Bennett R R, Buchan P B, Treherne J E
J Exp Biol. 1975 Feb;62(1):231-41. doi: 10.1242/jeb.62.1.231.
Exposure to sodium-deficient (tris) saline caused an appreciable decline in the sodium content of intact connectives in the absence of equivalent reduction in the amplitude of the recorded action potentials. Return of sodium-depleted connectives to normal saline resulted in a rapid recovery of axonal function despite only a partial (less than 70%) recovery in sodium content. Replacement of sodium ions by those of lithium in the bathing medium resulted in a substantial accumulation of this cation. Lithium movements exhibited a marked asymetry, no significant decline in concentration being observed upon return to normal saline. These results are tentatively interpreted in terms of an exchangeable glial sodium fraction and are discussed in relation to extra-axonal sodium regulation.
暴露于缺钠(三羟甲基氨基甲烷)盐溶液会导致完整结缔组织中的钠含量显著下降,而记录的动作电位幅度却没有相应降低。将缺钠的结缔组织放回正常盐溶液中,尽管钠含量仅部分(低于70%)恢复,但轴突功能迅速恢复。在浴液中用锂离子替代钠离子会导致这种阳离子大量蓄积。锂的移动表现出明显的不对称性,回到正常盐溶液后未观察到浓度有显著下降。这些结果初步解释为可交换的神经胶质钠部分,并结合轴突外钠调节进行了讨论。