The glucocorticoid analog dexamethasone alters the expression and the distribution of dopamine receptors and enkephalin within cortico-subcortical regions.
The glucocorticoid analog dexamethasone alters the expression and the distribution of dopamine receptors and enkephalin within cortico-subcortical regions.
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糖皮质激素类似物地塞米松改变皮质-皮质下区域内多巴胺受体和脑啡肽的表达和分布。
DOI:
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发表时间:
2013
影响因子:
2.7
通讯作者:
A. de Bartolomeis
中科院分区:
文献类型:
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作者:
F. Iasevoli;L. Aloj;G. Latte;L. Avvisati;F. Marmo;C. Tomasetti;E. Buonaguro;C. Simeoli;R. Pivonello;A. Colao;A. de Bartolomeis
In humans, glucocorticoid excess may cause neuropsychiatric symptoms, including psychosis and cognitive impairment, and glucocorticoid signaling hyperactivation may sensitize to substance of abuse. The aim of this work was to evaluate whether exposure to glucocorticoid excess triggers molecular changes in dopaminergic and opioidergic systems within relevant forebrain areas. We acutely exposed Sprague-Dawley rats to dexamethasone, a glucocorticoid analog, or vehicle and evaluated the mRNA expression of dopamine D1 and D2 receptors and enkephalin within the cortex, the striatum, and the midbrain. Dexamethasone reduced mRNA expression of D1 receptor and enkephalin in the cortex. In the striatum, dexamethasone reduced the expression of D1 receptor mRNA, but not that of D2 receptor and enkephalin. No significant changes in D2 receptor mRNA expression were observed in the midbrain. Basal distribution of D1 and D2 receptor mRNA showed a clear-cut striatal/cortical gradient, while this distribution was less obvious for enkephalin mRNA. Dexamethasone increased the cortico-striatal separation in terms of D1 and D2 receptor mRNA expression. These molecular changes may represent adaptive mechanisms to dexamethasone-induced potentiation of dopaminergic and opioidergic transmission, mostly in cortical areas.
DOI:
10.1073/pnas.0402208101
发表时间:
2004-08
影响因子:
11.1
作者:
Qiang Wei;Xin-Yun Lu;Li Liu;G. Schafer;K. Shieh;S. Burke;T. Robinson;S. Watson;A. Seasholtz;H. Akil
通讯作者:
Qiang Wei;Xin-Yun Lu;Li Liu;G. Schafer;K. Shieh;S. Burke;T. Robinson;S. Watson;A. Seasholtz;H. Akil