Abstract
Reactive oxygen species (ROS) typically are characterized as molecules involved in neurotoxicity and neurodegeneration. However, recent evidence from both neuronal and nonneuronal cells suggests that ROS also function as small messenger molecules that are normal components of signal transduction cascades during physiological processes. Consistent with this idea, ROS have been shown to be critical for hippocampal long-term potentiation (LTP), a form of synaptic plasticity widely studied as a cellular substrate for learning and memory. On the other hand, ROS also have been shown to be involved in aging-related impairment of LTP. This review discusses the evidence supporting the notion that ROS both contribute to normal LTP and are involved in age-related impairment of LTP. We also discuss possible sources that might be responsible for the production of ROS after the induction of LTP. Finally, we propose a functional ROS continuum to help explain this dichotomy of ROS function in hippocampal LTP.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1-7 |
| Number of pages | 7 |
| Journal | Journal of Neuroscience Research |
| Volume | 70 |
| Issue number | 1 |
| DOIs | |
| State | Published - Oct 1 2002 |
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Keywords
- Hydrogen peroxide
- Interleukin
- Learning and memory
- Protein kinases
- Superoxide
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Role of reactive oxygen species in hippocampal long-term potentiation : Contributory or inhibitory? / Knapp, Lauren T.; Klann, Eric.
In: Journal of Neuroscience Research, Vol. 70, No. 1, 01.10.2002, p. 1-7.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Role of reactive oxygen species in hippocampal long-term potentiation
T2 - Contributory or inhibitory?
AU - Knapp, Lauren T.
AU - Klann, Eric
PY - 2002/10/1
Y1 - 2002/10/1
N2 - Reactive oxygen species (ROS) typically are characterized as molecules involved in neurotoxicity and neurodegeneration. However, recent evidence from both neuronal and nonneuronal cells suggests that ROS also function as small messenger molecules that are normal components of signal transduction cascades during physiological processes. Consistent with this idea, ROS have been shown to be critical for hippocampal long-term potentiation (LTP), a form of synaptic plasticity widely studied as a cellular substrate for learning and memory. On the other hand, ROS also have been shown to be involved in aging-related impairment of LTP. This review discusses the evidence supporting the notion that ROS both contribute to normal LTP and are involved in age-related impairment of LTP. We also discuss possible sources that might be responsible for the production of ROS after the induction of LTP. Finally, we propose a functional ROS continuum to help explain this dichotomy of ROS function in hippocampal LTP.
AB - Reactive oxygen species (ROS) typically are characterized as molecules involved in neurotoxicity and neurodegeneration. However, recent evidence from both neuronal and nonneuronal cells suggests that ROS also function as small messenger molecules that are normal components of signal transduction cascades during physiological processes. Consistent with this idea, ROS have been shown to be critical for hippocampal long-term potentiation (LTP), a form of synaptic plasticity widely studied as a cellular substrate for learning and memory. On the other hand, ROS also have been shown to be involved in aging-related impairment of LTP. This review discusses the evidence supporting the notion that ROS both contribute to normal LTP and are involved in age-related impairment of LTP. We also discuss possible sources that might be responsible for the production of ROS after the induction of LTP. Finally, we propose a functional ROS continuum to help explain this dichotomy of ROS function in hippocampal LTP.
KW - Hydrogen peroxide
KW - Interleukin
KW - Learning and memory
KW - Protein kinases
KW - Superoxide
UR - http://www.scopus.com/inward/record.url?scp=0036785151&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036785151&partnerID=8YFLogxK
U2 - 10.1002/jnr.10371
DO - 10.1002/jnr.10371
M3 - Article
VL - 70
SP - 1
EP - 7
JO - Journal of Neuroscience Research
JF - Journal of Neuroscience Research
SN - 0360-4012
IS - 1
ER -