title: Glial nitric oxide and ischemia.
abstract: One of the responses to cerebral ischemia is an increase in the production of nitric oxide, catalyzed by enzymes expressed in both resident and infiltrating cells. The nitric oxide that is generated does contribute to the ensuing pathology, but it can also be beneficial. The effects of nitric oxide depend on the cell site of production, the amount generated, and the chemical nature of the products of further oxidation. Understanding how nitric oxide production from microglia and astrocytes contributes to ischemic pathology is important for the development and application of future therapeutics based on inhibiting or amplifying its production in the injured brain.
authors.affiliation: Institute of Cell Signaling, Medical School, University of Nottingham, Nottingham, United Kingdom.
authors.forename: Claire L
authors.initials: CL
authors.lastname: Gibson
authors.affiliation: Institute of Cell Signaling, Medical School, University of Nottingham, Nottingham, United Kingdom.
authors.forename: Teresa C
authors.initials: TC
authors.lastname: Coughlan
authors.affiliation: Institute of Cell Signaling, Medical School, University of Nottingham, Nottingham, United Kingdom.
authors.forename: Sean P
authors.initials: SP
authors.lastname: Murphy
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000188:drug therapy / Q000378:metabolism*; D004791:Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism*; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D004791:Enzyme Inhibitors; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase