髓鞘碱性蛋白使神经元膜去极化。

Myelin basic protein depolarizes neuronal membranes.

作者信息

Gähwiler B H, Honegger C G

出版信息

Neurosci Lett. 1979 Mar;11(3):317-21. doi: 10.1016/0304-3940(79)90015-6.

Abstract

Bath application of 10(-5) M myelin basic protein (MBP) to various types of cultured nerve cells resulted in a membrane depolarization amounting to a change of 41 +/- 15 mV. Excitability could be restored by repolarizing the membrane by means of current injection through the recording electrode. The action of MBP persisted in the presence of tetrodotoxin (TTX), Co2+ or D-600 as well as in low Na+ and low Cl- solutions, whereas it was abolished by increasing extracellular Ca2+ concentrations. The action MBP was mimicked by ouabain. We propose that the effect of the protein might be generated by blockade of an ion pump. It is speculated that MBP may exert a direct effect on neuronal membranes in demyelinating diseases.

摘要

将10⁻⁵ M髓鞘碱性蛋白（MBP）施加于各种类型的培养神经细胞上，会导致膜去极化，电位变化达41±15 mV。通过记录电极注入电流使膜复极化，可恢复兴奋性。在存在河豚毒素（TTX）、Co²⁺或D - 600的情况下，以及在低钠和低氯溶液中，MBP的作用仍然存在，而增加细胞外Ca²⁺浓度则可消除其作用。哇巴因可模拟MBP的作用。我们认为该蛋白的作用可能是由离子泵的阻断所产生的。据推测，MBP可能在脱髓鞘疾病中对神经元膜发挥直接作用。