Characterization of opioid receptors in rat nucleus accumbens following mesolimbic dopaminergic lesions

Ellen M. Unterwald, Ann Tempel, George F. Koob, R. Suzanne Zukin

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

The present study investigated the cellular localization of μ, δ and κ opioid receptors in the rat nucleus accumbens in relation to dopaminergic neurons. Dopaminergic terminals were destroyed by intra-accumbens injections of the neurotoxin 6-hydroxydopamine (6-OHDA). Fourteen days after dopaminergic denervation, receptor binding assays and quantitative in vitro autoradiography with highly selective radioligands demonstrated that the density of μ opioid receptors in the nucleus accumbens was decreased by 30 ± 6%. There was no change in δ or κ receptors in the accumbens, a finding which indicates that the loss of μ opioid receptors was specific. A time course study demonstrated that the loss of μ receptors lagged behind the depletion of dopamine by about 5 days. Destruction of intrinsic neuronal cell bodies and dendrites by injection of ibotenic acid into the accumbens resulted in a loss of 36 ± 3% of μ opioid receptors. Co-injection of 6-OHDA and ibotenic acid decreased μ receptors by 41 ± 4%, only slightly more than the loss caused by ibotenic acid alone. These results suggest that only a small number of μ opioid receptors in the nucleus accumbens are located on dopaminergic terminals and are consistent with the possibility that the loss of opioid receptors following denervation of dopaminergic fibers in the accumbens is the result of transsynaptic degeneration.

Original languageEnglish (US)
Pages (from-to)111-118
Number of pages8
JournalBrain Research
Volume505
Issue number1
DOIs
StatePublished - Dec 25 1989

Fingerprint

Nucleus Accumbens
Opioid Receptors
Ibotenic Acid
Oxidopamine
Denervation
Injections
Dopaminergic Neurons
Neurotoxins
Dendrites
Autoradiography
Dopamine

Keywords

  • Cellular localization
  • Lesion
  • Mesolimbic dopamine
  • Nucleus accumbens
  • Opioid receptor
  • Receptor autoradiography

ASJC Scopus subject areas

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

Cite this

Characterization of opioid receptors in rat nucleus accumbens following mesolimbic dopaminergic lesions. / Unterwald, Ellen M.; Tempel, Ann; Koob, George F.; Zukin, R. Suzanne.

In: Brain Research, Vol. 505, No. 1, 25.12.1989, p. 111-118.

Research output: Contribution to journalArticle

Unterwald, Ellen M. ; Tempel, Ann ; Koob, George F. ; Zukin, R. Suzanne. / Characterization of opioid receptors in rat nucleus accumbens following mesolimbic dopaminergic lesions. In: Brain Research. 1989 ; Vol. 505, No. 1. pp. 111-118.
@article{59f8774790c74793914ac0be60d33e16,
title = "Characterization of opioid receptors in rat nucleus accumbens following mesolimbic dopaminergic lesions",
abstract = "The present study investigated the cellular localization of μ, δ and κ opioid receptors in the rat nucleus accumbens in relation to dopaminergic neurons. Dopaminergic terminals were destroyed by intra-accumbens injections of the neurotoxin 6-hydroxydopamine (6-OHDA). Fourteen days after dopaminergic denervation, receptor binding assays and quantitative in vitro autoradiography with highly selective radioligands demonstrated that the density of μ opioid receptors in the nucleus accumbens was decreased by 30 ± 6{\%}. There was no change in δ or κ receptors in the accumbens, a finding which indicates that the loss of μ opioid receptors was specific. A time course study demonstrated that the loss of μ receptors lagged behind the depletion of dopamine by about 5 days. Destruction of intrinsic neuronal cell bodies and dendrites by injection of ibotenic acid into the accumbens resulted in a loss of 36 ± 3{\%} of μ opioid receptors. Co-injection of 6-OHDA and ibotenic acid decreased μ receptors by 41 ± 4{\%}, only slightly more than the loss caused by ibotenic acid alone. These results suggest that only a small number of μ opioid receptors in the nucleus accumbens are located on dopaminergic terminals and are consistent with the possibility that the loss of opioid receptors following denervation of dopaminergic fibers in the accumbens is the result of transsynaptic degeneration.",
keywords = "Cellular localization, Lesion, Mesolimbic dopamine, Nucleus accumbens, Opioid receptor, Receptor autoradiography",
author = "Unterwald, {Ellen M.} and Ann Tempel and Koob, {George F.} and Zukin, {R. Suzanne}",
year = "1989",
month = "12",
day = "25",
doi = "10.1016/0006-8993(89)90120-0",
language = "English (US)",
volume = "505",
pages = "111--118",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - Characterization of opioid receptors in rat nucleus accumbens following mesolimbic dopaminergic lesions

AU - Unterwald, Ellen M.

AU - Tempel, Ann

AU - Koob, George F.

AU - Zukin, R. Suzanne

PY - 1989/12/25

Y1 - 1989/12/25

N2 - The present study investigated the cellular localization of μ, δ and κ opioid receptors in the rat nucleus accumbens in relation to dopaminergic neurons. Dopaminergic terminals were destroyed by intra-accumbens injections of the neurotoxin 6-hydroxydopamine (6-OHDA). Fourteen days after dopaminergic denervation, receptor binding assays and quantitative in vitro autoradiography with highly selective radioligands demonstrated that the density of μ opioid receptors in the nucleus accumbens was decreased by 30 ± 6%. There was no change in δ or κ receptors in the accumbens, a finding which indicates that the loss of μ opioid receptors was specific. A time course study demonstrated that the loss of μ receptors lagged behind the depletion of dopamine by about 5 days. Destruction of intrinsic neuronal cell bodies and dendrites by injection of ibotenic acid into the accumbens resulted in a loss of 36 ± 3% of μ opioid receptors. Co-injection of 6-OHDA and ibotenic acid decreased μ receptors by 41 ± 4%, only slightly more than the loss caused by ibotenic acid alone. These results suggest that only a small number of μ opioid receptors in the nucleus accumbens are located on dopaminergic terminals and are consistent with the possibility that the loss of opioid receptors following denervation of dopaminergic fibers in the accumbens is the result of transsynaptic degeneration.

AB - The present study investigated the cellular localization of μ, δ and κ opioid receptors in the rat nucleus accumbens in relation to dopaminergic neurons. Dopaminergic terminals were destroyed by intra-accumbens injections of the neurotoxin 6-hydroxydopamine (6-OHDA). Fourteen days after dopaminergic denervation, receptor binding assays and quantitative in vitro autoradiography with highly selective radioligands demonstrated that the density of μ opioid receptors in the nucleus accumbens was decreased by 30 ± 6%. There was no change in δ or κ receptors in the accumbens, a finding which indicates that the loss of μ opioid receptors was specific. A time course study demonstrated that the loss of μ receptors lagged behind the depletion of dopamine by about 5 days. Destruction of intrinsic neuronal cell bodies and dendrites by injection of ibotenic acid into the accumbens resulted in a loss of 36 ± 3% of μ opioid receptors. Co-injection of 6-OHDA and ibotenic acid decreased μ receptors by 41 ± 4%, only slightly more than the loss caused by ibotenic acid alone. These results suggest that only a small number of μ opioid receptors in the nucleus accumbens are located on dopaminergic terminals and are consistent with the possibility that the loss of opioid receptors following denervation of dopaminergic fibers in the accumbens is the result of transsynaptic degeneration.

KW - Cellular localization

KW - Lesion

KW - Mesolimbic dopamine

KW - Nucleus accumbens

KW - Opioid receptor

KW - Receptor autoradiography

UR - http://www.scopus.com/inward/record.url?scp=0024805214&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024805214&partnerID=8YFLogxK

U2 - 10.1016/0006-8993(89)90120-0

DO - 10.1016/0006-8993(89)90120-0

M3 - Article

C2 - 2558779

AN - SCOPUS:0024805214

VL - 505

SP - 111

EP - 118

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1

ER -