Glucocorticoids (GC) exert multiple effects within the central nervous system via mineralocorticoid receptors (MR) and glucocorticoid receptors (GR) activation. MR expression is associated with a neuroprotective phenotype, whereas GR activation is implicated in the induction of an endangered neural phenotype and the opposite actions are most evident in hippocampus, where these receptors are predominantly present. Hippocampus has an overall inhibitory influence on the activity of the hypothalamic-pituitary-adrenal (HPA) axis and it has been suggested that efficient learning and adequate stress response depend on the appropriate functioning of the axis brought by coordinated activation of MR and GR in this region. There is a growing body of evidence that perinatal asphyxia causes irreversible damage to the brain leading to neurons loss in regions vulnerable to oxygen shortage especially in hippocampus. In the present review, some aspects of recently acquired insight in the role of GC receptors in promoting neuronal death and survival after hippocampal injury are discussed. Since the unbalance of MR and GR in hippocampus creates a condition of disturbed neuroendocrine regulation their potential impact on behavioral impairment will also be reviewed.
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