Abstract
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 language | English |
|---|---|
| Pages (from-to) | 223-235 |
| Number of pages | 13 |
| Journal | Molecular Neurobiology |
| Volume | 32 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2005 Jan 1 |
Fingerprint
All Science Journal Classification (ASJC) codes
- Cellular and Molecular Neuroscience
Cite this
}
Do stress and long-term potentiation share the same molecular mechanisms? / Huang, Chiung Chun; Yang, Chih Hao; Hsu, Kuei-Sen.
In: Molecular Neurobiology, Vol. 32, No. 3, 01.01.2005, p. 223-235.Research output: Contribution to journal › Review article
TY - JOUR
T1 - Do stress and long-term potentiation share the same molecular mechanisms?
AU - Huang, Chiung Chun
AU - Yang, Chih Hao
AU - Hsu, Kuei-Sen
PY - 2005/1/1
Y1 - 2005/1/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=28644432983&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=28644432983&partnerID=8YFLogxK
U2 - 10.1385/MN:32:3:223
DO - 10.1385/MN:32:3:223
M3 - Review article
C2 - 16385139
AN - SCOPUS:28644432983
VL - 32
SP - 223
EP - 235
JO - Molecular Neurobiology
JF - Molecular Neurobiology
SN - 0893-7648
IS - 3
ER -