Corticosteroid effects on cellular physiology of limbic cells

Abstract

After stress, circulating levels of stress hormones such as corticosterone are markedly increased. This will have an impact on the neurophysiology of limbic neurons that highly express corticosteroid receptors. Over the past decades several principles about the neurophysiological impact of corticosterone have emerged. First, corticosterone can quickly raise the excitability of hippocampal CA1 neurons shortly after stress exposure, via a nongenomic pathway involving mineralocorticoid receptors presumably located in the pre- as well as postsynaptic membrane. At the same time, gene-mediated actions via the glucocorticoid receptor are started which some hours later will result in enhanced calcium influx and impaired ability to induce long-term potentiation. These delayed actions are interpreted as a means to slowly normalize hippocampal activity and preserve information encoded early on after stress. Second, the full spectrum of neurophysiological actions by corticosterone is accomplished in interaction with other stress mediators, like noradrenaline. Third, these effects in the CA1 hippocampal region cannot be generalized to other brain regions such as the basolateral amygdala or paraventricular nucleus: There seems to be a highly differentiated response, which could serve to facilitate neuroendocrine/cognitive processing of some aspects of stress-related information, but attenuate other aspects. Finally, the time- and region-specific corticosteroid actions strongly depend on the individual's life history.