The Glucocorticoid Analog Dexamethasone Alters the Expression and the Distribution of Dopamine Receptors and Enkephalin within Cortico- Subcortical Regions
Elisabetta F. Buonaguro,
Andrea 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.
Keywords: Cognition, cortex, cortisol, dexamethasone, gene expression, glucocorticoid, schizophrenia, striatum.
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