Study on <Na^+> - <K^+> pump activity of glial cells in cortex from a warm-blooded animal.

用钴或海人酸致痫大鼠脑片，在体外研究了致痫皮层细胞外依赖的神经胶质泵的电生理、生物化学和组织化学特性。当细胞外~lt；K^+&gt；浓度([&lt；K^+&gt；])在4~40 mM范围内变化时，正常大脑皮质(A组织)胶质细胞的膜电位斜率平均值约为57 mV，致痫皮质(B组织)神经胶质细胞的平均膜电位斜率约为44 mV，而静息膜电位无明显差异。在B组织的胶质细胞中，用正常的培养液替换升高的[K^+]o&gt；可引起明显的一过性超极化。哇巴因可使B组织神经胶质细胞的上述现象消失，但对正常状态下的膜电位无明显影响。细胞外&lt；Na~(++)&gt；、&lt；Ca~(2+)&gt；和&lt；Cl~-&gt；对两种组织的神经胶质细胞膜电位均无明显影响。A组细胞内注射辣根过氧化物酶标记的细胞为原浆星形胶质细胞，B组以突起异常的纤维性星形胶质细胞为主。(&lt；K^+&gt；，&lt；Na^+&gt；，&lt；Na^+&gt；，&lt；K^+&gt；)-ATP酶活性在组织B的星形胶质细胞富集组分及其膜制剂中的活性明显高于组织A的。这些结果表明，致痫皮质可能被修饰以提高其活性。

The characteristics of a glial <Na^+> - <K^+> pump dependent on extracellular <K^+> within epileptogenic cortex were studied electrophysiologically, biochemically and histochemically in vitro using slices from either cobalt- or kainic acid-induced epileptogenic cortex of rat. When the extracellular <K^+> concentration ([ <K^+> ]) was varied between 4 and 40 mM, the mean slope of membrane potential plotted against <[K^+]+o> was about 57 mV in glia from the normal cortex (tissue A) and about 44 mV in glia from the epileptogenic cortex (tissue B); whereas no significant difference in the resting membrane potential of these tissues was observed. In glia from tissue B, a marked transient hyperpolarizarion above control level was caused by replacement of elevated <[K^+]_o> with the normal medium. Ouabain abolished these phenomena observed in glia from tissue B, but had no effect on the membrane potential during normal <[K^+]_o> . Reduction of extracellular <Na^+> , <Ca^(2+)> and <Cl^-> did not significantly affect the membrane potential of glia from either tissue, In tissue A, the cells marked by intracellular injection of horseradish peroxidase after intracellular recording were protoplasmic astrocytes; in tissue B, fibrous astrocyte with abnormal processes predominated. <K^+> -dependent stimulation of ( <Na^+> , <K^+> )-ATP-ase activity of the astrocyte-enriched fraction and its membrane preparation from tissue B was much larger than that from tissue A. A certain amount of the reaction product of <K^+> -pNPPase activity was seen on glial plasma membrane within tissue B but not on that from tissue A. These results suggest that epileptogenic cortex may be modified to increase in its activity.