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噻拉嗪对大鼠离体脑神经元ATP酶活性影响的研究 被引量:1
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作者 陈宇 杜雪曼 +4 位作者 连慧敏 唐赛男 刘文瀚 赵菁华 高利 《中国兽医杂志》 CAS 北大核心 2020年第1期26-30,共5页
为研究噻拉嗪对离体神经元Na^+-K^+-ATP酶和Ca^2+-Mg^2+-ATP酶活性的影响,明确噻拉嗪麻醉机制,为临床麻醉提供相应的理论依据。本试验分离培养胎鼠脑皮质神经元,在培养第8天加入浓度为15、25、35μg/mL和45μg/mL噻拉嗪,分别在加药后0、... 为研究噻拉嗪对离体神经元Na^+-K^+-ATP酶和Ca^2+-Mg^2+-ATP酶活性的影响,明确噻拉嗪麻醉机制,为临床麻醉提供相应的理论依据。本试验分离培养胎鼠脑皮质神经元,在培养第8天加入浓度为15、25、35μg/mL和45μg/mL噻拉嗪,分别在加药后0、5、10、15、20、25、30、45、60、90 min和120 min采用分光光度法测定离体神经元Na^+-K^+-ATP酶和Ca^2+-Mg^2+-ATP酶活性。试验结果显示,不同浓度噻拉嗪作用于离体培养的神经元后可见Na^+-K^+-ATP酶和Ca^2+-Mg^2+-ATP酶活性均呈现先下降后上升的趋势。25 min时,15、25μg/mL和45μg/mL组Na^+-K^+-ATP酶活性与0 min比分别降低了63.72%,66.77%和64.63%(P<0.01),这3组酶活性的最高值较最低值分别升高了188.9%、208.4%和181.8%(P<0.01)。35μg/mL组在15 min时为最低值,下降了67.04%(P<0.01),且最高值较最低值上升了196.2%(P<0.01)。不同浓度组Ca^2+-Mg^2+-ATP酶活性均在25 min降至最低值,分别较0 min下降了42.81%、68.91%、87.67%和80.14%(P<0.01)。4个组的最高值较最低值分别上升了46.95%、104.2%、420%和170.8%(P<0.01)。结果表明,噻拉嗪通过显著降低Na^+-K^+-ATP酶和Ca^2+-Mg^2+-ATP酶活性来发挥麻醉作用,其作用机制可能与改变神经元胞内外的离子平衡状态有关。 展开更多
关键词 噻拉嗪 离体神经元 NA^+-K^+-ATP酶 CA^2+-MG^2+-ATP酶
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He-Ne激光对大鼠离体颈上神经节后神经元膜电导的影响
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作者 莫华 何萍 +1 位作者 梁爱宣 莫宁 《激光生物学报》 CAS CSCD 2002年第5期368-371,共4页
应用细胞内生物电记录技术 ,观测不同功率、不同照射时间的 He- Ne激光 (脉冲频率 1Hz)对大鼠离体颈上神经节后神经元快兴奋性突触后电位 (f- EPSP)期间膜电导的影响。功率密度为 2 m W/ cm2 的 He- Ne激光在照射初期 (1min~ 2 min)引... 应用细胞内生物电记录技术 ,观测不同功率、不同照射时间的 He- Ne激光 (脉冲频率 1Hz)对大鼠离体颈上神经节后神经元快兴奋性突触后电位 (f- EPSP)期间膜电导的影响。功率密度为 2 m W/ cm2 的 He- Ne激光在照射初期 (1min~ 2 min)引起快兴奋性突触后电位 (f- EPSP)幅值增大 ,同时膜电导增大 ;而在激光照射后期 (后 3m in~8m in)引起节后神经元膜电导减少。功率密度为 5 m W/ cm2 的 He- Ne激光照射期膜电导无明显变化 .结果表明 :功率密度为 2 m W/ cm2 的 He- Ne激光照射初期引起膜电导 (Gl=34.6± 5 .4 n S)较照射前 (Gf=2 6 .8± 6 .2 n S)有明显增大 (P<0 .0 5 ) ,照射后期膜电导减少。提示 :He- Ne激光照射可能是通过两时相效应改变节后神经元膜电导来影响交感神经节内兴奋传递过程。这可能是低功率激光对神经细胞的一种作用机制。 展开更多
关键词 HE-NE激光 大鼠 离体颈上神经节后神经元 膜电导
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大鼠皮层神经元原代培养及毒胡萝卜素干预后的表现 被引量:2
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作者 容琼文 陈志斌 +3 位作者 蔡美华 欧小凡 陈蓉 苏庆杰 《中国热带医学》 CAS 2011年第2期138-140,共3页
目的探讨离体大鼠皮层神经元原代培养方法及毒胡萝卜素诱导大鼠皮层神经元内质网应激的作用特点。方法体外培养SD乳鼠皮层神经元细胞,免疫组织化学、免疫荧光染色鉴定神经元纯度,Hoechst33258单染法观察凋亡细胞核的形态变化及测出细胞... 目的探讨离体大鼠皮层神经元原代培养方法及毒胡萝卜素诱导大鼠皮层神经元内质网应激的作用特点。方法体外培养SD乳鼠皮层神经元细胞,免疫组织化学、免疫荧光染色鉴定神经元纯度,Hoechst33258单染法观察凋亡细胞核的形态变化及测出细胞凋亡率,透射电子显微镜观察神经元的亚细胞结构。结果 SD乳鼠皮层神经元可纯化体外培养,对培养7d后的神经元进行NSE免疫荧光染色显示计数NSE阳性细胞数占细胞总数的百分数为(95±3)%,在TG浓度为2μmol/L作用时间为24h时离体培养原代神经元细胞凋亡率最高为19%±0.54%,P<0.05。神经元细胞在2μmol/LTG作用24h后神经元呈现典型凋亡形态学改变,核周内质网,线粒体结构模糊不清,包膜破损,且出现染色质浓集、核固缩、细胞皱缩、核碎裂。结论体外改良的培养方法可以获得较高纯度的神经元,在毒胡萝卜素诱导的神经元内质网应激时,线粒体改变引起的变化可能是下游事件。 展开更多
关键词 离体神经元 毒胡萝卜素 内质网应激 透射电子显微镜
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PROPERTIES OF VOLTAGE-GATED SODIUM CHANNELS IN DEVELOPING AUDITORY NEURONS OF THE MOUSE IN VITRO
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作者 桂鸣 Lu-YangWang 《Chinese Medical Sciences Journal》 CAS CSCD 2003年第2期67-74,共8页
Objective. To investigate the properties of voltage-gated sodium (Na+) channels in developing auditoryneurons during early postnatal stages in the mammalian central nervous system.Methods. Using the whole-cell voltage... Objective. To investigate the properties of voltage-gated sodium (Na+) channels in developing auditoryneurons during early postnatal stages in the mammalian central nervous system.Methods. Using the whole-cell voltage-clamp technique, we have studied changes in the electrophysi-ological properties of Na+ channels in the principal neurons of the medial nucleus of the trapezoid body (MNTB).Results. We found that MNTB neurons already express functional Na+ channels at postnatal day 1 (P1),and that channel density begins to increase at P5 when the neurons receive synaptic innervation andreach its maximum (~3 fold) at P11 when functional hearing onsets. These changes were paralleled byan age-dependent acceleration in both inactivation and recovery from inactivation. In contrast, there wasvery little alteration in the voltage-dependence of inactivation.Conclusion. These profound changes in the properties of voltage-gated Na+ channels may increase theexcitability of MNTB neurons and enhance their phase-locking fidelity and capacity during high-frequencysynaptic transmission. 展开更多
关键词 voltage-gated sodium channels auditory neurons DEVELOPMENT
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Protein kinase C regulates neurite outgrowth in spinal cord neurons
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作者 杨萍 李振强 +1 位作者 宋林 殷玉芹 《Neuroscience Bulletin》 SCIE CAS CSCD 2010年第2期117-125,共9页
Objective The functional roles of protein kinase C (PKC) in the neurite outgrowth and nerve regeneration remain controversial. The present study was aimed to investigate the role of PKC in neurite outgrowth, by stud... Objective The functional roles of protein kinase C (PKC) in the neurite outgrowth and nerve regeneration remain controversial. The present study was aimed to investigate the role of PKC in neurite outgrowth, by studying their regulatory effects on neurite elongation in spinal cord neurons in vitro. Methods The anterior-horn neurons of spinal cord from embryonic day 14 (E14) Sprague-Dawley (SD) rats were dissociated, purified and cultured in the serum-containing medium. The ratio of membrane-PKC (mPKC) activity to cytoplasm-PKC (cPKC) activity (m/c-PKC) was studied at different time points during culture. Results Between 3-11 d of culture, the change of m/c-PKC activity ratio and PKC-βⅡ expression in the neurite were both significantly correlated with neurite outgrowth (r=0.95, P 〈 0.01; r=0.73, P 〈 0.01, respectively). Moreover, PMA, an activator of PKC, induced a dramatic elevation in the m/c-PKC activity ratio, accompanied with the increase in neurite length (r=-0.99, P 〈 0.01). In contrast, GF 109203X, an inhibitor of PKC, significantly inhibited neurite elongation, which could not be reversed by PMA. Conclusion PKC activity may be important in regulating neurite outgrowth in spinal cord neurons, and βⅡ isoform of PKC probably plays a major role in this process. 展开更多
关键词 protein kinase C spinal cord neurons neurite outgrowth in vitro
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