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dc.contributor.authorWiggins, Amanda Ken
dc.contributor.authorShen, Pei-Juanen
dc.contributor.authorGundlach, Andrew Len
dc.identifier.citationJournal of Neurochemistry; 87(6): 1368-80en
dc.description.abstractCortical spreading depression (CSD) is characterized by slowly propagating waves of neuronal/astrocytic depolarization and metabolic changes, followed by a period of quiescent neuronal and electroencephalographic activity. CSD acts as a preconditioning stimulus in brain, reducing cell death when elicited up to several days prior to an ischemic insult. Precise mechanisms associated with this neuroprotection are not known, although CSD increases the expression of a number of potentially neuroprotective genes/proteins. The nitric oxide (NO) system may be of particular importance, as it is acutely activated and chronically up-regulated in cerebral cortex by CSD, and NO can ameliorate and exacerbate cell death under different conditions. Several molecules have recently been identified that modulate the production and/or cellular actions of NO, but it is not known whether their expression is altered by CSD. Therefore, the present study examined the effect of CSD on the spatiotemporal expression of PIN, CAPON, PSD-95, Mn-SOD and Cu/Zn-SOD mRNA in the rat brain. In situ hybridization using specific [35S]-labelled oligonucleotides revealed that levels of PIN mRNA were significantly increased in the cortex and claustrum ( approximately 30-180%; p </= 0.01) after 6 h and 1 and 2 days, but were again equivalent to contralateral (control) cortical values at 7, 14 and 28 days. CAPON mRNA levels were increased ( approximately 30-180%; p </= 0.05) in the ipsilateral cortical hemisphere at 6 h and 2 days post treatment, but not at the other times examined. In contrast, levels of PSD-95, Mn- and Cu/Zn-SOD mRNA were not altered at any time after CSD. These results suggest that following CSD, nNOS activity and NO levels may be tightly regulated by both transcriptional and translational alterations in a range of nNOS adaptor proteins, which may contribute to CSD-induced neuroprotection against subsequent ischemia.en
dc.subject.otherAdaptor Proteins, Signal Transducingen
dc.subject.otherAdaptor Proteins, Vesicular Transport.metabolismen
dc.subject.otherCarrier Proteins.genetics.metabolismen
dc.subject.otherCell Cycle Proteins.genetics.metabolismen
dc.subject.otherCerebral Cortex.anatomy & histology.drug effects.physiologyen
dc.subject.otherCortical Spreading Depression.drug effects.physiologyen
dc.subject.otherDrosophila Proteins.genetics.metabolismen
dc.subject.otherFunctional Lateralityen
dc.subject.otherGene Expression Regulation.drug effectsen
dc.subject.otherGuanylate Kinaseen
dc.subject.otherIn Situ Hybridization.methodsen
dc.subject.otherIntracellular Signaling Peptides and Proteinsen
dc.subject.otherMembrane Proteinsen
dc.subject.otherMicrotubule-Associated Proteins.genetics.metabolismen
dc.subject.otherNerve Tissue Proteins.genetics.metabolismen
dc.subject.otherNitric Oxide.metabolismen
dc.subject.otherNitric Oxide Synthase.metabolismen
dc.subject.otherNitric Oxide Synthase Type Ien
dc.subject.otherOligonucleotide Probes.metabolismen
dc.subject.otherPotassium Chloride.pharmacologyen
dc.subject.otherRNA, Messenger.metabolismen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherSuperoxide Dismutase.genetics.metabolismen
dc.subject.otherTime Factorsen
dc.titleNeuronal-NOS adaptor protein expression after spreading depression: implications for NO production and ischemic tolerance.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of neurochemistryen
dc.identifier.affiliationHoward Florey Institute of Experimental Physiology and Medicine, Department of Medicine, Austin and Repatriation Medical Centre, The University of Melbourne, Victoria, Australiaen
dc.type.austinJournal Articleen
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
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