Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/9685
Title: Neuronal-NOS adaptor protein expression after spreading depression: implications for NO production and ischemic tolerance.
Authors: Wiggins, Amanda K;Shen, Pei-Juan;Gundlach, Andrew L
Affiliation: Howard Florey Institute of Experimental Physiology and Medicine, Department of Medicine, Austin and Repatriation Medical Centre, The University of Melbourne, Victoria, Australia.
Issue Date: 1-Dec-2003
Citation: Journal of Neurochemistry; 87(6): 1368-80
Abstract: Cortical 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.
Internal ID Number: 14713293
URI: http://ahro.austin.org.au/austinjspui/handle/1/9685
URL: http://www.ncbi.nlm.nih.gov/pubmed/14713293
Type: Journal Article
Subjects: Adaptor Proteins, Signal Transducing
Adaptor Proteins, Vesicular Transport.metabolism
Animals
Autoradiography
Carrier Proteins.genetics.metabolism
Cell Cycle Proteins.genetics.metabolism
Cerebral Cortex.anatomy & histology.drug effects.physiology
Cortical Spreading Depression.drug effects.physiology
Drosophila Proteins.genetics.metabolism
Dyneins.metabolism
Functional Laterality
Gene Expression Regulation.drug effects
Guanylate Kinase
In Situ Hybridization.methods
Intracellular Signaling Peptides and Proteins
Ischemia.metabolism
Male
Membrane Proteins
Microtubule-Associated Proteins.genetics.metabolism
Nerve Tissue Proteins.genetics.metabolism
Nitric Oxide.metabolism
Nitric Oxide Synthase.metabolism
Nitric Oxide Synthase Type I
Oligonucleotide Probes.metabolism
Potassium Chloride.pharmacology
RNA, Messenger.metabolism
Rats
Rats, Sprague-Dawley
Superoxide Dismutase.genetics.metabolism
Time Factors
Appears in Collections:Journal articles

Files in This Item:
There are no files associated with this item.


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.