptor upregulation in cultures of fetal mouse spinal cord-ganglion explants

AU - Tempel, Ann

AU - Crain, Stanley M.

AU - Peterson, Edith R.

AU - Simon, Eric J.

AU - Zukin, R. Suzanne

PY - 1986/3

Y1 - 1986/3

N2 - Chronic exposure of fetal mouse spinal cord-ganglion explants to the opioid antagonist naloxone (10 μM, 7 days) produced a pronounced upregulation of μ opioid receptors. The antagonist action was stereospecific, as it was produced by (-)-, but not by (+)-naloxone, and was dose-dependent. Half-maximal naloxone-induced receptor upregulation occurred after two days; receptor density was maximal at 5 days. Exposure of the explant cultures to naloxone (10 μM) in the presence of the protein synthesis inhibitor, cycloheximide (1 μM; a concentration which blocks >90% protein synthesis) resulted in receptor density changes that were similar to those observed in cultures exposed to naloxone alone. This finding suggests that antagonist-induced opiate receptor upregulation does not require the synthesis of new receptor molecules.

AB - Chronic exposure of fetal mouse spinal cord-ganglion explants to the opioid antagonist naloxone (10 μM, 7 days) produced a pronounced upregulation of μ opioid receptors. The antagonist action was stereospecific, as it was produced by (-)-, but not by (+)-naloxone, and was dose-dependent. Half-maximal naloxone-induced receptor upregulation occurred after two days; receptor density was maximal at 5 days. Exposure of the explant cultures to naloxone (10 μM) in the presence of the protein synthesis inhibitor, cycloheximide (1 μM; a concentration which blocks >90% protein synthesis) resulted in receptor density changes that were similar to those observed in cultures exposed to naloxone alone. This finding suggests that antagonist-induced opiate receptor upregulation does not require the synthesis of new receptor molecules.

KW - naloxone

KW - opiate receptor

KW - receptor upregulation

KW - sensory ganglion

KW - spinal cord

KW - tissue culture

UR - http://www.scopus.com/inward/record.url?scp=0022686726&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0022686726&partnerID=8YFLogxK

M3 - Article

VL - 390

SP - 287

EP - 291

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 2

ER -