Recent studies indicate that nitric oxide (NO) is involved in the pathogenesis of infarction and subsequent neurodegeneration following focal ischemia. Furthermore, expression of neuronal nitric oxide synthase (nNOS or type I NOS), the enzyme responsible for generation of NO, is upregulated during focal ischemia. To examine the mechanism of this upregulation of nNOS, I propose the following: 1) To characterize in detail the upregulation of nNOS mRNA, protein level, and catalytic activity in response to ischemia. 2) To identify regions of the nNOS promoter involved in upregulation of nNOS in response to ischemia. 3) To identify potential transcription factors involved in nNOS upregulation in response to ischemia.
