检索结果-南通市图书馆

Pertussis toxin modulation of sodium channels in the central neurons of cyhalothrin-resistant and cyhalothrinsusceptible cotton bollworm, Helicoverpa armigera

引用

Insect Science 2007年第2期14卷 107-115页

作者： QIANG ZHAO DE-LING KONG BING-JUN HE YAN-QIANG LIU XIAN-LIN FAN AN-XI LIU Key Laboratory of Bioactive Materials Ministry of Education College of Life Sciences Nankai University Tianjin Institute of Plant Protection Chinese Academy of Agricultural Sciences Beijing China

Pertussis toxin （FIX） inhibits the activation of the α-subunit of the inhibitory heterotrimeric G-proteins （Cαi/o） and modulates voltage-gated sodium channels, which may be one of the primary targets of pyrethroids. To investigate the potential mechanisms of agricultural pests resistance to pyrethroid insecticides, we examined the modulations by PTX on sodium channels in the central neurons of the 3rd-4th instar larvae of cyhalothrin-resistant （Cy-R） and cyhaiothrin-susceptible （Cy-S） Helicoverpa armigera by the whole-cell patch-clamp technique. The isolated neurons were cultured for 12-16 h in an improved L15 insect culture medium with or without PTX （400 ng/mL）. The results showed that both the Cy-R and Cy-S sodium channels exhibited fast kinetics and tetrodotoxin （TTX） sensitivity. The Cy-R sodium channels exhibited not only altered gating properties, including a 8.88-mV right shift in voltage-dependent activation （V0.5act） and a 6.54-mV right shift in voltage-dependent inactivation （V0.5inact）, but also a reduced peak in sodium channel density （Ⅰdensity）（55.2% of that in Cy-S neurons）. Cy-R sodium channels also showed low excitability, as evidenced by right shift of activation potential （Ⅴacti） by 5-10 mV and peak potential （Ⅴpcak） by 20 mV. FIX exerted significant effects on Cy-S sodium channels, reducing sodium channel density by 70.04%, right shifting V0.5act by 14.41 mV and V0.5inact by 9. 38 mV. It did not cause any significant changes of the parameters mentioned above in the Cy-R sodium channels. The activation time （Tpeak） from latency to peak at peak voltage and the fast inactivation time constant （τinact） in both Cy-S and Cy-R neurons were not affected. The results suggest that cotton bollworm resistant to pyrethroid insecticides involves not only mutations and allosteric alterations of voltage-gated sodium channels, but also might implicate perturbation of PTX-sensitive Gαi/o-COupled signaling Wansduction pathways.

关键词： cyhalothrin G proteins Helicoverpa armigera insecticide resistant neuron pertussis toxin sodium channels whole-cell patch-clamp technique

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

The anti-nociceptive effect of bufalin,an active ingredient from toad venom via modulating voltage-gated sodium channels

引用

中国药理学与毒理学杂志 2016年第10期30卷 1046-1046页

作者： SHEN Rui XU Jian YIN Pei-hao TAO Jie Department of Neurosurgery and Central Laboratory Putuo Hospital Shanghai University of Traditional Chinese Medicine

OBJECTIVE Toad venom(Venenum Bufonis)isalways used for analgesia in China from ancient to modern times,but the effective component of it remains unclear.METHODS In the present study,we investigated the anti-nociceptive effect and the underlying mechanism ofbufalin,an active ingredient fromtoad venom by animal behavior,patch clamp and calcium imaging.RESULTS Bufalin could significantly relieve formalin-induced spontaneous flinching and licking response as well as carrageenan-induced mechanical and thermal hyperalgesia.Using the whole-cel patch-clamp recording,bufalincaused remarkable suppressive effect on the peak currents of Na+channels in dorsal root ganglion neuroblastoma ND7-23 cel line in a U-shaped dependent manner.In addition,bufalinprompted the voltage-dependent activationand caused a negative shift of the fast-state inactivation of Na+channels.However,bufalin produced insignificant effect not onlyon voltage-dependent Kv4.2,Kv4.3 and BK channels,but also on the capsaicin induced Ca2+influx.CONCLUSION The present results indicate bufalin is capable of producing remarkable anti-nociceptive effects whichis probably ascribed to its specific modulation of voltage-gated Na+channels.

关键词： bufalin sodium channels formalin test carrageenan test patch clamp

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Blockade of paeoniflorin on sodium current in mouse hippocampal CA1 neurons

引用

Acta Pharmacologica Sinica 2003年第12期24卷 74-78页

作者： ZHANG Guang-Qin, HAO Xue-Mei, CHEN Shi-Zhong~1, ZHOU Pei-Ai, CHENG He-Ping, WU Cai-Hong~2 State Key Laboratory of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing 100871 ~1Department of Traditional Chinese Medicine, School of Pharmaceutical Science, Peking University, Beijing 100083, China College of Life Sciences Peking University State Key Laboratory of Biomembrane and Membrane Biotechnology 北京 100871 Department of Traditional Chinese Medicine School of Pharmaceutical Science Peking University 北京 100083

AIM: To study the blockade of paeoniflorin (Pae) on INain the acutely isolated hippocampus neurons of mice. METHODS: The whole-cell patch clamp technique was used. RESULTS: Pae inhibited INain frequency-dependent and concentration-dependent manners, with an IC50of 271μmol/L. Pae 0.3 mmol/L shifted the activation potential of the maximal INafrom -40 mV to -30 mV, shifted the steady-state activation and inactivation curves toward more positive and negative potentials by 10.8 mV, and 18.2 mV, respectively, and postponed the recovery of INainactivation state from (4.2±0.7) ms to (9.8±1.2) ms. CONCLUSION: Pae inhibited INain mouse hippocampus neurons.

关键词： hippocampus patch-clamp techniques paeoniflorin sodium channels

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Effect of hydrogen peroxide on persistent sodium current in guinea pig ventricular myocytes

引用

Acta Pharmacologica Sinica 2005年第7期26卷 828-834页

作者： Ji-hua MA~2 An-tao LUO Pei-hua ZHANG Cardio-Electrophysiological Research Laboratory,Medical College,Wuhan University of Science and Technology,Wuhan 430080,China Cardio-Electrophysiological Research Laboratory Medical College Wuhan University of Science and Technology Wuhan China

Aim:To study the effect of hydrogen peroxide(H202)on persistent sodium cur-rent(1Na.p)in guinea pig ventricular myocytes.Methods:The whole-cell,cell-attached,and inside-out patch-clamp techniques were applied on isolated ven-tricular myocytes from guinea pig.Results:H2O2(0.1 mmol/L,0.5 mmol/L and 1.0mmol/L)increased the amplitude of whole-cell INa.pin a concentration-dependentmanner,and glutathione(GSH 1 mmol/L)reversed the increased INa.p.H2O2(1mmol/L)increased persistent sodium channel activity in cell-attached and inside-out patches.The mean open probability was increased from control values of0.015±0.004 and 0.012±0.003 to 0.106±0.011 and 0.136e0.010,respectively(P<0.01 vs control).They were then decreased to 0.039±0.024 and 0.027±0.006,respectively,after the addition of 1 mmol/L GSH(P<0.01 vs H2O2).The time whenopen probability began to increase and reached a maximum was shorter in inside-out patches than that in cell-attached patches(4.8e 1.0 min vs 11.5+3.9 min,P<0.01;9.6±1.6 min vs 18.7±4.7 min,P<0.01).Conclusion:H2O2increased the INa.Pofguinea pig ventricular myocytes in a concentration-dependent manner,possiblyby directly oxidating the cell membrane.

关键词： hydrogen peroxide myocardium patch clamp techniques sodium channels

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Localization of molecular determinants in sensitivity of sodium channels to BmK I probing by surface plasmon resonance assay

Localization of molecular determinants in sensitivity of sod...

引用

中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Pin YE,Xing-Hua FENG,Hong-Tian YANG,Yong-Hua JI~* Lab of Neuropharmacology and Neurotoxicology,Shanghai University,Shanghai 200444,China

＜正＞Previously,domain IV S3/S4 linker was demonstrated to be an important region determing the sensitivity of sodium channels to BmK I,a sodium channel-specific site-3 modulator.But the localization of molecular determinants in sensitivity of sodium channels to BmK I remained unclear.In this study,through channel alignment,DIV/S3-S4 linker in BmK I-insensitive rNav1.8 was inserted by two amino acids（LE） compared with rNav1.5.By constructing channel mutants mimicing the rNav1.8 DIV S3/S4 region in rNav1.5 backbone,the sensitivity of rNav.15 mutants to BmK I was remarkably reduced.Furthermore,two peptides were synthesized according to the DIV/S3-S4 linker in rNav1.5（peptide P1） and rNav1.8（peptide P2）.The binding affinities of peptides to BmK I was investigated by surface Plasmon resonance（SPR）.The results showed that both P1 and P2 could bind with BmK I.But there were significantly differences in binding capability between these two peptides.The binding response（RU） of the peptide P2 was reduced to about 1/3 of the peptide P1.The association kinetics of P2 was also accelerated.It was presumed that the insensitivity of sodium channels to BmK I could be attributed to the alteration of microstructure of the receptor site by LE insertion.Thus,it may provide cludes for the diversity of spatial structure of receptor sites mapping for BmK I-sodium channel interaction.

关键词： sodium channels surface plasmon resonance BmK I

来源： cnki会议评论

在线全文

cnki会议

学校读者我要写书评

暂无评论

Puerarin blocks Na+ current in rat ventricular myocytes

引用

Acta Pharmacologica Sinica 2003年第12期24卷 38-42页

作者： ZHANG Guang-Qin, HAO Xue-Mei DAI De-Zai, FU Yu ZHOU Pei-Ai WU Cai-Hong Research Division of Pharmacology, China Pharmaceutical University, Nanjing 210009, China ~2National Laboratorv of Biomembrane and Membrane Biotechnology, College of Life Sciences, Peking University, Beijing 100871, China Research Division of Pharmacology China Pharmaceutical University Nanjing 210009 College of Life Sciences Peking University National Laboratory of Biomembrane and Membrane Biotechnology 北京 100871

AIM: To study the effect of puerarin （Pue） on Na+channel in rat ventricular myocytes. METHODS: Whole-cell patch-clamp technique was applied on isolated cardiomyocytes from rats. RESULTS: Pue inhibited cardiac INain a positive rate-dependent and dose-dependent manner, with an IC50of 349 μmol/L. The kinetics of blockage of cardiac sodium channel by Pue resembled the ClassIa/Ic of antiarrhythmic agents. Pue 300 μmol/L did not alter the shape of the I-V curve of INa, but markedly shifted the steady-state inactivation curve of INatowards more negative potential by 15.9 mV, and postponed the recovery of INainactivation state from （21.9±1.6） ms to （54.4±3.4） ms （Pchannels.

关键词： puerarin myocardium patch-clamp techniques sodium channels

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

Differential Inhibition of Nav1.7 and Neuropathic Pain by Hybridoma-Produced and Recombinant Monoclonal Antibodies that Target Nav1.7

引用

Neuroscience Bulletin 2018年第1期34卷 22-41页

作者： Sangsu Bang Jiho Yoo Xingrui Gong Di Liu Qingjian Han Xin Luo Wonseok Chang Gang Chen Sang-Taek Im Yong Ho Kim Judith A.Strong Ma-Zhong Zhang Jun-Ming Zhang Seok-Yong Lee Ru-Rong Ji Department of Anesthesiology Duke University Medical Center Department of Biochemistry Duke University Medical Center Pain Research Center Department of AnesthesiologyUniversity of Cincinnati Department of Anesthesiology Shanghai Children's Medical Center Department of Physiology and Biophysics College of Medicine Eulji University Department of Physiology College of Medicine Gachon University

Abstract The voltage-gated Na＋ channel subtype Nav1.7 is important for pain and itch in rodents and humans. We previously showed that a Nav1.7-targeting monoclonal antibody （SVmab） reduces Na＋ currents and pain and itch responses in mice. Here, we investigated whether recom- binant SVmab （rSVmab） binds to and blocks Nav1.7 similar to SVmab. ELISA tests revealed that SVmab was capable of binding to Nav1.7-expressing HEK293 cells, mouse DRG neurons, human nerve tissue, and the voltagesensor domain II of Nav1.7. In contrast, rSVmab showed no or weak binding to Nav1.7 in these tests. Patch-clamp recordings showed that SVmab, but not rSVmab, markedly inhibited Na＋ currents in Nav1.7-expressing HEK293 cells. Notably, electrical field stimulation increased the blocking activity of SVmab and rSVmab in Nav1.7- expressing HEK293 cells. SVmab was more effective than rSVmab in inhibiting paclitaxel-induced mechanical allodynia. SVmab also bound to human DRG neurons and inhibited their Na＋ currents. Finally, potential reasons for the differential efficacy of SVmab and rSVmab and future directions are discussed.

关键词： Primary afferent neuron Patch clamping （electrophysiology） sodium channels Animal models

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

Molecular evolution of Na^(+) channels in teleost fishes

引用

Integrative Zoology 2009年第1期4卷 64-74页

作者： Harold H.ZAKON Manda C.JOST Derrick J.ZWICKL Ying LU David M.HILLIS Section of Neurobiology Section of Integrative Biology The University of TexasAustinTXUSA

Voltage-dependent sodium channels are critical for electrical excitability.Invertebrates possess a single sodium channel gene;two rounds of genome duplication early in vertebrates increased the number to four.Since the teleost-tetrapod split,independent gene duplications in each lineage have further increased the number of sodium channel genes to 10 in tetrapods and 8 in teleosts.Here we review how the occurrence of multiple sodium channel paralogs has influenced the evolutionary history of three groups of fishes:pufferfish,gymnotiform and mor-myriform electric fish.Pufferfish(tetraodontidae)produce a neurotoxin,tetrodotoxin,that binds to and blocks the pore of sodium channels.Pufferfish evolved resistance to their own toxins by amino acid substitutions in the pore of their sodium channels.These substitutions had to occur in parallel across multiple paralogs for organismal re-sistance to evolve.Gymnotiform and mormyriform fishes independently evolved electric organs to generate elec-tricity for communication and object localization.Two sodium channel genes are expressed in muscle in most fishes.In both groups of weakly electric fishes,one gene lost its expression in muscle and became compartmen-talized in the evolutionary novel electric organ,which is a muscle derivative.This gene then evolved at elevated rates,whereas the gene that is still expressed in muscle does not show elevated rates of evolution.In the electric organ-expressing gene,amino acid substitutions occur in parts of the channel involved in determining how long the channel will be open or closed.The enhanced rate of sequence evolution of this gene likely underlies the spe-cies-level variations in the electric signal.

关键词： electric fish molecular evolution pufferfish sodium channels tetrodotoxin.

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Diabetes-induced changes in cardiac voltage-gated ion channels

引用

World Journal of Diabetes 2021年第1期12卷 1-18页

作者： Nihal Ozturk Serkan Uslu Semir Ozdemir Department of Biophysics Akdeniz University Faculty of MedicineAntalya 07058Turkey

Diabetes mellitus affects the heart through various mechanisms such as microvascular defects,metabolic abnormalities,autonomic dysfunction and incompatible immune response.Furthermore,it can also cause functional and structural changes in the myocardium by a disease known as diabetic cardiomyopathy(DCM)in the absence of coronary artery disease.As DCM progresses it causes electrical remodeling of the heart,left ventricular dysfunction and heart failure.Electrophysiological changes in the diabetic heart contribute significantly to the incidence of arrhythmias and sudden cardiac death in diabetes mellitus patients.In recent studies,significant changes in repolarizing K+currents,Na+currents and L-type Ca^(2+)currents along with impaired Ca^(2+ )homeostasis and defective contractile function have been identified in the diabetic heart.In addition,insulin levels and other trophic factors change significantly to maintain the ionic channel expression in diabetic patients.There are many diagnostic tools and management options for DCM,but it is difficult to detect its development and to effectively prevent its progress.In this review,diabetes-associated alterations in voltage-sensitive cardiac ion channels are comprehensively assessed to understand their potential role in the pathophysiology and pathogenesis of DCM.

关键词： Diabetes Action potential Cardiac ion channels L-type Ca^(2+)channels Potassium channels sodium channels

来源：

维普期刊数据库评论

在线全文

维普期刊数据库

学校读者我要写书评

暂无评论

Tetrahydroacridine inhibits voltage-dependent Na~+ current in guinea-pig ventricular myocytes

引用

Acta Pharmacologica Sinica 2004年第9期 36-42页

作者： Wei WANG, Yi-ping WANG, Guo-yuan HUState Key Laboratory of Drug Research, The First Department of Pharmacology, Shanghai Institute of Materia Medica, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 201203, China

AIM: To study the effects of tetrahydroacridine (tacrine) on voltage-gated Na+ channels in cardiac tissues. METHODS: Single ventricular myocytes were enzymatically dissociated from adult guinea-pig heart. Voltage-depe... 详细信息

关键词： Alzheimer disease cholinesterase inhibitors sodium channels tetrahydroacridine (tacrine) myocardium patch-clamp techniques

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：