Dopamine receptor mechanisms mediate corticotropin-releasing factor-induced long-term potentiation in the rat amygdala following cocaine withdrawal

Balaji Krishnan, Marjorie Centeno, Sebastian Pollandt, Yu Fu, Kathy Genzer, Jie Liu, Joel P. Gallagher, Patricia Shinnick-Gallagher

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

Corticotropin-releasing factor (CRF) in the amygdala is involved in stress responses. Moreover, dopaminergic neurotransmission in the brain reward system including the amygdala plays a significant role in the pathology of cocaine addiction. The present study analysed CRF-induced synaptic plasticity, its pharmacological sensitivity and interactions with the dopamine (DA) system in the basolateral to lateral capsula central amygdala (lcCeA) pathway after a 2-week withdrawal from repeated cocaine administration. A physiologically relevant CRF concentration (25 nm) induced long-term potentiation (LTP) that was enhanced after cocaine withdrawal. In saline-treated rats, CRF-induced LTP was mediated through N-methyl-d-aspartate (NMDA) receptors, L-type voltage-gated calcium channels (L-VGCCs) and CRF1 receptors. However, in cocaine-withdrawn animals, activation of CRF1 and CRF2 receptors was found to enhance LTP. This enhanced CRF-induced LTP after cocaine withdrawal was mediated through endogenous activation of both D1- and D2-like receptors. Furthermore, expression of the D1 receptor (D1R) but not the D2R, D3R, D4R or D5R was significantly increased after cocaine withdrawal. CRF 1 but not CRF2 protein expression was increased, suggesting that elevated levels of these proteins contributed to the enhancement of CRF-induced LTP during cocaine withdrawal. CRF interactions with the DA system in the amygdala may represent a fundamental neurochemical and cellular mechanism linking stress to cocaine-induced neuronal plasticity.

Original languageEnglish (US)
Pages (from-to)1027-1042
Number of pages16
JournalEuropean Journal of Neuroscience
Volume31
Issue number6
DOIs
StatePublished - Mar 2010

Fingerprint

Long-Term Potentiation
Corticotropin-Releasing Hormone
Dopamine Receptors
Amygdala
Cocaine
Neuronal Plasticity
Dopamine
Calcium-Sensing Receptors
Cocaine-Related Disorders
Calcium Channels
Reward
Synaptic Transmission
Proteins
Pharmacology
Pathology
Brain

Keywords

  • Basolateral amygdala to central amygdala
  • Cocaine withdrawal
  • CRF receptors
  • Field EPSP
  • GABAergic inhibition
  • Synaptic transmission

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Dopamine receptor mechanisms mediate corticotropin-releasing factor-induced long-term potentiation in the rat amygdala following cocaine withdrawal. / Krishnan, Balaji; Centeno, Marjorie; Pollandt, Sebastian; Fu, Yu; Genzer, Kathy; Liu, Jie; Gallagher, Joel P.; Shinnick-Gallagher, Patricia.

In: European Journal of Neuroscience, Vol. 31, No. 6, 03.2010, p. 1027-1042.

Research output: Contribution to journalArticle

Krishnan, Balaji ; Centeno, Marjorie ; Pollandt, Sebastian ; Fu, Yu ; Genzer, Kathy ; Liu, Jie ; Gallagher, Joel P. ; Shinnick-Gallagher, Patricia. / Dopamine receptor mechanisms mediate corticotropin-releasing factor-induced long-term potentiation in the rat amygdala following cocaine withdrawal. In: European Journal of Neuroscience. 2010 ; Vol. 31, No. 6. pp. 1027-1042.
@article{b76fae916ee045c597c1990be2515afa,
title = "Dopamine receptor mechanisms mediate corticotropin-releasing factor-induced long-term potentiation in the rat amygdala following cocaine withdrawal",
abstract = "Corticotropin-releasing factor (CRF) in the amygdala is involved in stress responses. Moreover, dopaminergic neurotransmission in the brain reward system including the amygdala plays a significant role in the pathology of cocaine addiction. The present study analysed CRF-induced synaptic plasticity, its pharmacological sensitivity and interactions with the dopamine (DA) system in the basolateral to lateral capsula central amygdala (lcCeA) pathway after a 2-week withdrawal from repeated cocaine administration. A physiologically relevant CRF concentration (25 nm) induced long-term potentiation (LTP) that was enhanced after cocaine withdrawal. In saline-treated rats, CRF-induced LTP was mediated through N-methyl-d-aspartate (NMDA) receptors, L-type voltage-gated calcium channels (L-VGCCs) and CRF1 receptors. However, in cocaine-withdrawn animals, activation of CRF1 and CRF2 receptors was found to enhance LTP. This enhanced CRF-induced LTP after cocaine withdrawal was mediated through endogenous activation of both D1- and D2-like receptors. Furthermore, expression of the D1 receptor (D1R) but not the D2R, D3R, D4R or D5R was significantly increased after cocaine withdrawal. CRF 1 but not CRF2 protein expression was increased, suggesting that elevated levels of these proteins contributed to the enhancement of CRF-induced LTP during cocaine withdrawal. CRF interactions with the DA system in the amygdala may represent a fundamental neurochemical and cellular mechanism linking stress to cocaine-induced neuronal plasticity.",
keywords = "Basolateral amygdala to central amygdala, Cocaine withdrawal, CRF receptors, Field EPSP, GABAergic inhibition, Synaptic transmission",
author = "Balaji Krishnan and Marjorie Centeno and Sebastian Pollandt and Yu Fu and Kathy Genzer and Jie Liu and Gallagher, {Joel P.} and Patricia Shinnick-Gallagher",
year = "2010",
month = "3",
doi = "10.1111/j.1460-9568.2010.07148.x",
language = "English (US)",
volume = "31",
pages = "1027--1042",
journal = "European Journal of Neuroscience",
issn = "0953-816X",
publisher = "Wiley-Blackwell",
number = "6",

}

TY - JOUR

T1 - Dopamine receptor mechanisms mediate corticotropin-releasing factor-induced long-term potentiation in the rat amygdala following cocaine withdrawal

AU - Krishnan, Balaji

AU - Centeno, Marjorie

AU - Pollandt, Sebastian

AU - Fu, Yu

AU - Genzer, Kathy

AU - Liu, Jie

AU - Gallagher, Joel P.

AU - Shinnick-Gallagher, Patricia

PY - 2010/3

Y1 - 2010/3

N2 - Corticotropin-releasing factor (CRF) in the amygdala is involved in stress responses. Moreover, dopaminergic neurotransmission in the brain reward system including the amygdala plays a significant role in the pathology of cocaine addiction. The present study analysed CRF-induced synaptic plasticity, its pharmacological sensitivity and interactions with the dopamine (DA) system in the basolateral to lateral capsula central amygdala (lcCeA) pathway after a 2-week withdrawal from repeated cocaine administration. A physiologically relevant CRF concentration (25 nm) induced long-term potentiation (LTP) that was enhanced after cocaine withdrawal. In saline-treated rats, CRF-induced LTP was mediated through N-methyl-d-aspartate (NMDA) receptors, L-type voltage-gated calcium channels (L-VGCCs) and CRF1 receptors. However, in cocaine-withdrawn animals, activation of CRF1 and CRF2 receptors was found to enhance LTP. This enhanced CRF-induced LTP after cocaine withdrawal was mediated through endogenous activation of both D1- and D2-like receptors. Furthermore, expression of the D1 receptor (D1R) but not the D2R, D3R, D4R or D5R was significantly increased after cocaine withdrawal. CRF 1 but not CRF2 protein expression was increased, suggesting that elevated levels of these proteins contributed to the enhancement of CRF-induced LTP during cocaine withdrawal. CRF interactions with the DA system in the amygdala may represent a fundamental neurochemical and cellular mechanism linking stress to cocaine-induced neuronal plasticity.

AB - Corticotropin-releasing factor (CRF) in the amygdala is involved in stress responses. Moreover, dopaminergic neurotransmission in the brain reward system including the amygdala plays a significant role in the pathology of cocaine addiction. The present study analysed CRF-induced synaptic plasticity, its pharmacological sensitivity and interactions with the dopamine (DA) system in the basolateral to lateral capsula central amygdala (lcCeA) pathway after a 2-week withdrawal from repeated cocaine administration. A physiologically relevant CRF concentration (25 nm) induced long-term potentiation (LTP) that was enhanced after cocaine withdrawal. In saline-treated rats, CRF-induced LTP was mediated through N-methyl-d-aspartate (NMDA) receptors, L-type voltage-gated calcium channels (L-VGCCs) and CRF1 receptors. However, in cocaine-withdrawn animals, activation of CRF1 and CRF2 receptors was found to enhance LTP. This enhanced CRF-induced LTP after cocaine withdrawal was mediated through endogenous activation of both D1- and D2-like receptors. Furthermore, expression of the D1 receptor (D1R) but not the D2R, D3R, D4R or D5R was significantly increased after cocaine withdrawal. CRF 1 but not CRF2 protein expression was increased, suggesting that elevated levels of these proteins contributed to the enhancement of CRF-induced LTP during cocaine withdrawal. CRF interactions with the DA system in the amygdala may represent a fundamental neurochemical and cellular mechanism linking stress to cocaine-induced neuronal plasticity.

KW - Basolateral amygdala to central amygdala

KW - Cocaine withdrawal

KW - CRF receptors

KW - Field EPSP

KW - GABAergic inhibition

KW - Synaptic transmission

UR - http://www.scopus.com/inward/record.url?scp=77949545007&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77949545007&partnerID=8YFLogxK

U2 - 10.1111/j.1460-9568.2010.07148.x

DO - 10.1111/j.1460-9568.2010.07148.x

M3 - Article

C2 - 20377617

AN - SCOPUS:77949545007

VL - 31

SP - 1027

EP - 1042

JO - European Journal of Neuroscience

JF - European Journal of Neuroscience

SN - 0953-816X

IS - 6

ER -