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蛋白激酶C激活剂和去氧肾上腺素通过降低钾离子通透性使星形胶质细胞膜去极化。

Activators of protein kinase C and phenylephrine depolarize the astrocyte membrane by reducing the K+ permeability.

作者信息

Akerman K E, Enkvist M O, Holopainen I

机构信息

Abo Akademi, Department of Biochemistry and Pharmacy, Finland.

出版信息

Neurosci Lett. 1988 Oct 17;92(3):265-9. doi: 10.1016/0304-3940(88)90600-3.

DOI:10.1016/0304-3940(88)90600-3
PMID:3200485
Abstract

The membrane potential of astrocytes has been measured by monitoring the absorbance of a cyanine dye DiS-C2-(5). Ba2+, the phorbol ester 12-tetradecanoylphorbol myristateacetate (TPA) and the diglyceride, dioctanoylglycerol (DiC8) depolarize the membrane. Valinomycin which makes the membrane potential dependent on the K+ electrochemical potential evokes a hyperpolarization when added subsequently. The alpha-adrenergic receptor agonist phenylephrine was blocked by Ba2+, TPA, DiC8 and valinomycin. The results suggest that a protein kinase C-mediated reduction in the K+ permeability is responsible for the depolarizing effect of TPA, DiC8 and phenylephrine.

摘要

通过监测花青染料DiS-C2-(5)的吸光度来测量星形胶质细胞的膜电位。钡离子、佛波酯12-十四酰佛波醇乙酸酯(TPA)和二甘油酯二辛酰甘油(DiC8)可使膜去极化。缬氨霉素使膜电位依赖于钾离子电化学势,随后加入时会引起超极化。α-肾上腺素能受体激动剂去氧肾上腺素被钡离子、TPA、DiC8和缬氨霉素阻断。结果表明,蛋白激酶C介导的钾离子通透性降低是TPA、DiC8和去氧肾上腺素去极化作用的原因。

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