Abstract
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.
Keywords: Cognition, cortex, cortisol, dexamethasone, gene expression, glucocorticoid, schizophrenia, striatum.
Current Molecular Pharmacology
Title:The Glucocorticoid Analog Dexamethasone Alters the Expression and the Distribution of Dopamine Receptors and Enkephalin within Cortico- Subcortical Regions
Volume: 6
Author(s): Felice Iasevoli, Luigi Aloj, Gianmarco Latte, Livia Avvisati, Federica Marmo, Carmine Tomasetti, Elisabetta F. Buonaguro, Chiara Simeoli, Rosario Pivonello, Annamaria Colao and Andrea de Bartolomeis
Affiliation:
Keywords: Cognition, cortex, cortisol, dexamethasone, gene expression, glucocorticoid, schizophrenia, striatum.
Abstract: 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.
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Cite this article as:
Iasevoli Felice, Aloj Luigi, Latte Gianmarco, Avvisati Livia, Marmo Federica, Tomasetti Carmine, Buonaguro F. Elisabetta, Simeoli Chiara, Pivonello Rosario, Colao Annamaria and Bartolomeis de Andrea, The Glucocorticoid Analog Dexamethasone Alters the Expression and the Distribution of Dopamine Receptors and Enkephalin within Cortico- Subcortical Regions, Current Molecular Pharmacology 2013; 6 (3) . https://dx.doi.org/10.2174/187446720603140415215941
DOI https://dx.doi.org/10.2174/187446720603140415215941 |
Print ISSN 1874-4672 |
Publisher Name Bentham Science Publisher |
Online ISSN 1874-4702 |
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