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

Abstract 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.