CNS glycogen is predominantly localized in astrocytes, where it is converted to lactate and shuttled to axons as an energy source. Thus, any event affecting glycogen 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 S-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 CNS. In previous studies using C6 astroglioma cell line we have shown that glycogen accumulation was inhibited by NO but without affecting cell redox status. Here we have extended the studies using rat astrocytes primary culture and intact cells of rat spinal cord. Results have confirmed that glycogen levels are regulated in the presence of NO in all system tested, with generation of S-nitroso-proteins, and S-nitrosylation of some enzymes involved in glycogen and glucose metabolism.Since astrocyte glycogen 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.
