FERRIER LECTURE - NEUROGLIAL CELLS - PHYSIOLOGICAL PROPERTIES AND A POTASSIUM MEDIATED EFFECT OF NEURONAL ACTIVITY ON GLIAL MEMBRANE POTENTIAL
FERRIER LECTURE - NEUROGLIAL CELLS - PHYSIOLOGICAL PROPERTIES AND A POTASSIUM MEDIATED EFFECT OF NEURONAL ACTIVITY ON GLIAL MEMBRANE POTENTIAL
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DOI：
10.1098/rspb.1967.0047
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发表时间：
1967-01-01
期刊：
影响因子：
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通讯作者：
KUFFLER, SW
中科院分区：
文献类型：
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作者：
KUFFLER, SW
作为测试各种假说和关于神经胶质作用的广泛持有的假设的第一步，进行实验以确定神经胶质细胞的一些生理特性。还研究了细胞间隙（通常为100至200 A宽）在物质通过神经系统运动中的作用。此外，钾介导的神经元活性对神经胶质细胞的影响进行了描述。两个相对简单的准备工作：水蛭（水蛭）的中枢神经系统和两栖动物的视神经，泥小狗（Necturus maculosus）和青蛙（蛙）。以下结果进行了讨论：神经胶质细胞被包围，像神经元一样，由高电阻膜，并含有高浓度的K+，约100毫当量。/升。神经胶质细胞不产生传播冲动，其静息电位比神经元的静息电位大（在Necturus中接近90 mV）。神经胶质细胞膜的行为就像一个精确的K+电极，并且在生理范围内以及当环境中的K+增加时，处于K+的平衡电位。与大多数神经元不同，神经胶质细胞通过特殊的低电阻连接（紧密连接）相互连接。水蛭体内的神经元在周围的神经胶质细胞被移除后仍能持续数小时传导冲动;这些“暴露”的细胞仍能吸收葡萄糖并将其转化为糖原。通过使用神经胶质细胞和神经元的膜作为其离子环境的指示剂，发现神经系统中的细胞间裂隙作为Na+和K+等离子以及蔗糖、菊粉、葡聚糖或胆碱等分子扩散的快速有效途径。因此，这些物质的主要运动途径是通过裂隙而不是通过胶质细胞质围绕胶质细胞运动。视神经内的无髓鞘轴突中的冲动活动使周围的神经胶质细胞去极化。已发现以下机制的证据：在冲动期间，K+释放，积聚在细胞间隙中并降低胶质细胞膜电位。在各种实验情况下，据估计，裂隙中的K+浓度从正常的3毫当量增加到20毫当量。L或更多。当光线照射到眼睛时，在自然刺激期间，循环动物的视神经也会发生胶质去极化。讨论了脑内细胞间隙K+浓度波动的后果。虽然接近生理范围的神经元对K+浓度的变化相对不敏感，但预计观察到的波动会影响突触区域的神经元活动。K+去极化对神经胶质细胞生理活性的影响尚不清楚。由于神经胶质细胞膜是其环境中整体神经元活性的良好指标，因此K+释放可作为引起神经胶质细胞反应的信号，可能是营养性反应。神经胶质细胞群的激活产生电流，这有助于从视神经表面记录的缓慢的电位变化，并且在大脑其他地方的局灶性活动期间可能也是如此。关于神经胶质细胞的作用，可能会出现各种功能。目前的知识中存在着明显的空白，这阻碍了更精确的假说的形成，这些假说与各种神经胶质细胞的生化特性和神经元-神经胶质相互作用机制的详细信息有关。
As an initial step in testing various hypotheses and widely held assumptions concerning the role of neuroglia, experiments were made to establish some of the physiological properties of glial cells. The role of intercellular spaces, usually 100 to 200 A wide, for the movement of materials through the nervous system was also studied. In addition, a potassium-mediated effect of neuronal activity on glial cells was described. Two relatively simple preparations were used: the central nervous system of the leech (Hirudo medicinalis) and the optic nerves of amphibia, the mud puppy (Necturus maculosus) and the frog (Rana pipiens). The following results were discussed: Neuroglial cells are surrounded, like neurons, by a high resistance membrane and contain a high internal concentration of K+, about 100 mequiv. /l. Glial cells do not generate propagated impulses and their resting potential is larger (near 90 mV in Necturus) than that of neurons. The glial membrane behaves like an accurate K+ electrode and is at the equilibrium potential for K+ in the physiological range, as well as when K+ in the environment increased. Unlike most neurons, glial cells are linked to each other by special low resistance connections (tight junctions). Neurons in the leech continue to conduct impulses for many hours after their surrounding glial cells have been removed; such ''exposed'' cells still take up glucose and convert it to glycogen. By using the membranes of glial cells and of neurons as indicators of their ionic environment, it was found that the intercellular clefts in the nervous system serve as a rapid and effective pathway for the diffusion of ions like Na+ and K+, and for molecules like sucrose, inulin, dextran or choline. The principal pathway, therefore, for the movement of such substances is around the glial cells through the clefts rather than through the glial cytoplasm. Impulse activity in the non-myelinated axons within optic nerves depolarizes the surrounding glial cells. Evidence for the following mechanism has been found: during the impulses K+ is released, accumulates in the intercellular spaces and reduces the glial membrane potential. In various experimental situations the K+ concentration in the cleft has been estimated to increase from the normal 3 to 20 mequiv./L or more. Glial depolarization also occurs in the optic nerves of circulated animals during natural stimulation when light is shone into the eye. The consequence of the fluctuations of K+ concentrations in the intercellular clefts within the brain were discussed. While near the physiological range neurons were relatively insensitive to changes in K+ concentrations, it is to be expected that the observed fluctuations would influence neuronal activity in synaptic regions. The effect of K+ depolarization on the physiological activity of glial cells is not known. Since the glial membranes are good indicators of overall neuronal activity in their environment, K+ liberation may serve as a signal for evoking a response in glial cells, possibly a trophic one. Activation of groups of glial cells generates current flow which contributes to slow potential changes recorded from the surface of optic nerves, and the same is likely to be true during focal activity elsewhere in the brain. Concerning the role of glial cells, a variety of functions will probably emerge. Obvious gaps in present knowledge which prevent the form-ulation of more precise hypotheses relate to detailed information about the biochemical properties of various glial cells and the mechanism of neuron-glia interaction.