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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Role of transglutaminase in (3H)5-HT release from synaptosomes and in the inhibitory effect of tetanus toxin.
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Role of transglutaminase in (3H)5-HT release from synaptosomes and in the inhibitory effect of tetanus toxin.

机译：转谷氨酰胺酶在突触小体中（3H）5-HT释放以及破伤风毒素抑制作用中的作用。

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It has been suggested that the Ca(2+)-dependent enzyme transglutaminase (TGase) may suppress vesicular neurotransmitter release and mediate the inhibitory effect of tetanus toxin (TetTx) on exocytosis. The aim of the present study was to test this in a model of [3H]5-HT release from superfused rat cortical synaptosomes. Monodansylcadaverine, a synthetic amine that acts as an alternative substrate for TGase, showed dose-dependent releasing activity which, however, was Ca(2+)-independent, being maintained in a Ca(2+)-free buffer (containing EGTA) or using synaptosomes preloaded with the intracellular Ca2+ chelator BAPTA. Preincubation of synaptosomes with RS-48373, an irreversible TGase inactivator, resulted in marked (64%) and persistent inhibition of endogenous TGase but did not alter basal and K(+)-induced [3H]5-HT release. Preincubation of synaptosomes with 10 nM TetTx resulted in 52% inhibition of K(+)-induced [3H]5-HT release, and this effect was not antagonized in RS-48373-treated synaptosomes. The inhibitory effect of TetTx was significantly antagonized by 20 mM captopril, a metalloendoprotease inhibitor, confirming in rat brain synaptosomes that TetTx inhibits exocytosis by acting as a metalloendoprotease. These results suggest that TGase is not involved in controlling [3H]5-HT release from resting and depolarized synaptosomes, or in the inhibitory effect of TetTx.
机译：有人提出，Ca（2+）依赖酶转谷氨酰胺酶（TGase）可能抑制囊泡神经递质的释放，并介导破伤风毒素（TetTx）对胞吐作用的抑制作用。本研究的目的是在从超融合大鼠皮质突触小体中释放[3H] 5-HT的模型中对此进行测试。 Monodansylcadaverine，一种用作TGase替代底物的合成胺，显示出剂量依赖性的释放活性，然而，它是Ca（2+）依赖性的，被保持在不含Ca（2+）的缓冲液（含EGTA）中或使用预装有细胞内Ca2 +螯合剂BAPTA的突触小体。用不可逆的TGase灭活剂RS-48373对突触小体进行预温育，可导致内源性TGase显着（64％）和持续抑制，但不会改变基础和K（+）诱导的[3H] 5-HT释放。突触体与10 nM TetTx的预温育导致K（+）诱导的[3H] 5-HT释放抑制52％，在RS-48373处理的突触体中没有拮抗这种作用。 TetTx的抑制作用被20mM卡托普利（一种金属内切蛋白酶抑制剂）明显拮抗，证实在大鼠脑突触小体中TetTx通过充当金属内切蛋白酶来抑制胞吐作用。这些结果表明，TGase不参与控制[3H] 5-HT从静止和去极化的突触小体中释放，也不参与TetTx的抑制作用。

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