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大鼠钴诱导致痫皮层内胶质细胞钠钾泵的改变

Modification of the Na+,K+-pump of glial cells within cobalt-induced epileptogenic cortex of rat.

作者信息

Onozuka M, Kishii K, Imai S, Ozono S

机构信息

Department of Anatomy, Gifu University School of Medicine, Japan.

出版信息

Brain Res. 1987 Sep 15;420(2):259-67. doi: 10.1016/0006-8993(87)91246-7.

Abstract

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 cobalt-induced epileptogenic cortex of rat. When the extracellular K+ concentration ([K+]o) 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 hyperpolarization 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+, Ca2+ 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 astrocytes with abnormal processes predominated. K+-dependent stimulation of Na+,K+-ATPase 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. The above findings suggest that a glial Na+,K+-pump within actively firing epileptogenic cortex may be modified to increase in its activity.

摘要

利用大鼠钴诱导致痫皮层切片,在体外从电生理、生化和组织化学方面研究了致痫皮层内依赖细胞外钾的胶质细胞钠钾泵的特性。当细胞外钾浓度([K⁺]ₒ)在4至40 mM之间变化时,正常皮层(组织A)胶质细胞中膜电位相对于[K⁺]ₒ的平均斜率约为57 mV,致痫皮层(组织B)胶质细胞中约为44 mV;而这些组织的静息膜电位未观察到显著差异。在组织B的胶质细胞中,用正常培养基替代升高的[K⁺]ₒ会引起明显的短暂超极化,超过对照水平。哇巴因消除了在组织B的胶质细胞中观察到的这些现象,但在正常[K⁺]ₒ期间对膜电位没有影响。细胞外钠、钙和氯的减少对两种组织的胶质细胞膜电位均无显著影响。在组织A中,细胞内记录后通过细胞内注射辣根过氧化物酶标记的细胞是原浆性星形胶质细胞;在组织B中,具有异常突起的纤维性星形胶质细胞占主导。组织B富含星形胶质细胞部分及其膜制剂的钠钾ATP酶活性的钾依赖性刺激比组织A大得多。在组织B的胶质细胞质膜上可见一定量的钾-pNPP酶活性反应产物,而组织A的质膜上未见。上述发现表明,活跃放电的致痫皮层内的胶质细胞钠钾泵可能发生改变以增加其活性。

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