Effect of Allocryptopine on Late sodium current of atrial myocytes in spontaneously hypertensive rats

Objective To explore the effect of allocryptopine （All） on the Late sodium current （INa,Late） of atrial myocytes in spontaneously hyper- tensive rats （SHR）. Method The enzyme digestion method was used to separate single atrial myocytes from SHR and Wistar-Kyoto rat （WKY） rats. INa,Late was record by patch-clamp technique and the effect of All on the current was evaluated. Results Comparing with WKY cells, markedly increasing of INa,Late current in SHR myocytes was found from 0.24 ± 0.02 pA/pF of WKY cells to 1.73± 0.04 pA/pF of SHR cells （P 〈 0.01, n = 15）. After treament with 30 μmol/L All; the current densities was reduced to 0.92 ± 0.03 pA/pF. The ratio of INa,Late/INa,peak of WKY and SHR were 0.09% ± 0.01% and 0.71% ± 0.02%, INa, Late/INa,peak of SHR was reduced to 0.37% ± 0.02% by 30 μmol/L All （P 〈 0.01, n = 15）. We also determined the effect of All on the gating mechanism of the INa,Late in the SHR cells. It was found that All decreased the INa,Late by alleviating the inactivation of the channels and increasing the window current of sodium channel. Conclusion Increased INa,Late in SHR atrial myocytes and the prolonged APD were inhibited by All coming from Chinese herb medicine.

Effects of hypoxia on sodium current in rat cardiomyocytes

The aim of this study was to investigate the effect of hypoxia on the sodium current of rat cardiomyocytes in order to explore ion channel mechanism of cardiomyocyte hypoxia.The rat cardiomyocytes were isolated by acute enzymatic hydrolysis.A group of untreated cells were used to record sodium currents using whole-cell patch-clamp technique,another group was subjected to hypoxia and record sodium currents using same technique.The results showed that the morphological trajectory of sodium hypoxia was not changed compared with that of normal cells.The I-V curve of hypoxic cells was significantly higher than that of normal cells,and the peak current of INa was 15.68%higher than that of normal cells(P<0.0001).Activation potential of normal and hypoxia cells was about-40mV,the maximum peak current corresponds to the stimulation voltage of-25mV.The above results suggest that rat cardiomyocytes sodium current increases in the case of hypoxia.

Voltage- and Use-dependent Effect of 7-chlor-benzylte-trahydropalmatine on Sodium Currents in Guinea Pig Ventricular Myocytes

The whole-cell patch-clamp technique was employed to obtain information about the voltage-dependence and kinetics of interaction of 7-chlor-benzylte-trahydropalmatine (7-Cl-BTHP) with cardiac sodium channels. 7-Cl-BTHP (30 mol/L) significantly decreased the peak sodium current (from 7. 8±1. 8 nA to 5. 3±1. 4 nA, P<0. 01, n=5), without producing a shift of the current-voltage curve. It shifted the inactivation curves of sodium current to hyperpolarized potentials, and the V(0.5) was shifted from - (82. 5±2. 5) mV to - (95±2.4) mV (P <0. 05, n=4). 7-Cl-BTHP produced a significant use-dependent effect that was proportional to the duration of the voltage step. In addition, 7-Cl-BTHP slowed the recovery of sodium channel from inactivation, which could explain its use-dependent effects on sodium current. The characteristics of 7-Cl-BTHP blockage suggest that this agent binds preferentially to inactivated sodium channels.

Effects of curcumin on sodium currents of dorsal root ganglion neurons in type 2 diabetic neuropathic pain rats

Along with the development of economy and society, type 2 diabetic mellitus(T2DM) has become one of the most common diseases at the global level. As one of the complications of T2 DM, diabetic neuropathic pain(DNP) stubbornly and chronically affects the health and life of human beings. In the pain field, dorsal root ganglion(DRG) is generally considered as the first stage of the sensory pathway where the hyperexcitability of injured neurons is associated with different kinds of peripheral neuropathic pains. The abnormal electrophysiology is mainly due to the changed properties of voltage-gated sodium channels(VGSCs) and the increased sodium currents(INa). Curcumin is an active ingredient extracted from turmeric and has been demonstrated to ameliorate T2 DM and its various complications including DNP effectively. The present study demonstrates that the INa of small-sized DRG neurons are significantly increased with the abnormal electrophysiological characteristics of VGSCs in type 2 diabetic neuropathic pain rats. And these abnormalities can be ameliorated efficaciously by a period of treatment with curcumin.

Antiarrhythmic ionic mechanism of Guanfu base A—Selective inhibition of late sodium current in isolated ventricular myocytes from guinea pigs

The present study was designed to determine the effects of Guanfu base A(GFA) on the late sodium current(INa.L),transient sodium current(INa.T),HERG current(IHERG),and Kv1.5 current(IKv1.5).The values of INa.L,INa.T,IHERG and IKv1.5 were recorded using the whole-cell patch clamp technique.Compared with other channels,GFA showed selective blocking activity in late sodium channel.It inhibited INa.L in a concentration-dependent manner with an IC50 of(1.57 ± 0.14) μmol·L-1,which was significantly lower than its IC50 values of(21.17 ± 4.51) μmol·L-1 for the INa.T.The inhibitory effect of GFA on INa,L was not affected by 200μmol·L-1 H2O2.It inhibited IHERG with an IC50 of(273 ± 34) μmol·L-1 and has slight blocking effect on IKv1.5,decreasing IKv1.5 by only 20.6% at 200 μmol·L-1.In summary,GFA inhibited INa.L selectively and remained similar inhibition in presence of reactive oxygen species..These findings may suggest a novel molecular mechanism for the potential clinical application of GFA in the treatment of cardiovascular disorders.

Sodium current kinetics of transitional myocytes in Koch triangle of rabbit hearts

Background Few studies have explored the inward sodium current （INa） kinetics of transitional cardiomyocytes. This study aimed to explore the kinetics of transitional cardiomyocytes types α and β. Methods The whole-cell patch clamp technique was used to study the rapid INa of isolated transitional cardiomyocytes in the Koch triangle of rabbit hearts. Results Maximal amplitude and density of INa in type a and type β was （-1627±288） pA （α）, （-35.17±6.56） pA/pF （β） and （-3845±467） pA （α）, （-65.64±10.23） pA/pF （β） （P 〈0.05）. Steady state activation curves of INa, fitted to a Boltzmann distribution for both types, were sigmoid in shape. Half activation voltage and slope factors did not significantly differ between types at （-43.46±0.85） mV （α）, （-41.39±0.47） mV （β） or （9.04±0.66） mV （α）, （11.08±0.89） mV （β）. Steady state inactivation curves of INa, fitted to a Boltzmann distribution in both types were inverse ＂S＂ shape. Half inactivation voltage and slope factors were （-109.9±0.62） mV （α）, （-107.5±0.49） mV （β） and （11.78±0.36） mV （α）, （11.57±0.27） mV （β）, （P〉0.05）, but time constants of inactivation were significantly different at （1.10±0.19） mV （α） and （2.37±0.33） ms （β）, （P 〈0.05）. Time constants of recovery from inactivation of INa for both types were （122.16±27.43） mV （α） and （103.84±2.8.97） ms （β） （P 〈0.05）. Conclusions Transitional cardiomyocytes in rabbit hearts show a heterogeneous, voltage gated and time dependent fast inward sodium current. Types α and β show the features of INa similar to those in slow- and fast-response myocytes, with probably better automaticity and conductivity, respectively.

CRYSTALLIZATION OF SODIUM TUNGSTEN BRONZE USING ELECTROLYSIS WITHREVERSE CURRENT~＋

Utilizing the technique of electrolysis with reverse current,sodium tungsten bronze (Na_xWO_3) crystals were prepared from a molten mixture of sodium tungstate (Na_2WO_4 ) and tungstic trioxide (WO_3) at 800℃. Crystal structure, lattice parameter, and s

Effects of sodium ferulate on the ultrarapid delayed rectifier K^+ current in human atrial myocytes

Objective：To study the effects of sodium ferulate on the ultrarapid delayed rectifier K^＋ current（IKur） in human atrial myocytes. Methods：Human atrial myocytes were isolated by enzyme dispersion method. IKur, in human atrial myocytes were recorded by using the whole cell patch clamp. The changes of IKur were compared in the absence and the presence of sodium ferulate. Results：There was no effect of 0.4 g/L sodium ferulate on I-V relation of IKur. However, 0.4 g/L sodium ferulate inhibited IKur to some degrees at each test pulse. The current densities of IKur at ＋60 mV decreased from 4.997 ± 0.35 PA/PF to 3.331 ± 0.26 PA/PF（n = 6, P 〈 0.05）. The inhibitory effect was concentration-dependent. IC50 was（0.41 ±0.03）g/L and the Hill coefficient was 0.95 ± 0.05. Conclusion：Sodium ferulate as a potassium channel blocker can inhibit IKur in human atrial myocytes effectively.

马钱子碱抑制豚鼠心室肌细胞钠电流的作用研究

目的本研究旨在分析马钱子碱(brucine)对分离的单个豚鼠心室肌细胞钠电流(INa+)的作用,并探索其抗心律失常的可能机制。方法共选取24只健康的成年豚鼠作为实验对象,雌雄不拘,随机分为4组,每组6只:第1组是未接受任何处理的对照组,之后通过微量加样器使培养皿中brucine药物的终浓度分别达到3μmol/L、10μmol/L、30μmol/L。采用急性酶解法分离获得单个豚鼠心室肌细胞,通过全细胞膜片钳技术测量离子通道电流,以检测不同浓度的brucine对豚鼠心室肌细胞INa+的影响。结果正常的对照组没有明显的INa+电流峰值的变化,而brucine 3μmol/L组给药前后基本不影响INa+电流峰值,当brucine的浓度增加到10μmol/L时,给药前后INa+电流峰值显著下降(P<0.05),在30μmol/L组给药前后INa+电流峰值大幅度减少(P<0.01),并且这种抑制作用呈浓度依赖性。正常对照组及brucine 3μmol/L剂量组中,电流-电压曲线(Ⅰ~Ⅴ曲线)并未受到显著的影响;然而,10μmol/L、30μmol/L剂量组与对照组比较,INa+的Ⅰ~Ⅴ曲线上移,无平行移动,且曲线形状不变。结论Brucine能够通过抑制心室肌细胞钠通道电流发挥抗心律失常作用。

Transforming growth factor-beta 1 enhances discharge activity of cortical neurons

Transforming growth factor-beta 1(TGF-β1)has been extensively studied for its pleiotropic effects on central nervous system diseases.The neuroprotective or neurotoxic effects of TGF-β1 in specific brain areas may depend on the pathological process and cell types involved.Voltage-gated sodium channels(VGSCs)are essential ion channels for the generation of action potentials in neurons,and are involved in various neuroexcitation-related diseases.However,the effects of TGF-β1 on the functional properties of VGSCs and firing properties in cortical neurons remain unclear.In this study,we investigated the effects of TGF-β1 on VGSC function and firing properties in primary cortical neurons from mice.We found that TGF-β1 increased VGSC current density in a dose-and time-dependent manner,which was attributable to the upregulation of Nav1.3 expression.Increased VGSC current density and Nav1.3 expression were significantly abolished by preincubation with inhibitors of mitogen-activated protein kinase kinase(PD98059),p38 mitogen-activated protein kinase(SB203580),and Jun NH2-terminal kinase 1/2 inhibitor(SP600125).Interestingly,TGF-β1 significantly increased the firing threshold of action potentials but did not change their firing rate in cortical neurons.These findings suggest that TGF-β1 can increase Nav1.3 expression through activation of the ERK1/2-JNK-MAPK pathway,which leads to a decrease in the firing threshold of action potentials in cortical neurons under pathological conditions.Thus,this contributes to the occurrence and progression of neuroexcitatory-related diseases of the central nervous system.

Activin A maintains cerebral cortex neuronal survival and increases voltage-gated Na^+ neuronal current

Activin A, which was first described in 1986, has been shown to maintain hippocampal neuronal survival. Activin A increases intracellular free Ca2＋ via L-type Ca2＋ channels. Our previous study showed that activin A promotes neurite growth of dorsal root ganglia in embryonic chickens and inhibits nitric oxide secretion. The present study demonstrated for the first time that activin A could maintain cerebral cortex neuronal survival in vitro for a long period, and that activin A was shown to increase voltage-gated Na＋ current （/Na） in Neuro-2a cells, which was recorded by patch clamp technique. The present study revealed a novel mechanism for activin A, as well as the influence of activin A on neurons by regulating expressions of vasoactive intestine peptide and inducible nitric oxide synthase.

次氯酸钠电解工艺动力学调控及在污水处理中消毒效果

为提升次氯酸钠电解工艺的产氯量和满足城镇污水处理站深度处理单元出水的消毒要求,从反应动力学角度,探究次氯酸钠电解工艺的电解参数如盐水浓度、电流密度和电解温度对次氯酸钠生产过程的影响,分析深度处理单元出水水质对次氯酸钠消毒效果的影响,明晰电解参数和出水水质的影响机制。结果表明:当盐水浓度、电流密度、电解温度和电解时间分别为40 g/L、20 A/dm^(2)、32℃和2.5 h时,能够有效控制温度影响、析氯电位、歧化反应和活化能,并使次氯酸钠产量提高到9.28 g/L。当次氯酸钠的投加量至少为5 mg/L和控制接触反应时间为5 min时,次氯酸钠对粪大肠杆菌群的灭菌性比其对COD和氨氮的氧化性更占竞争优势,并将水样中粪大肠杆菌群数减少至102.97个/L,达到了GB 18918—2002《城镇污水处理厂污染物排放标准》一级A排放标准中细菌学指标要求。

电解沉积法碲提纯技术的研究

本文以粗二氧化碲为原料,加入到氢氧化钠溶液中在60~80℃加热条件下搅拌反应,反应完后将溶液进行过滤除杂,滤去不溶性的杂质,所得滤液中加入助剂配制成含Te 200~230(g/L),NaOH 90~100(g/L),Se<0.3(g/L),Pb<0.003(g/L)的电解液。然后将配制好的电解液放入电解槽中,设置电解槽电流密度为50A/m^(2),电解沉积时间120~144 h。将在阴极板上析出的碲刮下并用纯水洗涤至中性,放入真空干燥箱中进行干燥。干燥好的电解碲进行熔融、扒渣、真空铸型等工序制得碲锭,得到的碲锭经检测分析其品级可达到4 N及以上。

Effects of Intrathecally Administerd NaV1.8 Antisense Oligonucleotide on the Expression of Sodium Channel mRNA in Dorsal Root Ganglion

Neuropathic pain has been hypothesized to be the result of aberrant expression and function of sodium channels at the site of injury. To investigate the effects of NaV1.8 antisense oligonucleotide on the expression of sodium channel mRNA in dorsal root ganglion （DRG） neurons in chronic neuropathic pain. 24 Sprague-Dawley rats weighing 200--260 g were anesthetized with the intraperitoneal injection of 300 mg· kg^-1 choral hydrate. The CCI model was made by loose ligation of sciatic nerve trunk by 4--0 chromic gut. The mechanical and thermal pain threshold were measured before operation and 1, 3, 5, 7, 9, 11, 13 days after operation. A PE-10 catheter was implanted in subarachnoid space at lumbar region. On the 7th postoperative day the animals were randomly divided into 4 groups. The drugs were injected intrathecally twice a day for 5 consecutive days in group 2--4. The animals were decapitated 14 days after the surgery. The L4--L6 DRG of the operated side was removed and crushed, and total RNA was extracted with Trizol reagent. The contralateral side was used as control. The change of NaV1.8 sodium channel transcripts was determined by RT-PCR. Pain threshold was significantly lowered after CCI as compared with that in control group and was elevated 3 days after antisense oligonucleotide injection. Sensory neuron specific TTX-R sodium channel NaV1.8 transcript was down-regulated after antisense oligonucleotide injection at the dosage of 45 μg as compared with that in CCI group （P〈0.01）, and it was even greater at the dosage of 90 μg. The intrathecally injected NaV1.8 antisense oligonucleotide can reduce the mechanical allodynia and thermal hyperalgesia partially by downregulating the SNS transcript expression.

304不锈钢在熔融多硫化钠中的高温腐蚀行为研究

钠硫电池不锈钢集流体材料在熔融多硫化钠中易发生高温腐蚀,影响电池的性能并引发安全问题。本工作采用电化学阻抗谱技术研究了304不锈钢在350℃熔融多硫化钠熔盐中的高温腐蚀行为,结合微观组织分析,探索其高温腐蚀机理。结果表明,304不锈钢的电化学阻抗谱由高频段的容抗弧和低频段的直线组成,呈典型的扩散反应控制。电荷转移电阻较小,介于0.918~2.014Ω·cm^(2)之间,表明不锈钢的腐蚀速率较快。腐蚀产物层主要由外层的FeS_(2)、FeNiS_(2)和内层的Crr_(2)S_(3)组成。在腐蚀过程中,合金表面的产物膜经历生长、溶解与脱落的过程。

熔融氯化钠晶体介电常数的模拟计算方法

由于分子模拟过程中存在周期性边界的影响,离子偶极矩定义模糊,导致传统的偶极矩涨落方法在计算熔融盐晶体或含有自由电荷体系的介电常数时存在一定阻碍。根据经典介电理论,通过电流关联函数计算熔融氯化钠(NaCl)晶体体系的介电常数,研究了不同温度下氯化钠的频率相关介电谱,并分析了晶体相变对介电特性的影响。结果表明:当NaCl为晶体状态时,介电谱显示出明显的共振吸收峰;在NaCl熔化以后,介电谱的共振吸收峰的带宽变宽,波形发生了明显变化。分别利用电流法和外加电场法计算了不同温度下NaCl的静态介电常数,结果显示:两种方法的计算结果的一致性良好,从而验证了本文方法的准确性;NaCl晶体在发生固液相变时,静态介电常数会在相变点发生跳变。

氧化苦参碱对豚鼠心室肌细胞钠电流的影响

目的 :观察氧化苦参碱 (OMT)对豚鼠心室肌细胞钠电流的影响。方法 :采用全细胞膜片钳技术。结果 :OMT 0 .1、0 .3和 1mmol/ L对钠电流均呈现不同程度的抑制作用 ,且呈现剂量依赖性。结论 :OMT对钠通道的阻滞作用可能是其抗心律失常的作用机制之一。

马钱子碱对大鼠海马神经元钠通道的影响

目的 研究马钱子碱镇痛作用的机制。方法 用全细胞膜片钳技术 ,首先在大鼠海马CA1锥体神经元记录出钠电流 ,然后观察马钱子碱对钠电流的影响。结果 马钱子碱可以浓度依赖的方式可逆地抑制钠电流。

成年蜜蜂脑神经细胞的培养和电生理特征

为了研究杀虫剂等对蜜蜂毒性作用的神经机制,需在体外建立成年蜜蜂脑神经细胞的分离培养和电生理记录技术并研究其正常电生理特征,而对成年蜜蜂脑神经细胞的分离培养和电生理特性的研究报道甚少。我们采用酶解和机械吹打相结合的方法获得了数量较多且活力较好的成年意大利蜜蜂Apismellifera脑神经细胞,并用全细胞膜片钳技术研究了成年意大利蜜蜂脑神经细胞对电流和电压刺激的反应,获得了成年意蜂脑神经细胞的基本电生理特征以及钠电流和钾电流的特性。全细胞电流钳的记录结果表明,在体外培养条件下,细胞无自发放电发生,注射电流后仅引起细胞单次放电,引起细胞放电的阈电流平均为60.8±6.3pA;细胞动作电位产生的阈电位平均为-27.4±2.3mV。用全细胞电压钳记录了神经细胞的钠电流和钾电流。钠电流的分离是在电压刺激下通过阻断钾通道和钙通道实现。细胞的内向钠电流在指令电压为-40～-30mV左右激活,-10mV达峰值,钠通道的稳态失活电压V1/2为-58.4mV;外向钾电流成份至少包括较小的快速失活钾电流和和较大的缓慢失活钾电流(占总钾电流的80%),其半激活膜电位V1/2为3.86mV,无明显的稳态失活。结果提示缓慢失活钾电流的特征可能是细胞单次放电的机制之一。

三种蜘蛛粗毒对NG108-15细胞电压门控钠通道的抑制作用

利用小鼠神经细胞瘤×大鼠神经胶质细胞的杂交细胞 NG1 0 8-1 5,通过全细胞记录 ( whole-cellrecording)模式的膜片钳技术 ,检验了虎纹捕鸟蛛 ( Selenocosmia huwena)、海南捕鸟蛛 ( Selenocosmia hainana)和广西大疣蛛 ( Macrotheleguangxia sp)的粗毒对 NG1 0 8-1 5细胞膜上电压门控 TTX敏感型钠电流和延迟整流钾电流的作用 .结果表明 ,三种蜘蛛粗毒对外向延迟整流钾电流没有明显作用 ,但对 TTX敏感型的快钠电流表现出较强的抑制效应 .抑制效应呈量效关系 .三种粗毒抑制钠电流的 EC5 0 相应约为 :3.4 mg/L;1 .8mg/L和 1 1 .0 mg/L.