TY - JOUR
T1 - Hippocampal long-term potentiation, memory, and longevity in mice that overexpress mitochondrial superoxide dismutase
AU - Hu, Daoying
AU - Cao, Peng
AU - Thiels, Edda
AU - Chu, Charleen T.
AU - Wu, Gang yi
AU - Oury, Tim D.
AU - Klann, Eric
N1 - Funding Information:
This work was supported by National Institutes of Health grants NS034007 and NS047384 (E.K.), HL63700 (T.D.O.) and an Investigator-Initiated Research Grant from the Alzheimer’s Association (E.K.). We thank Laura Villasana and Monica Garcia for technical assistance.
PY - 2007/3
Y1 - 2007/3
N2 - Superoxide has been shown to be critically involved in several pathological manifestations of aging animals. In contrast, superoxide also can act as a signaling molecule to modulate signal transduction cascades required for hippocampal synaptic plasticity. Mitochondrial superoxide dismutase (SOD-2 or Mn-SOD) is a key antioxidant enzyme that scavenges superoxide. Thus, SOD-2 may not only prevent aging-related oxidative stress, but may also regulate redox signaling in young animals. We used transgenic mice overexpressing SOD-2 to study the role of mitochondrial superoxide in aging, synaptic plasticity, and memory-associated behavior. We found that overexpression of SOD-2 had no obvious effect on synaptic plasticity and memory formation in young mice, and could not rescue the age-related impairments in either synaptic plasticity or memory in old mice. However, SOD-2 overexpression did decrease mitochondrial superoxide in hippocampal neurons, and extended the lifespan of the mice. These findings increase our knowledge of the role of mitochondrial superoxide in physiological and pathological processes in the brain.
AB - Superoxide has been shown to be critically involved in several pathological manifestations of aging animals. In contrast, superoxide also can act as a signaling molecule to modulate signal transduction cascades required for hippocampal synaptic plasticity. Mitochondrial superoxide dismutase (SOD-2 or Mn-SOD) is a key antioxidant enzyme that scavenges superoxide. Thus, SOD-2 may not only prevent aging-related oxidative stress, but may also regulate redox signaling in young animals. We used transgenic mice overexpressing SOD-2 to study the role of mitochondrial superoxide in aging, synaptic plasticity, and memory-associated behavior. We found that overexpression of SOD-2 had no obvious effect on synaptic plasticity and memory formation in young mice, and could not rescue the age-related impairments in either synaptic plasticity or memory in old mice. However, SOD-2 overexpression did decrease mitochondrial superoxide in hippocampal neurons, and extended the lifespan of the mice. These findings increase our knowledge of the role of mitochondrial superoxide in physiological and pathological processes in the brain.
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U2 - 10.1016/j.nlm.2006.10.003
DO - 10.1016/j.nlm.2006.10.003
M3 - Article
C2 - 17129739
AN - SCOPUS:33846345418
SN - 1074-7427
VL - 87
SP - 372
EP - 384
JO - Neurobiology of Learning and Memory
JF - Neurobiology of Learning and Memory
IS - 3
ER -