Effects of atropine and pralidoxime on neuronal actions of paraoxon in rat hippocampal slices
Effects of atropine and pralidoxime on neuronal actions of paraoxon in rat hippocampal slices
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DOI：
10.1016/j.neures.2010.08.008
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发表时间：
2010-12-01
影响因子：
2.9
通讯作者：
Yamakage, Michiaki
中科院分区：
文献类型：
--
作者：
Narimatsu, Eichi;Niiya, Tomohisa;Yamakage, Michiaki
本文研究了有机磷胆碱酯酶（ChE）抑制剂对氧磷（paraoxon）对中枢突触传递和躯体兴奋性的作用，以及非选择性毒蕈碱型乙酰胆碱受体（mAChR）拮抗剂阿托品（atropine）和肟类药物解磷定（PAM）对上述作用的抑制作用。用多电极阵列（MEA）系统记录大鼠海马脑片0.1Hz的CA 1区群锋电位（PS）和CA 1区兴奋性突触后电位（fEPSPs）。使用ANOVA和Bonferroni/Dunn检验进行统计（所有数据中n = 6）。对氧磷（1 μ M）抑制fEPSPs，但没有显着影响PS。用阿托品（10 μ M，p < 0.01）预处理、同时处理和后处理以及用PAM（10 μ M，p <0.01）预处理抑制fEPSP抑制。阿托品预处理、同时处理和后处理以及PAM预处理和后处理均未改变对氧磷诱导的PS变化的不显著性;然而，对氧磷和PAM同时处理显著抑制了PS（p < 0.01）。对氧磷诱导的胆碱酯酶抑制可抑制兴奋性突触传递并促进mAChRs介导的躯体兴奋性，后者可抵消抑制的突触传递对躯体动作电位的影响。阿托品和PAM预防和抑制对氧磷的作用，早期治疗效果更好。(C)2010年爱思唯尔爱尔兰有限公司和日本神经科学学会。All rights reserved.
The actions of paraoxon, an organophosphorus cholinesterase (ChE) inhibitor, on central synaptic transmission and somatic excitability, and the inhibitory effects of atropine, a non-selective muscarinic acetylcholine receptor (mAChR) antagonist, and pralidoxime (PAM), an oxime, on these actions were investigated. From rat hippocampal slices, CA1-population spikes (PSs) and CA1-field excitatory postsynaptic potentials (fEPSPs) at 0.1 Hz were recorded using a multi-electrode array (MEA) system. Statistics were performed using ANOVA with Bonferroni/Dunn testing (n = 6 in all data). Paraoxon (1 mu M) depressed fEPSPs but did not significantly influence PSs. The fEPSP depression was inhibited by pre-, simultaneous and post-treatments with atropine (10 mu M, p < 0.01) and pre-treatment with PAM (10 mu M, p < 0.01). The insignificance of the paraoxon-induced PS change was not altered by pre-, simultaneous and post-treatments with atropine or by pre- and post-treatments with PAM; however, PSs were significantly depressed by simultaneous treatment with paraoxon and PAM (p < 0.01). Paraoxon-induced ChE inhibition depresses excitatory synaptic transmission and facilitates somatic excitability mediated by mAChRs, and the latter counteracts influence of the depressed synaptic transmission on somatic action potentials. Atropine and PAM prevent and depress the actions of paraoxon and are more effective with earlier treatment. (C) 2010 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.