Dopamine receptor mechanisms mediate corticotropin-releasing factor-induced long-term potentiation in the rat amygdala following cocaine withdrawal.
Dopamine receptor mechanisms mediate corticotropin-releasing factor-induced long-term potentiation in the rat amygdala following cocaine withdrawal.
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DOI:
10.1111/j.1460-9568.2010.07148.x
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发表时间:
2010-03
期刊:
影响因子:
--
通讯作者:
Shinnick-Gallagher P
中科院分区:
文献类型:
--
作者:
Krishnan B;Centeno M;Pollandt S;Fu Y;Genzer K;Liu J;Gallagher JP;Shinnick-Gallagher P
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. Our study analyzed CRF-induced synaptic plasticity, its pharmacological sensitivity, and interactions with the dopamine (DA) system in the basolateral (BLA) to lateral capsula central amygdala (lcCeA) pathway after a two 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 However, in cocaine-withdrawn animals, activation of CRF1 and CRF2 receptors was found to enhance LTP.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-like 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. It was also found that CRF1 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. In summary, CRF interactions with the DA system in the amygdala may represent a fundamental neurochemical and cellular mechanism linking stress to cocaine-induced neuronal plasticity.
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影响因子:
4.7
作者:
Chatzaki, E;Murphy, BJ;Grigoriadis, DE
通讯作者:
Grigoriadis, DE
影响因子:
5.3
作者:
Erb, S;Shaham, Y;Stewart, J
通讯作者:
Stewart, J
影响因子:
4.8
作者:
Avishai-Eliner, S;Eghbal-Ahmadi, M;Baram, TZ
通讯作者:
Baram, TZ
影响因子:
25
作者:
Bissière, S;Humeau, Y;Lüthi, A
通讯作者:
Lüthi, A
DOI:
10.1111/j.1749-6632.1997.tb46161.x
发表时间:
1997-01-01
期刊:
NEUROPEPTIDES IN DEVELOPMENT AND AGING
影响因子:
--
作者:
Baram, TZ;Yi, SJ;Schultz, L
通讯作者:
Schultz, L