Communication between neurons and glial cells is not limited to the synapses; axonal high frequency stimuli cause phosphorylation of myelin basic protein (MBP), a component of myelin in the white matter tracts. The signaling directed toward oligodendrocytes, dependent axonal activity, is mediated by nitric oxide, which is released from axons and stimulates the phosphorylation of MBP in oligodendrocytes through a mechanism dependent of kinase mitogenactivated protein (MAP-K) [1,2]. Moreover, studies in both the Central Nervous System (CNS) and Peripheral Nervous System (PNS) activity indicate that neuronal impulses in fetuses (as well as in early postnatal stage) influence the development of myelin forming glia [3]. This communication is mediated by ionic changes in the extracellular space and influences neuronal activity; as well as non-synaptic release of neurotransmitters, growth factors or signaling molecules specialized in axon-glia communication. Blocking of K+ channels in oligodendrocyte precursor cells, by either depolarizing agents or ion channel specific toxins, prevents the proliferation and differentiation of this type of glial cell [2]. Thus, it can be observed that the large and complex communication network between axons and myelin-forming cells is part of the proper functioning of the CNS, which can be affected

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