Nitric oxide (NO) has been implicated in the neurodegeneration associated to inflammatory processes inflammatory processes in the CNS. There is abundant literature on the induction of glial reactivity and NO synthase (NOS) activity by inflammatory cytokines in rodent astroglia and microglia and on the neurotoxicity caused by the generated NO. However, there are no reports about the effect of glial reactivity on the enzymes involved in the metabolism of cyclic GMP (cGMP), important intracellular physiological second messenger of NO or about the effects of neurotrophic factors liberated by reactive glia on the NO/cGMP system of neurons. In human cells, there is little information about the effects of inflammatory agents on neuronal and astroglial NOS activities and the presence of other enzymatic components of the NO/cGMP system has not been described. The aim of the present project is to study the regulation of the NO/cGMP system in cultures of astroglia and neurons of rodent and human brain by agents whose levels are elevated during inflammatory processes of the CNS (cytokines, \beta-amyloid peptides, neurotrophic factors) and how it relates to alterations in cellular functions in which NO and/or cGMP have been implicated (glial glutamate uptake, proliferation, differentiation or cell death)
|Effective start/end date||1/10/98 → 1/10/01|
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