过氧化氢引起的突触传递的变化

Carol A. Colton , Joel S. Colton , Daniel L. Gilbert
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引用次数: 35

摘要

研究了过氧化氢(H2O2)对龙虾神经肌肉连接处兴奋性和抑制性突触传递的影响。H2O2使结电位(Vejp)的振幅呈剂量依赖性下降。这种减少是由于突触前递质释放和突触后对神经递质反应的变化。观察到H2O2对突触前的影响是递质释放量(即量子含量)的减少,以及快速促进作用的降低,即连续兴奋连接电位的幅度以3hz的速率增加。为了辨别突触后的变化,为了绕过突触前的释放过程,我们将该制剂中假定的兴奋性神经递质谷氨酸直接应用于沐浴介质中。H2O2降低了谷氨酸受体/离子载体的反应。H2O2对兴奋性(谷氨酸介导)传递没有选择性,因为抑制性(gaba介导)传递也被H2O2抑制。这种效应主要发生在突触前,因为H2O2对施加GABA的突触后反应没有产生变化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Changes in synaptic transmission produced by hydrogen peroxide

The effect of hydrogen peroxide (H2O2) on excitatory and inhibitory synaptic transmission was studied at the lobster neuromuscular junction. H2O2 produced a dose dependent decrease in the amplitude of the junction potential (Vejp). This decrease was due to changes in both presynaptic transmitter release and the postsynaptic response to the neurotransmitter. Observed presynaptic changes due to exposure to H2O2 were a decrease in the amount of transmitter released, that is, quantal content, as well as a decrease in the fast facilitation, that is, the amplitude increase of successive excitatory junction potentials at a rate of 3 Hz. To discern postsynaptic changes, glutamate, the putative excitatory neurotransmitter for this preparation was applied directly to the bathing medium in order to bypass the presynaptic release process. H2O2 produced a decreased response of the glutamate receptor/ ionophore. The action of H2O2 was not selective to excitatory (glutamate-mediated) transmission because inhibitory (GABA-mediated) transmission was also depressed by H2O2. This effect was primarily presynaptic since H2O2 produced no change in the postsynaptic response to applied GABA.

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