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1.
采用三阶统计法的离子通道电流起伏的参数建模及其估算单离子通道运动参数的应用[英]/MinoH…//IEEETransBME.-1993,40(9).-970本文提出了一种采用三阶累积量法的稳定离子通道电流摆动(Stationaryionic-chan...  相似文献   

2.
心肌细胞中由拉伸刺激离子通道产生的肌电反馈〔英]/AkayM…//IEEETransBME.1993,40(8).811对新生鼠心肌细胞拉伸刺激离子通道(SAC)采用接触细胞薄片进行研究,用记录吸量管吸膜片引起的拉伸产生的动作电位突发被记录为动作电流...  相似文献   

3.
恶性心律失常和室颤是心血管疾病中造成人类死亡的主要原因之一。建立在Hodgkin-Huxley方程基础上的心肌细胞动作电位数学模型由离子通道、泵及交换体电流组成,与细胞内外离子浓度、通道状况、神经递质和药物影响密切相关,可使细胞电生理和临床病理生理间建立确切的联系。基于这种模型的计算机仿真研究可以通过改变细胞内外环境,观察心肌组织乃至整个心脏电生理功能的变化,探讨和揭示心律失常或心源性猝死的机制。本文重点阐述了心肌细胞动作电位数学模型的构成及其计算机仿真研究的概况。  相似文献   

4.
自从人们在蛙神经肌肉按合处发现膜电流波动以来,这些波动已进一步地研究以分析生物膜单离子通道的动态特性。在膜电流波动分析中,功率谱通常起着一个关键的作用,由于其与单离子通道的动态特性有关(即由于单离子通道的失敏感状态)。在分析中,对快速精确地估计功率  相似文献   

5.
目的:传统的全细胞膜片钳技术在离子通道电流的记录中存在机械稳定性差,对细胞的损伤大,以及胞内液的被渗析影响与细胞内信号转导和离子通道调控有关的第二信使物质的正常运行。而穿孔全细胞膜片钳技术应用二性霉素B或制霉菌素在细胞膜上形成特定的孔道,选择性地允许一些离子和大分子物质,从而使细胞内环境保持相对稳定,在一定程度上弥补了上述缺陷,实验成功率也相应提高。本文就穿孔膜片钳技术在全细胞离子通道电流记录中的应用进行探讨。  相似文献   

6.
膜片钳实验技术系列讲座──第十二部分单一离子通道记录数据的分析法陈军译李继硕校阅(第四军医大学基础部解剖学教研室,梁球琚脑研究中心,西安710032)(曾我部正博:日本生理学杂志1995;57:247~260)前言什么是单一离子通道电流?对处于功能状...  相似文献   

7.
目的:单通道平面脂质双分子层电生理平台是目前研究离子通道特性最直接、最有效的技术手段。为扩展平台研究温度对离子通道电生理特性、通道稳定性等的研究的能力,本文借助循环水浴对平台的温控模块进行设计与实现。方法:本文以Warner公司的脂质双分子层电生理实验平台为操作平台搭建循环水浴温控模块。通过分析温控模块中循环水对平台电流测量的干扰并比较不同循环水排布方式对电流测量的干扰强度,我们设计了折返对偶排布的循环水排布回路,并借助α-溶血素七聚体大孔径离子通道检验该设计的实用效果。该排布方式能够降低循环水回路与电流测量回路间的电磁耦合,进而降低由循环水引入的电磁干扰,保证皮安级小电流的测量。结果:电流噪音可受循环水流回路的排布影响,其中在采用折返对偶排布的情况下,电流噪音与无温控系统空白对照的电流噪音无显著区别。结论:折返对偶排布的循环水流设计能够有效降低循环水温控模块对电流测量的电磁干扰。  相似文献   

8.
仿真研究心衰情况下心室肌细胞离子通道的变异对细胞电生理和透壁特异性的影响机制,以及心力衰竭下心室透壁复极化的改变与心律失常之间的关系.基于反映正常和衰竭人体心肌细胞离子通道透壁特异性的实验数据,建立离子通道水平的心肌细胞电生理数学模型,模拟仿真研究心衰情况下心室肌心外膜、中层、心内膜细胞电生理透壁特异性的变化.结果:仿真研究发现心衰导致透壁心室肌细胞电生理重建,透壁细胞的动作电位持续时间都有明显的延长,改变了动作电位的透壁特异性,进而减小了动作电位的透壁梯度,同时衰竭心脏中快步率时动作电位的比率依赖性会增加.模型研究认为这可能与心衰细胞中离子电流ICaL和Iks的透壁特异性的电生理重构有关.所发展的细胞模型不仅可以辅助细胞电生理实验分析研究,同时也是今后仿真研究心衰情况下心肌细胞兴奋-收缩耦联力学特性的重要基础.  相似文献   

9.
目的:研究手机900MHz射频磁场对小鼠皮层神经元动作电位的影响。方法:低发射功率为398.1 mW、频率为900 MHz的射频磁场照射急性分离小鼠脑皮层神经元。采用膜片钳技术,观察对照组和暴露组的Na+通道电流I Na、瞬时外向K+通道电流I A和延迟整流K+通道电流I K。结果:900 MHz磁场暴露对神经元离子通道有明显影响:(1)Na+通道激活电位向超极化方向移动,钠电流峰值增大,激活和失活曲线向超极化方向移动;(2)瞬时外向钾通道的激活过程受到抑制;(3)延迟整流钾电流I K受到抑制,且呈时间依赖性。结论:低功率900 MHz射频磁场暴露影响离子通道的I-V特性和动力学特性,神经元动作电位发放阈值变小,动作电位发放频率变缓,改变了动作电位的形状和时程,影响了神经细胞电传导特性,对脑神经元的生理功能产生了一定的影响。  相似文献   

10.
<正> 70年代初期,细胞内透析技术的进展及其在神经细胞体的应用使人们首次得以在全细胞水平将Ca~(2+)电流与其它跨膜电流区别开进行研究。这些研究表明:(1),Ca~(2+)离子通道的活动是按m~2 Hodgkin-Huxley模式进行的;(2),首次指出细胞内Ca~(2+)对Ca~(2+)离子通道的功能是至关重要的;(3),Ca_2~+离子通道的一个基本特性是在细胞外有Ca~(2+)螯合剂存在的情况下,它转变为单价离子可透过的形式[Kostyuk and Krishtal, J.Physiol. (London)270:545(1977);ibid,P.569]。对后一现象的进一步研究发现Ca~(2+)本身可调节Ca_2~+离子通道的选择性,这一调节可能是通过将Ca~(2+)与Ca~(2+)离子通道的外口附近的高亲合  相似文献   

11.
基于HMM的低信噪比离子通道信号的恢复及参数估计   总被引:1,自引:0,他引:1  
细胞膜离子单通道信号是皮安级的随机电流 ,膜片钳技术可以记录这些信号。一般认为它是一阶的、状态有限的 Markov过程。某些种类的离子通道 ,电流信号特别微弱 ,完全淹没在背景噪声中 ,传统的膜片钳技术很难检测到 ,只能运用数学方法恢复和估计。在低采样频率情况下 ,由于混叠效应 ,可认为背景噪声是白色的 ;在高采样频率条件下 (高于奈奎斯特频率 ) ,背景噪声是有色的。本文分别综述了白色背景噪声条件下基于隐式 Markov模型和有色背景噪声条件下基于隐式矢量 Markov模型的低信噪比离子单通道信号的恢复和参数估计 ,主要包括前后向算法、EM算法等  相似文献   

12.
Single channel currents activated by glutamate were recorded by means of the patch-clamp technique in the abdominal superficial extensor muscle and the claw opener muscle of small (1-3 months old) and large (greater than 16 months old) crayfish. It was found that in small crayfish the time course of glutamate-operated single channel currents was prolonged by a factor of about 4 in these two preparations. In the abdominal superficial extensor muscle, single channel currents activated by 5 mmol/l glutamate had a mean burst length of tau = 2-3 ms in large crayfish and a mean burst length of tau = 8-9 ms in small crayfish. In the claw opener, for large crayfish tau congruent to 0.5 ms and for small crayfish tau = 1.5-2.5 ms resulted (500 mumol/l glutamate). Moreover, single channel currents with long time courses often slowly increased their amplitudes during the open time of the channel and current amplitudes did not decline completely to the baseline after channel closing. In addition, single channel currents with relatively constant amplitude were often followed by a small increasing and decreasing membrane current. The latter results suggest that glutamate channel gating might trigger a membrane current.  相似文献   

13.
在单通道信号处理中引入尺度能量分布的概念 ,利用小波变换 ,通过提取具有特征频率的高频信号 ,可以在不失真的条件下将单通道信号清晰地检测出来 ,消除噪声干扰。本文提供的方法在离子通道信号处理中具有较普遍的意义  相似文献   

14.
15.
In cardiac ventricular myocytes, membrane depolarization leads to the inactivation of the Na channel and Ca channel ionic currents. The inactivation of the ionic currents has been associated with a reduction of the gating charge movement (“immobilization”) which governs the activation of Na channels and Ca channels. The nature of the apparent “immobilization” of the charge movement following depolarization was explored in embryonic chick ventricular myocytes using voltage protocols applied from depolarized holding potentials. It was found that although all of the charge was mobile following inactivation, the voltage dependence of its movement was shifted to more negative potentials. In addition, the shift in the distribution of the Na channel charge could be differentiated from that of the Ca channel charge on the basis of kinetic as well as steady-state criteria. These results suggest that the voltage-dependent activation of Na channel and Ca channel charge movements leads to conformational changes and charge rearrangements that differentially bias the movements of these voltage sensors, and concomitantly produce channel inactivation. Received: 26 September 1995 / Accepted: 7 November 1995  相似文献   

16.
 The rabbit cardiac Ca2+ channel (α1C) expressed in Xenopus oocytes exhibited a complete run-down of ionic currents when cell-attached patches were excised. The α1C channel was expressed alone or was coexpressed with the accessory β2a or β1b subunit. The catalytic subunit of protein kinase A (PKAc) and MgATP were capable of delaying the run-down of single-channel currents. In 33% of the α1C patches, and 26% of the α1C2a patches, inclusion of PKAc in the bath solution delayed the run-down for a maximum of 20 min. In experiments where PKAc in the bath was not sufficient to delay the run-down of channel activity, insertion of the patch back into the oocyte (patch-cramming) could restore channel activity. Gating currents were also measured in the α1C1b channel and were not subject to any run-down, even after the complete run-down of ionic currents. The results presented here reveal that PKAc is capable of delaying the run-down of currents in a subset of patches. The patch-cramming results suggest that a cytoplasmic factor, in addition to phosphorylation of the channel (by PKAc), may be involved in the maintenance of channel activity. Received: 29 October 1998 / Accepted: 4 January 1999  相似文献   

17.
We examined changes in ionic and gating currents in CaV1.2 channels when extracellular Ca2+ was reduced from 10 m m to 0.1 μ m . Saturating gating currents decreased by two-thirds ( K D≈ 40 μ m ) and ionic currents increased 5-fold ( K D≈ 0.5 μ m ) due to increasing Na+ conductance. A biphasic time dependence for the activation of ionic currents was observed at low [Ca2+], which appeared to reflect the rapid activation of channels that were not blocked by Ca2+ and a slower reversal of Ca2+ blockade of the remaining channels. Removal of Ca2+ following inactivation of Ca2+ currents showed that Na+ currents were not affected by Ca2+-dependent inactivation. Ca2+-dependent inactivation also induced a negative shift of the reversal potential for ionic currents suggesting that inactivation alters channel selectivity. Our findings suggest that activation of Ca2+ conductance and Ca2+-dependent inactivation depend on extracellular Ca2+ and are linked to changes in selectivity.  相似文献   

18.
Recent studies have shown that cholinergic amacrine cells possess unique membrane properties. However, voltage-gated ionic channels in cholinergic amacrine cells have not been characterized systematically. In this study, using electrophysiological and immunohistochemical techniques, we examined voltage-gated ionic channels in a transgenic mouse line the cholinergic amacrine cells of which were selectively labeled with green fluorescent protein (GFP). Voltage-gated K(+) currents contained a 4-aminopyridine-sensitive current (A current) and a tetraethylammonium-sensitive current (delayed rectifier K(+) current). Voltage-gated Ca(2+) currents contained a omega-conotoxin GVIA-sensitive component (N-type) and a omega-Aga IVA-sensitive component (P/Q-type). Tetrodotoxin-sensitive Na(+) currents and dihydropyridine-sensitive Ca(2+) currents (L-type) were not observed. Immunoreactivity for the Na channel subunit (Pan Nav), the K channel subunits (the A-current subunits [Kv. 3.3 and Kv 3.4]) and the Ca channel subunits (alpha1(A) [P/Q-type], alpha1(B) [N-type] and alpha1(C) [L-type]) was detected in the membrane fraction of the mouse retina by Western blot analysis. Immunoreactivity for the Kv. 3.3, Kv 3.4, alpha1(A) [P/Q-type], and alpha1(B) [N-type] was colocalized with the GFP signals. Immunoreactivity for alpha1(C) [L-type] was not colocalized with the GFP signals. Immunoreactivity for Pan Nav did not exist on the membrane surface of the GFP-positive cells. Our findings indicate that signal propagation in cholinergic amacrine cells is mediated by a combination of two types of voltage-gated K(+) currents (the A current and the delayed rectifier K(+) current) and two types of voltage-gated Ca(2+) currents (the P/Q-type and the N-type) in the mouse retina.  相似文献   

19.
It is well known that neuronal firing properties are determined by synaptic inputs and inherent membrane functions such as specific ionic currents. To characterize the ionic currents of brainstem cardio-respiratory neurons, cells from the hypoglossal (XII) nucleus and the dorsal motor nucleus of the vagus (DMX) were freshly dissociated and membrane ionic currents were studied under whole-cell voltage and current clamp. Both of these neurons showed a TTX-sensitive Na+ current with a much larger current density in XII than DMX neurons. This Na+ current had two (fast and slow) distinct inactivation decay components. The ratio of the magnitudes of the fast to slow component was roughly two-fold greater in DMX than in XII cells. Both DMX and XII neurons also showed a high voltage-activated Ca2+ current, but this current density was significantly greater (three-fold) in DMX than XII neurons. A relatively small amount of low-voltage activated Ca2+ current was also observed in DMX neurons, but not in the majority of XII cells. A transient and a sustained outward current components were observed in DMX cells, but only sustained currents were present in XII neurons. These outward currents had a reversal potential of about -70 mV with 3 mM external K+ and -30mV with 25 mM K+, and substitution of K+ with cesium and tetraethylammonium suppressed more than 90% the outward currents, indicating that most outward currents were carried by K+. The transient outward current consisted of two components with one sensitive to 4-aminopyridine and the other to intracellular Ca2+. In XII neurons, BRL 38227 (lemakalim), an ATP-sensitive K+ (KATP) channel activator, increased the sustained K+ currents by 10% of control, and glibenclamide, a KATP channel blocker, decreased the sustained K+ currents by 20%. Evidence for the presence of an inward rectifier K+ current was also obtained from both XII and DMX neurons. These results on XII and DMX neurons indicate that (1) the methods used to dissociate neurons provide a useful means to overcome voltage clamp technical difficulties; (2) ion channel characteristics such as density and biophysical properties of DMX neurons are very different from those of XII neurons; and (3) several newly discovered membrane ionic currents are present in these cells.  相似文献   

20.
It is well known that neuronal firing properties are determined by synaptic inputs and inherent membrane functions such as specific ionic currents. To characterize the ionic currents of brainstem cardio-respiratory neurons, cells from the hypoglossal (XII) nucleus and the dorsal motor nucleus of the vagus (DMX) were freshly dissociated and membrane ionic currents were studied under whole-cell voltage and current clamp. Both of these neurons showed a TTX-sensitive Na+ current with a much larger current density in XII than DMX neurons. This Na+ current had two (fast and slow) distinct inactivation decay components. The ratio of the magnitudes of the fast to slow component was roughly two-fold greater in DMX than in XII cells. Both DMX and XII neurons also showed a high voltage-activated Ca2+ current, but this current density was significantly greater (three-fold) in DMX than XII neurons. A relatively small amount of low-voltage activated Ca2+ current was also observed in DMX neurons, but not in the majority of XII cells. A transient and a sustained outward current components were observed in DMX cells, but only sustained currents were present in XII neurons. These outward currents had a reversal potential of about − 70 mV with 3 mM external K+ and −30 mV with 25 mM K+, and substitution of K+ with cesium and tetraethylammonium suppressed more than 90% the outward currents, indicating that most outward currents were carried by K+. The transient outward current consisted of two components with onesensitive to 4-aminopyridine and the other to intracellular Ca2+. In XII neurons, BRL 38227 (lemakalim), an ATP-sensitive K+ (KATP) channel activator, increased the sustained K+ currents by 10% of control, and glibenclamide, a KATP channel blocker, decreased the sustained K+ currents by 20%. Evidence for the presence of an inward rectifier K+ current was also obtained from both XII and DMX neurons. These results on XII and DMX neurons indicate that (1) the methods used to dissociate neurons provide a useful means to overcome voltage clamp technical difficulties; (2) ion channel characteristics such as density and biophysical properties of DMX neurons are very different from those of XII neurons; and (3) several newly discovered membrane ionic currents are present in these cells.  相似文献   

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