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一氧化氮相关物质抑制中枢神经元培养物中的诱发神经传递,但增强自发微小突触电流。

Nitric oxide-related species inhibit evoked neurotransmission but enhance spontaneous miniature synaptic currents in central neuronal cultures.

作者信息

Pan Z H, Segal M M, Lipton S A

机构信息

Department of Neurology, Children's Hospital, Boston, MA 02115, USA.

出版信息

Proc Natl Acad Sci U S A. 1996 Dec 24;93(26):15423-8. doi: 10.1073/pnas.93.26.15423.

DOI:10.1073/pnas.93.26.15423
PMID:8986827
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC26420/
Abstract

Nitric oxide (NO.) does not react significantly with thiol groups under physiological conditions, whereas a variety of endogenous NO donor molecules facilitate rapid transfer to thiol of nitrosonium ion (NO+, with one less electron than NO.). Here, nitrosonium donors are shown to decrease the efficacy of evoked neurotransmission while increasing the frequency of spontaneous miniature excitatory postsynaptic currents (mEPSCs). In contrast, pure NO donors have little effect (displaying at most only a slight increase) on the amplitude of evoked EPSCs and frequency of spontaneous mEPSCs in our preparations. These findings may help explain heretofore paradoxical observations that the NO moiety can either increase, decrease, or have no net effect on synaptic activity in various preparations.

摘要

在生理条件下,一氧化氮(NO.)与巯基的反应并不显著,而多种内源性一氧化氮供体分子则有助于硝鎓离子(NO+,比NO.少一个电子)快速转移至巯基。在此,已表明硝鎓供体可降低诱发神经传递的效能,同时增加自发性微小兴奋性突触后电流(mEPSCs)的频率。相比之下,在我们的实验制剂中,纯一氧化氮供体对诱发的兴奋性突触后电流(EPSCs)幅度和自发性mEPSCs频率几乎没有影响(至多仅显示轻微增加)。这些发现可能有助于解释迄今为止自相矛盾的观察结果,即一氧化氮部分在各种制剂中对突触活动既可以增加、减少,也可以没有净效应。