Salgado A H, Gomez M V, Romano-Silva M A, Prado M A
Departamento de Farmacologia, ICB, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Neurosci Lett. 1996 Feb 2;204(1-2):37-40. doi: 10.1016/0304-3940(96)12310-7.
The aim of the present experiments was to test whether vesamicol alters the evoked release of ATP from nerve terminals. Continuous or cumulative release of ATP evoked by 33 mM KC1 from rat cerebrocortical synaptosomes was largely calcium-dependent. Vesamicol interfered with release of ATP from synaptosomes depolarized with KCl (33 mM) in a dose-dependent and stereoselective way. The (-)-vesamicol decreased the output of ATP in doses much lower than (+)-vesamicol. The release of the major excitatory neurotransmitter glutamate from depolarized nerve endings was not impaired by vesamicol. We suggest that vesamicol may alter the release of ATP specifically, probably by interacting with a protein similar to the vesamicol receptor found in cholinergic synaptic vesicles.
本实验的目的是测试维生霉素是否会改变神经末梢诱发的ATP释放。33 mM氯化钾从大鼠大脑皮质突触体诱发的ATP持续或累积释放很大程度上依赖于钙。维生霉素以剂量依赖性和立体选择性的方式干扰用氯化钾（33 mM）去极化的突触体中ATP的释放。（-）-维生霉素以远低于（+）-维生霉素的剂量降低了ATP的输出量。维生霉素不会损害去极化神经末梢释放主要兴奋性神经递质谷氨酸。我们认为，维生霉素可能特异性地改变ATP的释放，可能是通过与一种类似于在胆碱能突触小泡中发现的维生霉素受体的蛋白质相互作用来实现的。
