Carol A. Colton , Joel S. Colton , Daniel L. Gilbert
{"title":"过氧化氢引起的突触传递的变化","authors":"Carol A. Colton , Joel S. Colton , Daniel L. Gilbert","doi":"10.1016/S0748-5514(86)80063-0","DOIUrl":null,"url":null,"abstract":"<div><p>The effect of hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) on excitatory and inhibitory synaptic transmission was studied at the lobster neuromuscular junction. H<sub>2</sub>O<sub>2</sub> produced a dose dependent decrease in the amplitude of the junction potential (<em>V<sub>ejp</sub></em>). 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 H<sub>2</sub>O<sub>2</sub> 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. H<sub>2</sub>O<sub>2</sub> produced a decreased response of the glutamate receptor/ ionophore. The action of H<sub>2</sub>O<sub>2</sub> was not selective to excitatory (glutamate-mediated) transmission because inhibitory (GABA-mediated) transmission was also depressed by H<sub>2</sub>O<sub>2</sub>. This effect was primarily presynaptic since H<sub>2</sub>O<sub>2</sub> produced no change in the postsynaptic response to applied GABA.</p></div>","PeriodicalId":77737,"journal":{"name":"Journal of free radicals in biology & medicine","volume":"2 2","pages":"Pages 141-148"},"PeriodicalIF":0.0000,"publicationDate":"1986-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0748-5514(86)80063-0","citationCount":"35","resultStr":"{\"title\":\"Changes in synaptic transmission produced by hydrogen peroxide\",\"authors\":\"Carol A. Colton , Joel S. Colton , Daniel L. Gilbert\",\"doi\":\"10.1016/S0748-5514(86)80063-0\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>The effect of hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) on excitatory and inhibitory synaptic transmission was studied at the lobster neuromuscular junction. H<sub>2</sub>O<sub>2</sub> produced a dose dependent decrease in the amplitude of the junction potential (<em>V<sub>ejp</sub></em>). 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 H<sub>2</sub>O<sub>2</sub> 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. H<sub>2</sub>O<sub>2</sub> produced a decreased response of the glutamate receptor/ ionophore. The action of H<sub>2</sub>O<sub>2</sub> was not selective to excitatory (glutamate-mediated) transmission because inhibitory (GABA-mediated) transmission was also depressed by H<sub>2</sub>O<sub>2</sub>. This effect was primarily presynaptic since H<sub>2</sub>O<sub>2</sub> produced no change in the postsynaptic response to applied GABA.</p></div>\",\"PeriodicalId\":77737,\"journal\":{\"name\":\"Journal of free radicals in biology & medicine\",\"volume\":\"2 2\",\"pages\":\"Pages 141-148\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1986-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/S0748-5514(86)80063-0\",\"citationCount\":\"35\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of free radicals in biology & medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S0748551486800630\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of free radicals in biology & medicine","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0748551486800630","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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.