蜘蛛神经毒素PnTx3-6抑制突触体中钾离子诱发的细胞内钙离子浓度升高以及钙离子依赖性谷氨酸释放。
PnTx3-6 a spider neurotoxin inhibits K+-evoked increase in [Ca2+](i) and Ca2+-dependent glutamate release in synaptosomes.
作者信息
Vieira Luciene B, Kushmerick C, Reis Helton J, Diniz Carlos R, Cordeiro Marta N, Prado Marco A M, Kalapothakis E, Romano-Silva Marco A, Gomez Marcus V
机构信息
Laboratório de Neurofarmacologia, Departamento de Farmacologia, ICB, Universidade Federal de Minas Gerais, Caixa Postal 2486, 31270-901 Belo Horizonte, MG, Brazil.
出版信息
Neurochem Int. 2003 Mar;42(4):277-82. doi: 10.1016/s0197-0186(02)00130-4.
The present experiments investigated the effect of a neurotoxin purified from the venom of the spider Phoneutria nigriventer. This toxic component, P. nigriventer toxin 3-6 (PnTx3-6), abolished Ca(2+)-dependent glutamate release with an IC(50) of 74.4nM but did not alter Ca(2+)-independent secretion of glutamate when brain cortical synaptosomes were depolarized by KCl (33mM). This effect was most likely due to interference with the entry of calcium through voltage activated calcium channels (VACC), reducing the increase in the intrasynaptosomal free calcium induced by membrane depolarization with an IC(50) of 9.5nM. We compared the alterations induced by PnTx3-6 with the actions of toxins known to block calcium channels coupled to exocytosis. Our results indicate that PnTx3-6 inhibition of glutamate release and intrasynaptosomal calcium involves P/Q type calcium channels and this toxin can be a valuable tool in the investigation of calcium channels.
本实验研究了从黑腹捕鸟蛛毒液中纯化得到的一种神经毒素的作用。这种毒性成分，即黑腹捕鸟蛛毒素3-6（PnTx3-6），能消除Ca(2+)依赖性谷氨酸释放，其IC(50)为74.4nM，但当脑皮质突触体被33mM KCl去极化时，它不会改变Ca(2+)非依赖性谷氨酸分泌。这种作用很可能是由于干扰了钙通过电压激活钙通道（VACC）的进入，减少了膜去极化诱导的突触体内游离钙的增加，其IC(50)为9.5nM。我们将PnTx3-6诱导的改变与已知能阻断与胞吐作用偶联的钙通道的毒素的作用进行了比较。我们的结果表明，PnTx3-6对谷氨酸释放和突触体内钙的抑制涉及P/Q型钙通道，并且这种毒素可能是研究钙通道的一种有价值的工具。
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