Stress is a biological, significant factor shown to influence hippocampal synaptic plasticity and cognitive functions. Although numerous studies have reported that stress produces a suppression in long-term potentiation (LTP; a putative synaptic mechanism underlying learning and memory), little is known about the mechanism by which this occurs. Because the effects of stress on LTP and its converse process, long-term depression (LTD), parallel the changes in synaptic plasticity that occur following the establishment of LTP with tetanic stimulation (i.e., occluding LTP and enhancing LTD induction), it has been proposed that stress affects subsequent hippocampal plasticity by sharing the same molecular machinery required to support LTP This article summarizes recent findings from ours and other laboratories to assess this view and discusses relevant hypotheses in the study of stress-related modifications of synaptic plasticity.
- Extracellular signal-related kinase (ERK)
- Glucocorticoid receptor
- Long-term potentiation (LTP)
- Mitogen-activated protein kinase (MAPK)
- N-methyl-D-aspartate (NMDA) receptors
ASJC Scopus subject areas