Do stress and long-term potentiation share the same molecular mechanisms?

Chiung Chun Huang, Chih Hao Yang, Kuei Sen Hsu

Research output: Contribution to journalReview articlepeer-review

44 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)223-235
Number of pages13
JournalMolecular Neurobiology
Issue number3
Publication statusPublished - Dec 2005
Externally publishedYes


  • Extracellular signal-related kinase (ERK)
  • Glucocorticoid receptor
  • Hippocampus
  • Long-term potentiation (LTP)
  • Mitogen-activated protein kinase (MAPK)
  • N-methyl-D-aspartate (NMDA) receptors
  • Stress

ASJC Scopus subject areas

  • Neurology
  • Cellular and Molecular Neuroscience


Dive into the research topics of 'Do stress and long-term potentiation share the same molecular mechanisms?'. Together they form a unique fingerprint.

Cite this