Our lab is interested in understanding the molecular mechanisms underlying synaptic plasticity and memory formation. I am specifically interested in the role that reactive oxygen species (ROS) play in these processes. Examples of ROS are superoxide, hydrogen peroxide, and nitric oxide (also known as a reactive nitrogen species). ROS are known to be involved in neurodegeneration caused by oxidative stress; however there is also considerable evidence for a role of ROS in signal transduction. We have shown that ROS are necessary for synaptic plasticity and memory formation, yet it is not well understood how the required ROS are generated. I am interested in determining how ROS are generated in a controlled manner such that they can be utilized as signaling molecules during synaptic plasticity and memory formation while avoiding the generation of neurodegenerative conditions. In my studies, I will concentrate on determining whether NADPH oxidase is the principle source for ROS production during synaptic plasticity and memory formation. Thus, I hypothesize that that ROS generated by NADPH oxidase is required during synaptic plasticity and memory formation. I propose to test these hypotheses using neuropharmacological, electrophysiological, and behavioral analysis of wild-type, and knockout mice.
|Kishida, Kenneth T; Klann, Eric (2007) Sources and targets of reactive oxygen species in synaptic plasticity and memory. Antioxid Redox Signal 9:233-44|
|Kishida, Kenneth T; Hoeffer, Charles A; Hu, Daoying et al. (2006) Synaptic plasticity deficits and mild memory impairments in mouse models of chronic granulomatous disease. Mol Cell Biol 26:5908-20|