Abstract
Hormones secreted from the pituitary-adrenal system during stress affect learning and memory processes. The phenomenon of long-term potentiation (LTP) is a robust example of neuronal plasticity and has become widely regarded as a possible physiological substrate for learning and memory in the mammalian brain. The current study supports our previous finding that stress impairs LTP in the in vitro hippocampal slice. In addition, manipulation of the pituitary-adrenal axis by dexamethasone (DEX), a synthetic glucocorticoid that blocks the pituitary-adrenal response to stress, appears to influence the temporal patterns of the development of the neuronal plastic changes which occur immediately after tetanus (post-tetanic potentiation period, or PTP). Since the stress-induced impairment of LTP occurs, regardless of DEX treatment, we suggest the action of DEX is to modulate the temporal pattern of the PTP/LTP interaction in response to stress.
Get full access to this article
View all access options for this article.