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小膠質(zhì)細(xì)胞p38 MAPK在ATP抑制海馬CA1區(qū)長時程增強(qiáng)中的作用

發(fā)布時間:2018-05-12 17:53

  本文選題:長時程增強(qiáng) + 三磷酸腺苷 ; 參考:《臨床麻醉學(xué)雜志》2014年02期


【摘要】:目的探討p38絲裂原激活的蛋白激酶(MAPK)在三磷酸腺苷(ATP)抑制海馬CA1區(qū)長時程增強(qiáng)(LTP)中的作用。方法成年雄性SD大鼠20只,體重250~280g,隨機(jī)均分為四組:生理鹽水組(NS組)、ATP組、p38 MAPK抑制劑組(SB203580組)和SB203580+ATP組。前三組在高頻刺激(HFS)前30min側(cè)腦室分別注射生理鹽水、ATP和p38 MAPK;SB203580+ATP組在注射ATP前30min側(cè)腦室給予p38MAPK抑制劑。采用海馬在體電生理記錄和免疫組織化學(xué)方法,記錄HFS 5、60min海馬CA1區(qū)興奮性突觸后電位(fEPSPs)及HFS誘導(dǎo)時LTP,免疫組織化學(xué)觀察海馬CA1區(qū)p38MAPK的磷酸化水平。結(jié)果與NS組比較,ATP組HFS 5、60min fEPSPs幅度明顯降低(P0.01)。與ATP組比較,SB203580+ATP組高頻刺激后fEPSPs幅度明顯增加(P0.01),NS組、SB203580組和SB203580+ATP組海馬CA1區(qū)p38MAPK的磷酸化水平明顯降低(P0.01)。p-p38僅與小膠質(zhì)細(xì)胞標(biāo)記物Iba-1存在共染。結(jié)論 ATP可能通過激活小膠質(zhì)細(xì)胞內(nèi)的p38 MAPK抑制海馬CA1區(qū)LTP。
[Abstract]:Objective to investigate the role of p38 mitogen-activated protein kinase MAPK (MAPK) in inhibiting the long-term potentiation of CA1 in hippocampus by adenosine triphosphate (ATP). Methods Twenty adult male Sprague-Dawley rats, weighing 250 ~ 280 g, were randomly divided into four groups: normal saline group (NS group), p38 MAPK inhibitor group (SB203580) and SB203580 ATP group. The first three groups were injected with normal saline ATP and p38 MAPKK SB203580 ATP before high frequency stimulation. The 30min side ventricle was treated with p38MAPK inhibitor before ATP injection. The excitatory postsynaptic potential (fEPSPs) of hippocampal CA1 and the level of p38MAPK phosphorylation in hippocampal CA1 region were observed by immunohistochemistry and electrophysiological recording of hippocampal in vivo and immunohistochemical method. The excitatory postsynaptic potential (fEPSPs) in hippocampal CA1 area and the level of p38MAPK in CA1 region of hippocampus induced by HFS were recorded by immunohistochemistry. Results compared with the NS group, the fEPSPs amplitude of the HFS group was significantly lower than that of the NS group (P 0.01). Compared with ATP group, the amplitude of fEPSPs in SB203580 ATP group increased significantly after high frequency stimulation, and the phosphorylation level of p38MAPK in CA1 region of hippocampus in SB203580 group and SB203580 ATP group decreased significantly after high frequency stimulation. It was only costained with Iba-1, a microglial marker. Conclusion ATP may inhibit LTP in CA1 area of hippocampus by activating p38 MAPK in microglia.
【作者單位】: 廣州醫(yī)科大學(xué)附屬第二醫(yī)院疼痛科;中華疼痛學(xué)會第一臨床中心;
【基金】:國家自然科學(xué)基金青年基金(31100805) 廣州市珠江科技新星項目(2012J2200036) 廣東省中醫(yī)藥基金(20112154)
【分類號】:R749.16

【參考文獻(xiàn)】

相關(guān)期刊論文 前3條

1 張桂蓮;姚麗;杜峗;張茹;卜寧;劉t熃,

本文編號:1879563


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