| Autor: |
Sean Murphy, Dana M. Grzybicki, Martha L. Simmons |
| Rok vydání: |
1995 |
| Předmět: |
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| Zdroj: |
Nitric Oxide in the Nervous System ISBN: 9780127219851 |
| DOI: |
10.1016/b978-012721985-1/50011-3 |
| Popis: |
Publisher Summary This chapter discusses glial cells as nitric oxide sources and targets. Nitric oxide (NO) production by microglia required transcription and translation and needed L-arginine and nicotinamide adenine dinucleotide phosphate (NADPH), but not calcium and calmodulin. The microglial form of the enzyme shared most of the characteristics of the macrophage nitric oxide synthase (NOS), including the ability to cause cytotoxicity when microglia are cocultured with oligodendrocytes. The ability of the astrocyte cytosol to activate soluble guanylyl cyclase (sGC) in fibroblasts was enhanced by the presence of superoxide dismutase (SOD), suggesting the involvement of an unstable mediator such as NO. The rat astrocyte iNOS cDNA is 92% identical in sequence to the mouse macrophage sequence in the coding region and 81% identical in the untranslated regions. The deduced amino acid sequence is 93% identical to that of the mouse macrophage enzyme and most of the substitutions are conservative. In cells undergoing transcriptional induction of NOS, removal of the NO being formed or prevention of its formation will amplify the transcription of NOS evoked by cytokines. It is found that inducible NOS message is expressed in vivo in the brain during acute viral infection. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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