Glucocorticoid Receptor Blocking Increases Hippocampal CNTF Levels after Acute Ischemic Stroke

Ischemic stroke is one of the most common neurological pathologies, leading to a decrease in the quality of life. After stroke, the area of primary damage is most often localized in the neocortex, but later damage can spread to structures distant from the infarction zone, in particular, to the hippocampus. Activation of the hypothalamic-pituitary-adrenal system (HPAS) is one of the early neuroendocrine responses to cerebral ischemia, an increase in the release of corticosterone (CS) by the adrenal glands into the blood leads to its increased accumulation in the hippocampus, which, according to our hypothesis, may predetermine its damage and the development of delayed cognitive and affective disorders. The state of the neurotrophic factor system may determine the neuroprotective potential of the hippocampus when the HPAS is activated. The present work investigated the effect of glucocorticoid signaling on CNTF expression in the hippocampus of rats in the acute period after middle cerebral artery occlusion (MCAO). An increase in the level of CS in the blood occurred early after MCAO and was accompanied by the accumulation of stress hormone in the hippocampus of the ischemic hemisphere. MCAO combined with the administration of the glucocorticoid receptor blocker Mifepristone was followed by an increase in CNTF levels, which was not observed with the administration of a vehicle, which may indicate the participation of glucocorticoid receptors in modulating the content of this neurotrophic factor in the hippocampus.