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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Chronic dexamethasone-treatment alters mineralocorticoid receptor, truncated trkB and selected glutamate receptor subunit mRNA expression in the porcine hippocampus.

Prepubertal boars (n = 4/treatment) were killed 24 h after a 5 day course of intravenous injections of dexamethasone (Dex, 1 and 5 mg kg(-1)), or saline vehicle. Gene expression was quantified in brain sections following in situ hybridisation histochemistry. The objective was to determine whether chronic glucocorticoid treatment would alter the expression of mRNAs for gluco- and mineralocorticoid receptors (GR and MR), brain-derived neurotrophic factor (BDNF), its receptor, trkB, and selected ionotropic glutamate receptor (iGluR) subunits in the hippocampus. Although Dex did not alter GR message, the higher dose reduced MR mRNA in all hippocampal subfields studied. There was no effect of Dex on the expression of BDNF, or the full-length form of its receptor but there was evidence to suggest that mRNA for the truncated form of trkB was increased. Expression of mRNA for glutamate receptor subunits was either unaffected (NR1) or decreased (GluR2 and GluR3). These findings indicate that acute and chronic glucocorticoid treatment has differential effects on hippocampal gene expression in the porcine brain.[1]

References

  1. Chronic dexamethasone-treatment alters mineralocorticoid receptor, truncated trkB and selected glutamate receptor subunit mRNA expression in the porcine hippocampus. Vellucci, S.V., Parrott, R.F., Mimmack, M.L. Neuropeptides (2002) [Pubmed]
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