IONIC CHANNELS IN MYELINATED NERVES

可激发离子通道（Na+和K+），属于经典的 参与神经冲动的产生，并存在于两个轴突上 哺乳动物周围神经中的成鞘神经胶质细胞 系统 长期的目标是阐明离子的作用 通道，特别是它们在轴突和神经胶质中的可塑性， 正常和异常的轴-神经胶质相互作用，特别强调 脱髓鞘疾病 这项提案的具体目标集中在神经胶质细胞的可塑性， 离子通道及其与两种细胞行为的关系 哺乳动物雪旺细胞，即增殖和髓鞘形成。 神经胶质通道表达的可塑性将用 膜片钳技术对雪旺细胞的研究 行为要么在基因上改变（神经突变体）， 通过组织培养中的胶质细胞有丝分裂原，或通过其他实验 轴神经胶质关系的紊乱，（脱髓鞘， 髓鞘再生、再生和神经移植）。 职能联系 神经胶质通道和细胞反应之间的关系将被检查， 离子通道阻断剂和荧光探针 细胞内离子的运输。 轴突调节的问题 神经胶质通道，密切相关的推测， 可激发离子通道的转移，将被探索。 具体 待检验假设是神经胶质K通道的上调 在功能上与增殖有关， 兴奋性神经胶质通道与正常的 髓鞘形成

Excitable ion channels (Na+ and K+), of the types classically involved in nerve impulse generation, and present on both the axons and the ensheathing glial cells in the mammalian peripheral nervous system. The long-term goal is to elucidate the role of ion channels, particularly their plasticity in both axons and glia, in normal and abnormal axo-glial interactions with special emphasis on demyelinating diseases. The specific aims of this proposal focus on the plasticity of glial ion channels and its relation to two cellular behaviors of mammalian Schwann cells, namely, proliferation and myelinogenesis. Plasticity in glial channel expression will be measured with the patch-clamp on Schwann cell whose myelinogenic and proliferative behaviors are altered either genetically (neurological mutants), by glial mitogens in tissue culture, or by other experimental perturbations of the axo-glial relations, (demyelination, remyelination, regeneration and nerve-grafting). Functional links between glial channels and cellular responses will be examined with ion channel blockers and fluorescent probes for monitoring trafficking of intracellular ions. The issue of axonal regulation of glial channels, germane to the speculation of a glia-to-axon transfer of excitable ion channels, will be explored. The specific hypothesis to be tested is that up-regulation of glial K channels is linked functionally to proliferation, and that down-regulation of excitable glial channels is associated with normal myelinogenesis.