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Glucocorticoid and Mineralocorticoid Receptor mRNA Expression in Rat Brain
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1989
Year
GlucocorticoidType IiSocial SciencesRat BrainAdrenal GlandReceptor MrnasType Ii ReceptorNeuroendocrine MechanismNeuroimmunologyNeurochemistryNeuropharmacologyMineralocorticoid Receptor BiologyNervous SystemEndocrinologyPharmacologyNeurophysiologyPhysiologyNeuroscienceBiological PsychiatryMedicine
Corticosterone in the rat brain signals through two receptor types, type I (MR) and type II (GR), encoded by the MR and GR genes. The authors examined glucocorticoid regulation of these receptors using a cytosol receptor binding assay and molecular probes to quantify GR and MR mRNA levels. Type II receptor binding and GR mRNA were uniformly distributed across brain regions, whereas type I binding and MR mRNA were concentrated in the hippocampus; adrenalectomy increased, and corticosterone decreased, hippocampal binding of both receptor types, yet neither treatment altered MR or GR mRNA, indicating that binding changes are not driven by steady‑state mRNA levels.
In the rat brain, the binding of corticosterone is mediated through two receptor types, the type I receptor and the type II receptor, which are presumed to be encoded by genes designated as MR and GR, respectively. We have studied the regulation of these receptors by glucocorticoids, utilizing a cytosol receptor binding assay. In addition, we have employed molecular probes for the GR and the MR to measure receptor mRNAs. The level of type II receptor binding is uniform across several brain regions, as is the expression of GR (type II) mRNA. In contrast, type I receptor binding is concentrated in the hippocampus, and the MR (type I) mRNA similarly shows a higher level of expression in hippocampus than in the other brain regions studied. Removal of endogenous glucocorticoids by adrenalectomy (ADX) induces an increase, and corticosterone administration results in a decrease, in the level of type I and type II binding in the hippocampus; however, no significant changes in the MR (type I) or GR (type II) mRNA levels are seen with these treatments. The diurnal variation of serum corticosterone in intact rats is correlated with a circadian regulation of type I receptor binding in the hippocampus, while MR (type I) mRNA expression is unaffected. Thus, the changes in type I and type II receptor binding capacity elicited by differing steroid conditions cannot be attributed to modulation of the steady state levels of MR (type I) or GR (type II) mRNA.