Aim To study the effects of cyclovirobuxine D on inward rectifier K^- current(I_(k1) ) > transient outward K^+ current (I_(to)), L-type Ca^(2+) current (I_(Ca-L)), and actionpotential duration (APD) in isolated rat...Aim To study the effects of cyclovirobuxine D on inward rectifier K^- current(I_(k1) ) > transient outward K^+ current (I_(to)), L-type Ca^(2+) current (I_(Ca-L)), and actionpotential duration (APD) in isolated rat ventricular myocytes. Methods The whole cell patch-clamptechniques were used to study the changes of I_(k1), I_(to), I_(Ca-L) and APD in rat ventricularmyocytes. Results Cyclovirobuxine D (1-10 μmol·L^(-1)) significantly prolonged APD_(50) andAPD_(90) in isolated rat ventricular myocytes. Resting potential (RP) was decreased by 10μmol·L^(-1) of cyclovirobuxine D. Cyclovirobuxine D significantly decreased both inward andoutward components of I_(k1) . At - 100 mV, 1 and 10 μmol·L^(-1) of cyclovirobuxine D decreasedI_(k1), density from (-8.0+- 1.1) pA/pF to ( - 4.1 +- 0.7) pA/pF and ( - 3.4 +- 0.8) pA/pF,respectively, whereas at - 30 mV, I-(k1) density was decreased from (1.10 +-0.24) pA/pF to (0.61+-0.18) pA/pF and (0.36+- 0.11) pA/pF, respectively. 1_(to) was markedly inhibited bycyclovirobuxine D from the test potential of 0 mV to + 60 mV. At + 40 mV, 1 and 10μmol·L^(-1) ofcyclovirobuxine D decreased I_(to) density from (8.9+- 2.0) pA/pF to (5.5 +- 1.2) pA/pF and (4.9+-0.9) pA/pF, respectively. Cyclovirobuxine D inhibited I_(Ca-L) in a concentration-dependentmanner. At 10 mV, 1 and 10μmol·L^(-1) of cyclovirobuxine D decreased I_(Ca-L) density from ( - 9.9+- 1.8) pA/pF to ( - 6.4 +- 1.4) pA/pF and (-4.2+-0.6) pA/pF, respectively. ConclusionCyclovirobuxine D significantly prolonged APD and inhibited I_(k1), I_(to), and I_(Ca-L) in ratventricular myocytes. The inhibitory effects of cyclovirobuxine D on _(k1) and I_(to) are majormolecular mechanisms of APD prolongation in rat.展开更多
Using patch clamp whole cell recording techiques, we examined the effects ofIQ_23, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential (AP) andpotassium currents in single guinea p...Using patch clamp whole cell recording techiques, we examined the effects ofIQ_23, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential (AP) andpotassium currents in single guinea pig ventricular myocytes. The results showed that IQ_23 at 10, 30and 100 μmol ·L_-1 slowed the repolarization in AP dose-dependently. The APD_90 were prolonged by15%, 28% and 31% respectively. This effect did not depend on the extracellular Ca^2+. In voltageclamp mode, IQ_23 effectively blocked both the components of the delayed rectifier potassium current(I_k), i.e., I_ks and I_kr. At concentrations of 30 and 100 μmol· L^-1, IQ_23 suppressed I_ks by 21% and 26%and suppressed I_kr by 67% and 86% respectively. But even at 100 μmol·L^-1, IQ_23 had little effect onthe inward rectifier potassium current (I_k1). It is concluded: 1. IQ_23 can dose-dependently prolongAPD in the ventriculas myocytes of guinea pig, the effect does not depend on the extracellular Ca^2+; 2.IQ_23 blocks both I_ks and Ikr in the ventricular myocytes without obvious specificities between them.展开更多
The effects of 2-[p-(Dimethylamino)styryl] pyridine methiodide(DSPM)on slow response action potential(SRAP)and slow inward current(Isi) of guinea pig papillary muscles were studied by intracellular microelectrodes and...The effects of 2-[p-(Dimethylamino)styryl] pyridine methiodide(DSPM)on slow response action potential(SRAP)and slow inward current(Isi) of guinea pig papillary muscles were studied by intracellular microelectrodes and voltage clamp techniques.The APA and V_(max) of SRAP induced by high K ̄+were decreased after 50 min of perfusion with DSPM solu- tion. Isi was suppressed from a peak value of8.8± 1.6μA to 5.7± 1.8μA, The results indicated that DSPM has a selective blocking effect on calcium channel.展开更多
Non-injurious local stimuli, such as a cold shock, and injurious stimuli, such as local burning, punctures or chemicals, were applied to study electrical wave transmission in black pine (Pinus thunbergii) seedlings. T...Non-injurious local stimuli, such as a cold shock, and injurious stimuli, such as local burning, punctures or chemicals, were applied to study electrical wave transmission in black pine (Pinus thunbergii) seedlings. The results showed that non-injurious stimuli evoked the action potential (AP) transmission and injurious stimulation induced both AP transmission and the more complex variation (VP) transmission in the seedlings. The causes of these phenomena were discussed. Key words Black pine - Pinus thunbergii - Action potential (AP) - Variation potential (VP) - Electrical wave transmission CLC number S791.256 Document code A Foundation item: This paper was supported by the National Nature Science Foundation of China (grant No. 39670613).Biography: GUO Jian (1971-), male, lecturer in Haikou Bureau of Forestry. Hainan, P. R. China.Responsible editor: Song Funan展开更多
Using patch clamp whole cell recording techiques, we examined the effects ofIQ<sub>2</sub>3, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential (AP) andpotassium cur...Using patch clamp whole cell recording techiques, we examined the effects ofIQ<sub>2</sub>3, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential (AP) andpotassium currents in single guinea pig ventricular myocytes. The results showed that IQ<sub>2</sub>3 at 10, 30and 100 μmol ·L<sub>-</sub>1 slowed the repolarization in AP dose-dependently. The APD<sub>9</sub>0 were prolonged by15%, 28% and 31% respectively. This effect did not depend on the extracellular Ca<sup>2</sup>+. In voltageclamp mode, IQ<sub>2</sub>3 effectively blocked both the components of the delayed rectifier potassium current(I<sub>k</sub>), i.e., I<sub>k</sub>s and I<sub>k</sub>r. At concentrations of 30 and 100 μmol· L<sup>-</sup>1, IQ<sub>2</sub>3 suppressed I<sub>k</sub>s by 21% and 26%and suppressed I<sub>k</sub>r by 67% and 86% respectively. But even at 100 μmol·L<sup>-</sup>1, IQ<sub>2</sub>3 had little effect onthe inward rectifier potassium current (I<sub>k</sub>1). It is concluded: 1. IQ<sub>2</sub>3 can dose-dependently prolongAPD in the ventriculas myocytes of guinea pig, the effect does not depend on the extracellular Ca<sup>2</sup>+; 2.IQ<sub>2</sub>3 blocks both I<sub>k</sub>s and Ikr in the ventricular myocytes without obvious specificities between them.展开更多
Objectives To evaluate the association between a KCNQ 1 mutation, R259H, and short QT syndrome (SQTS) and to explore the elec- trophysiological mechanisms underlying their association. Methods We performed genetic s...Objectives To evaluate the association between a KCNQ 1 mutation, R259H, and short QT syndrome (SQTS) and to explore the elec- trophysiological mechanisms underlying their association. Methods We performed genetic screening of SQTS genes in 25 probands and their family members (63 patients). We used direct sequencing to screen the exons and intron-exon boundaries of candidate genes that en- code ion channels which contribute to the repolarization of the ventricular action potential, including KCNQI, KCNH2, KCNE1, KCNE2, KCNJ2, CACNAlc, CACNB2b and CACNA2D1. In one of the 25 SQTS probands screened, we discovered a KCNQ1 mutation, R259H. We cloned R259H and transiently expressed it in HEK-293 cells; then, currents were recorded using whole cell patch clamp techniques. Results R259H-KCNQ 1 showed significantly increased current density, which was approximately 3-fold larger than that of wild type (WT) after a depolarizing pulse at 1 s. The steady state voltage dependence of the activation and inactivation did not show significant differences between the WT and R259H mutation (P 〉 0.05), whereas the time constant of deactivation was markedly prolonged in the mutant compared with the WT in terms of the test potentials, which indicated that the deactivation of R259H was markedly slower than that of the WT. These results suggested that the R259H mutation can effectively increase the slowly activated delayed rectifier potassium current (Irs) in phase 3 of the cardiac action potential, which may be an infrequent cause of QT interval shortening. Conclusions R259H is a gain-of-function muta- tion of the KCNQ1 channel that is responsible for SQTS2. This is the first time that the R259H mutation was detected in Chinese people.展开更多
Action potentials generated in the sinoatrial node (SAN) dominate the rhythm and rate of a healthy human heart. Subsequently, these action potentials propagate to the whole heart via its conduction system. Abnormali...Action potentials generated in the sinoatrial node (SAN) dominate the rhythm and rate of a healthy human heart. Subsequently, these action potentials propagate to the whole heart via its conduction system. Abnormalities of impulse generation and/or propagation in a heart can cause arrhythmias. For example, SAN dysfunction or conduction block of the atrioventricular node can lead to serious bradycardia which is currently treated with an implanted electronic pacemaker. On the other hand, conduction damage may cause reentrant tachyarrhythmias which are primarily treated pharmacologically or by medical device-based therapies, including defibrillation and tissue ablation. However, drug therapies sometimes may not be effective or are associated with serious side effects. Device-based therapies for cardiac arrhythmias, even with well developed technology, still face inadequacies, limitations, hardware complications, and other challenges. Therefore, scientists are actively seeking other alternatives for antiarrhythmic therapy. In particular, cells and genes used for repairing cardiac conduction damage/defect have been investigated in various studies both in vitro and in vivo. Despite the complexities of the excitation and conduction systems of the heart, cell and gene-based strategies provide novel alternatives for treatment or cure of cardiac arrhythmias. This review summarizes some highlights of recent research progress in this field.展开更多
Brugada syndrome is a primary arrhythmia syndrome characterized by loss-of-function mutations in the SCN5A gene, which encodes for the cardiac Na^+ channel. In affected individuals, the risk of developing malignant v...Brugada syndrome is a primary arrhythmia syndrome characterized by loss-of-function mutations in the SCN5A gene, which encodes for the cardiac Na^+ channel. In affected individuals, the risk of developing malignant ventricular arrhythmias and sudden cardiac death are increased.展开更多
Objective To characterize early afterdepolarizations (EADs) caused triggered activity (TA) among calsequestrin-2 (CASQ2) knock-in (CASQ2 KI) mice and its relationship with aging. Methods Electrophysiological p...Objective To characterize early afterdepolarizations (EADs) caused triggered activity (TA) among calsequestrin-2 (CASQ2) knock-in (CASQ2 KI) mice and its relationship with aging. Methods Electrophysiological properties of ventricular myocytes from 3- month (mo, young), 9-mo (adult-l) and 12-too (adult-2) in wild-type (WT) and CASQ2 KI mice were investigated with patch-clamp technique. Results The incidences of EADs and TA in CASQ2 KI cardiomyocytes increased with increasing age. In contrast, WT mice cardiomyocytes showed no significant change in matched-age groups. Compared with that in 3-mo CASQ2 KI mice, the 50% repolarization of action potential (APD50) showed prolongation in both 9-mo and 12-mo ones (9.2±0.9 ms of 9-mo and 10.3 ± 1.2 ms of 12- mo vs. 5.6± 0.3 ms of 3-mo), while the 90 % repolarization of action potential (APD90) was similar among 3 age groups. Compared with 3-mo mice, the 9-mo and 12-mo CASQ2 KI mice showed markedly reduced transient outward potassium current (Ito) densities but increased L-type calcium current (ICa-L) densities. Conlcusion This study suggested that events of EADs and TA in CASQ2 KI mice increased with increasing age, It might be associated partly with the augment of cellular calcium concentration and the prolongation of APD50 induced by decrease of Ito and increase of ICa-L in adult CASQ2 KI mice展开更多
Gold nanoparticles(GNPs)have been extensively used in nanomedicine and neuroscience owing to their biological inertness,peculiar opto-electronic and physico-chemical features.However,the effect of GNPs shape on the ne...Gold nanoparticles(GNPs)have been extensively used in nanomedicine and neuroscience owing to their biological inertness,peculiar opto-electronic and physico-chemical features.However,the effect of GNPs shape on the neurophysiological properties of single neuron is still unclear.To tackle this issue,different shape GNPs(nanosphere,nanotriakisoctahedron and nanoflower)were synthesized to investigate the effect of GNPs on the voltage-dependent sodium channel and the action potential(AP)of hippocampal CA1 neurons in mice.The results indicated that GNPs inhibited the amplitudes of voltage-gated sodium current(I_(Na))and led to a hyperpolarizing shift in the voltage-dependence curve of both activation and inactivation of I_(Na).GNPs also increased neuronal excitability and altered some properties of AP.Moreover,most alterations in AP properties were observed in nanoflower GNPs treated CA1 neurons,suggesting that the neurotoxicity of gold nanoparticles is surface roughness-dependent.These results may provide a valuable direction in the clinical application of GNPs.展开更多
文摘Aim To study the effects of cyclovirobuxine D on inward rectifier K^- current(I_(k1) ) > transient outward K^+ current (I_(to)), L-type Ca^(2+) current (I_(Ca-L)), and actionpotential duration (APD) in isolated rat ventricular myocytes. Methods The whole cell patch-clamptechniques were used to study the changes of I_(k1), I_(to), I_(Ca-L) and APD in rat ventricularmyocytes. Results Cyclovirobuxine D (1-10 μmol·L^(-1)) significantly prolonged APD_(50) andAPD_(90) in isolated rat ventricular myocytes. Resting potential (RP) was decreased by 10μmol·L^(-1) of cyclovirobuxine D. Cyclovirobuxine D significantly decreased both inward andoutward components of I_(k1) . At - 100 mV, 1 and 10 μmol·L^(-1) of cyclovirobuxine D decreasedI_(k1), density from (-8.0+- 1.1) pA/pF to ( - 4.1 +- 0.7) pA/pF and ( - 3.4 +- 0.8) pA/pF,respectively, whereas at - 30 mV, I-(k1) density was decreased from (1.10 +-0.24) pA/pF to (0.61+-0.18) pA/pF and (0.36+- 0.11) pA/pF, respectively. 1_(to) was markedly inhibited bycyclovirobuxine D from the test potential of 0 mV to + 60 mV. At + 40 mV, 1 and 10μmol·L^(-1) ofcyclovirobuxine D decreased I_(to) density from (8.9+- 2.0) pA/pF to (5.5 +- 1.2) pA/pF and (4.9+-0.9) pA/pF, respectively. Cyclovirobuxine D inhibited I_(Ca-L) in a concentration-dependentmanner. At 10 mV, 1 and 10μmol·L^(-1) of cyclovirobuxine D decreased I_(Ca-L) density from ( - 9.9+- 1.8) pA/pF to ( - 6.4 +- 1.4) pA/pF and (-4.2+-0.6) pA/pF, respectively. ConclusionCyclovirobuxine D significantly prolonged APD and inhibited I_(k1), I_(to), and I_(Ca-L) in ratventricular myocytes. The inhibitory effects of cyclovirobuxine D on _(k1) and I_(to) are majormolecular mechanisms of APD prolongation in rat.
文摘Using patch clamp whole cell recording techiques, we examined the effects ofIQ_23, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential (AP) andpotassium currents in single guinea pig ventricular myocytes. The results showed that IQ_23 at 10, 30and 100 μmol ·L_-1 slowed the repolarization in AP dose-dependently. The APD_90 were prolonged by15%, 28% and 31% respectively. This effect did not depend on the extracellular Ca^2+. In voltageclamp mode, IQ_23 effectively blocked both the components of the delayed rectifier potassium current(I_k), i.e., I_ks and I_kr. At concentrations of 30 and 100 μmol· L^-1, IQ_23 suppressed I_ks by 21% and 26%and suppressed I_kr by 67% and 86% respectively. But even at 100 μmol·L^-1, IQ_23 had little effect onthe inward rectifier potassium current (I_k1). It is concluded: 1. IQ_23 can dose-dependently prolongAPD in the ventriculas myocytes of guinea pig, the effect does not depend on the extracellular Ca^2+; 2.IQ_23 blocks both I_ks and Ikr in the ventricular myocytes without obvious specificities between them.
文摘The effects of 2-[p-(Dimethylamino)styryl] pyridine methiodide(DSPM)on slow response action potential(SRAP)and slow inward current(Isi) of guinea pig papillary muscles were studied by intracellular microelectrodes and voltage clamp techniques.The APA and V_(max) of SRAP induced by high K ̄+were decreased after 50 min of perfusion with DSPM solu- tion. Isi was suppressed from a peak value of8.8± 1.6μA to 5.7± 1.8μA, The results indicated that DSPM has a selective blocking effect on calcium channel.
基金This paper was supported by the National Nature Science Foundation of China (grant No. 39670613).
文摘Non-injurious local stimuli, such as a cold shock, and injurious stimuli, such as local burning, punctures or chemicals, were applied to study electrical wave transmission in black pine (Pinus thunbergii) seedlings. The results showed that non-injurious stimuli evoked the action potential (AP) transmission and injurious stimulation induced both AP transmission and the more complex variation (VP) transmission in the seedlings. The causes of these phenomena were discussed. Key words Black pine - Pinus thunbergii - Action potential (AP) - Variation potential (VP) - Electrical wave transmission CLC number S791.256 Document code A Foundation item: This paper was supported by the National Nature Science Foundation of China (grant No. 39670613).Biography: GUO Jian (1971-), male, lecturer in Haikou Bureau of Forestry. Hainan, P. R. China.Responsible editor: Song Funan
文摘Using patch clamp whole cell recording techiques, we examined the effects ofIQ<sub>2</sub>3, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential (AP) andpotassium currents in single guinea pig ventricular myocytes. The results showed that IQ<sub>2</sub>3 at 10, 30and 100 μmol ·L<sub>-</sub>1 slowed the repolarization in AP dose-dependently. The APD<sub>9</sub>0 were prolonged by15%, 28% and 31% respectively. This effect did not depend on the extracellular Ca<sup>2</sup>+. In voltageclamp mode, IQ<sub>2</sub>3 effectively blocked both the components of the delayed rectifier potassium current(I<sub>k</sub>), i.e., I<sub>k</sub>s and I<sub>k</sub>r. At concentrations of 30 and 100 μmol· L<sup>-</sup>1, IQ<sub>2</sub>3 suppressed I<sub>k</sub>s by 21% and 26%and suppressed I<sub>k</sub>r by 67% and 86% respectively. But even at 100 μmol·L<sup>-</sup>1, IQ<sub>2</sub>3 had little effect onthe inward rectifier potassium current (I<sub>k</sub>1). It is concluded: 1. IQ<sub>2</sub>3 can dose-dependently prolongAPD in the ventriculas myocytes of guinea pig, the effect does not depend on the extracellular Ca<sup>2</sup>+; 2.IQ<sub>2</sub>3 blocks both I<sub>k</sub>s and Ikr in the ventricular myocytes without obvious specificities between them.
基金grants obtained from the National Natural Science Foundation of China (No.: 81170177, 81030002) and science and Technology De- partment of Gansu Province Project (145RJZ104).
文摘Objectives To evaluate the association between a KCNQ 1 mutation, R259H, and short QT syndrome (SQTS) and to explore the elec- trophysiological mechanisms underlying their association. Methods We performed genetic screening of SQTS genes in 25 probands and their family members (63 patients). We used direct sequencing to screen the exons and intron-exon boundaries of candidate genes that en- code ion channels which contribute to the repolarization of the ventricular action potential, including KCNQI, KCNH2, KCNE1, KCNE2, KCNJ2, CACNAlc, CACNB2b and CACNA2D1. In one of the 25 SQTS probands screened, we discovered a KCNQ1 mutation, R259H. We cloned R259H and transiently expressed it in HEK-293 cells; then, currents were recorded using whole cell patch clamp techniques. Results R259H-KCNQ 1 showed significantly increased current density, which was approximately 3-fold larger than that of wild type (WT) after a depolarizing pulse at 1 s. The steady state voltage dependence of the activation and inactivation did not show significant differences between the WT and R259H mutation (P 〉 0.05), whereas the time constant of deactivation was markedly prolonged in the mutant compared with the WT in terms of the test potentials, which indicated that the deactivation of R259H was markedly slower than that of the WT. These results suggested that the R259H mutation can effectively increase the slowly activated delayed rectifier potassium current (Irs) in phase 3 of the cardiac action potential, which may be an infrequent cause of QT interval shortening. Conclusions R259H is a gain-of-function muta- tion of the KCNQ1 channel that is responsible for SQTS2. This is the first time that the R259H mutation was detected in Chinese people.
文摘Action potentials generated in the sinoatrial node (SAN) dominate the rhythm and rate of a healthy human heart. Subsequently, these action potentials propagate to the whole heart via its conduction system. Abnormalities of impulse generation and/or propagation in a heart can cause arrhythmias. For example, SAN dysfunction or conduction block of the atrioventricular node can lead to serious bradycardia which is currently treated with an implanted electronic pacemaker. On the other hand, conduction damage may cause reentrant tachyarrhythmias which are primarily treated pharmacologically or by medical device-based therapies, including defibrillation and tissue ablation. However, drug therapies sometimes may not be effective or are associated with serious side effects. Device-based therapies for cardiac arrhythmias, even with well developed technology, still face inadequacies, limitations, hardware complications, and other challenges. Therefore, scientists are actively seeking other alternatives for antiarrhythmic therapy. In particular, cells and genes used for repairing cardiac conduction damage/defect have been investigated in various studies both in vitro and in vivo. Despite the complexities of the excitation and conduction systems of the heart, cell and gene-based strategies provide novel alternatives for treatment or cure of cardiac arrhythmias. This review summarizes some highlights of recent research progress in this field.
文摘Brugada syndrome is a primary arrhythmia syndrome characterized by loss-of-function mutations in the SCN5A gene, which encodes for the cardiac Na^+ channel. In affected individuals, the risk of developing malignant ventricular arrhythmias and sudden cardiac death are increased.
文摘Objective To characterize early afterdepolarizations (EADs) caused triggered activity (TA) among calsequestrin-2 (CASQ2) knock-in (CASQ2 KI) mice and its relationship with aging. Methods Electrophysiological properties of ventricular myocytes from 3- month (mo, young), 9-mo (adult-l) and 12-too (adult-2) in wild-type (WT) and CASQ2 KI mice were investigated with patch-clamp technique. Results The incidences of EADs and TA in CASQ2 KI cardiomyocytes increased with increasing age. In contrast, WT mice cardiomyocytes showed no significant change in matched-age groups. Compared with that in 3-mo CASQ2 KI mice, the 50% repolarization of action potential (APD50) showed prolongation in both 9-mo and 12-mo ones (9.2±0.9 ms of 9-mo and 10.3 ± 1.2 ms of 12- mo vs. 5.6± 0.3 ms of 3-mo), while the 90 % repolarization of action potential (APD90) was similar among 3 age groups. Compared with 3-mo mice, the 9-mo and 12-mo CASQ2 KI mice showed markedly reduced transient outward potassium current (Ito) densities but increased L-type calcium current (ICa-L) densities. Conlcusion This study suggested that events of EADs and TA in CASQ2 KI mice increased with increasing age, It might be associated partly with the augment of cellular calcium concentration and the prolongation of APD50 induced by decrease of Ito and increase of ICa-L in adult CASQ2 KI mice
基金Project(LY19C090004)supported by the Natural Science Foundation of Zhejiang Province,ChinaProjects(BK20200710,BK2018077)supported by the Natural Science Foundation of Jiangsu Province,China+1 种基金Project(NHKY-2019-19)supported by the Nanjing Polytechnic Institute Start Fund,ChinaProject(202012920026Y)supported by the Innovation and Entrepreneurship Training Program of Jiangsu Province College Students,China。
文摘Gold nanoparticles(GNPs)have been extensively used in nanomedicine and neuroscience owing to their biological inertness,peculiar opto-electronic and physico-chemical features.However,the effect of GNPs shape on the neurophysiological properties of single neuron is still unclear.To tackle this issue,different shape GNPs(nanosphere,nanotriakisoctahedron and nanoflower)were synthesized to investigate the effect of GNPs on the voltage-dependent sodium channel and the action potential(AP)of hippocampal CA1 neurons in mice.The results indicated that GNPs inhibited the amplitudes of voltage-gated sodium current(I_(Na))and led to a hyperpolarizing shift in the voltage-dependence curve of both activation and inactivation of I_(Na).GNPs also increased neuronal excitability and altered some properties of AP.Moreover,most alterations in AP properties were observed in nanoflower GNPs treated CA1 neurons,suggesting that the neurotoxicity of gold nanoparticles is surface roughness-dependent.These results may provide a valuable direction in the clinical application of GNPs.