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

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Down-regulation of BDNF mRNA, with no effect on trkB or glucocorticoid receptor m RNAs, in the porcine hippocampus after acute dexamethasone treatment.

Glucocorticoids bind to hippocampal mineralo-(MR) and gluco-(GR) corticoid receptors and, at high concentrations (e.g. as seen following treatment with pharmacological doses of corticosteroids or during stress), may affect hippocampal neuronal function. Such actions could involve brain-derived neurotrophic factor (BDNF), its receptor, trkB, and the excitatory neurotransmitter, glutamate. This experiment investigated the effect of a single intravenous (i.v.) injection of the synthetic glucocorticoid, dexamethasone (Dex, 5 mg kg(-1)) on gene expression for MR s, GR s, BDNF, trkB, and selected ionotropic glutamate receptor subunits (iGluRs), in the porcine hippocampus. Quantification of m RNA s in the brains of pigs (n = 4/treatment) killed 24 hours after saline or Dex administration indicated a significant Dex-induced decrease in BDNF m RNA in all hippocampal regions. However, gene expression for MR s, GR s, trkB and iGluRs was unaffected at this time-point.[1]

References

  1. Down-regulation of BDNF mRNA, with no effect on trkB or glucocorticoid receptor m RNAs, in the porcine hippocampus after acute dexamethasone treatment. Vellucci, S.V., Parrott, R.F., Mimmack, M.L. Res. Vet. Sci. (2001) [Pubmed]
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