Sources and targets of reactive oxygen species in synaptic plasticity and memory

Kenneth T. Kishida, Eric Klann

Research output: Contribution to journalArticle

Abstract

Increasing evidence suggests that reactive oxygen species (ROS), such as superoxide and hydrogen peroxide, act as necessary signaling molecules in processes underlying cognition. Moreover, ROS have been shown to be necessary in molecular process underlying signal transduction, synaptic plasticity, and memory formation. Research from several laboratories suggests that NADPH oxidase is an important source of superoxide in the brain. Evidence is presented here to show that ROS are in fact important signaling molecules involved in synaptic plasticity and memory formation. Moreover, evidence that the NADPH oxidase complex is a key regulator of ROS generation in synaptic plasticity and memory formation is discussed. Understanding redox signaling in the brain, including the sources and molecular targets of ROS, are important for a full understanding of the signaling pathways that underlie synaptic plasticity and memory. Knowledge of ROS function in the brain also is critical for understanding aging and neurodegenerative diseases of the brain given that several of these disorders, including Alzheimer's disease and Parkinson disease, may be exacerbated by the unregulated generation of ROS.

Original languageEnglish (US)
Pages (from-to)233-244
Number of pages12
JournalAntioxidants and Redox Signaling
Volume9
Issue number2
DOIs
StatePublished - Feb 2007

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Neuronal Plasticity
Plasticity
Reactive Oxygen Species
Data storage equipment
Brain
NADPH Oxidase
Superoxides
Neurodegenerative diseases
Signal transduction
Molecules
Neurodegenerative Diseases
Cognition
Hydrogen Peroxide
Oxidation-Reduction
Parkinson Disease
Signal Transduction
Alzheimer Disease
Aging of materials
Research

ASJC Scopus subject areas

  • Biochemistry

Cite this

Sources and targets of reactive oxygen species in synaptic plasticity and memory. / Kishida, Kenneth T.; Klann, Eric.

In: Antioxidants and Redox Signaling, Vol. 9, No. 2, 02.2007, p. 233-244.

Research output: Contribution to journalArticle

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