In CNS glycogen (G) is localized in astrocytes, where it is metabolized to lactate and delivered to neurons for the supply of energy substrate. Thus, any event affecting G metabolism, will affect the normal function of neurons. Several CNS disorders are characterized by excessive nitric oxide (NO) production. The exposure to NO results in nitrosylation of protein thiols which can alter protein function. It was previously established that S-nitrosoglutathione (GSNO) is a viable intercellular S-nitrosylating agent. In the present work we have studied the effect of NO on astrocytic G metabolism. For this, C6 cells were stimulated for either, G accumulation or G degradation. In the presence of GSNO, both, G accumulation and G synthase activity were inhibited. However S-nitrosylated proteins (PrNOs) were not detected, probably due to antioxidant events preventing nitrosylation. PrSNOs did form and could be detected during G degradation in the presence of GSNO, but degradation was unaffected. These preliminary results points to both, a NO damage dependence upon the cell energetic charge, and G metabolism regulation by NO in the astrocyte. Since astrocyte G plays an important role in supporting neuronal activity, this study would be relevant to those CNS diseases characterized by excessive NO production like multiple sclerosis, stroke, Parkinson?s and Alzheimer?s diseases.
