Villegas J
Fed Proc. 1975 Apr;34(5):1370-3.
The effects of acetylcholine, carbamylcholine, D-tubocurarine, eserine, and alpha-bungarotoxin on the Schwann cell electrical potential of resting and stimulated squid nerve fibers were studied. Acetylcholine (10-7 M) and barbamylcholine (10-6 M) induce a prolonged hyper polarization in the Schwann cells of the unstimulated nerve fiber. In the presence of carbamylcholine (10-6 M) the behavior of the Schwann cell membrane to changes in the external potassium concentration approximates the behavior of an ideal potassium electrode. D-Tubocurarine (10-9 M) blocks the hyperpolarizing effects of nerve impulse trains and carbamylcholine (10-6 M), whereas at the same concentration eserine prolongs the Schwann cell hyperpolarizations induced by axon stimulation or by acetylcholine (10-7 M). alpha-Bungarotoxin (10-9M) also blocks the hyperpolarizing effect of nerve impulse trains and of carbamylcholine. D-Tubocurarine (10-5M) protects the Schwann cells against the irreversible action of alpha-bungarotoxin. These results show the existence of acetylcholine receptors in the Schwann cell membrane. Preliminary measurements of the binding of 125I-alpha bungarotoxin to the plasma membranes isolated from squid nerves also indicate the presence of acetylcholine receptors. These findings support the involvement of cholinergic mechanisms in the axon-Schwann cell relationship previously described.
研究了乙酰胆碱、氨甲酰胆碱、d -筒箭毒碱、毒扁豆碱和α -银环蛇毒素对静息和受刺激的鱿鱼神经纤维雪旺氏细胞膜电位的影响。乙酰胆碱（10⁻⁷M）和氨甲酰胆碱（10⁻⁶M）可使未受刺激神经纤维的雪旺氏细胞产生长时间的超极化。在氨甲酰胆碱（10⁻⁶M）存在的情况下，雪旺氏细胞膜对细胞外钾离子浓度变化的反应近似于理想钾电极的反应。d -筒箭毒碱（10⁻⁹M）可阻断神经冲动序列和氨甲酰胆碱（10⁻⁶M）引起的超极化作用，而在相同浓度下毒扁豆碱可延长轴突刺激或乙酰胆碱（10⁻⁷M）引起的雪旺氏细胞超极化时间。α -银环蛇毒素（10⁻⁹M）也可阻断神经冲动序列和氨甲酰胆碱引起的超极化作用。d -筒箭毒碱（10⁻⁵M）可保护雪旺氏细胞免受α -银环蛇毒素的不可逆作用。这些结果表明雪旺氏细胞膜上存在乙酰胆碱受体。对125I-α银环蛇毒素与从鱿鱼神经分离的质膜结合的初步测量也表明存在乙酰胆碱受体。这些发现支持了胆碱能机制参与先前描述的轴突-雪旺氏细胞关系。
