检索结果-南通市图书馆

Cyproheptadine Regulates Pyramidal Neuron Excitability in Mouse Medial Prefrontal Cortex

Neuroscience Bulletin 2018年第5期34卷 759-768页

作者： yan-Lin He Kai Wang Qian-Ru Zhao yan-ai mei Institutes of Brain Science State Key Laboratory of Medical Neurobiology and School of Life Sciences Fudan University

Cyproheptadine （CPH）, a first-generation anti- histamine, enhances the delayed rectifier outward K＋ current （IK） in mouse cortical neurons through a sigma-1 receptor-mediated protein kinase A pathway. In this study, we aimed to determine the effects of CPH on neuronal excitability in current-clamped pyramidal neurons in mouse medial prefrontal cortex slices. CPH （10 μmol/L） significantly reduced the current density required to generate action potentials （APs） and increased the instan- taneous frequency evoked by a depolarizing current. CPH also depolarized the resting membrane potential （RMP）, decreased the delay time to elicit an AP, and reduced the spike threshold potential. This effect of CPH was mim- icked by a sigma-1 receptor agonist and eliminated by an antagonist. Application of tetraethylammonium （TEA） to block IK channels hyperpolarized the RMP and reduced the instantaneous frequency of APs. TEA eliminated the effects of CPH on AP frequency and delay time, but had no effect on spike threshold or RMP. The current-voltage relationship showed that CPH increased the membrane depolarization in response to positive current pulses and hyperpolarization in response to negative current pulses, suggesting that other types of membrane ion channels might also be affected by CPH. These results suggest that CPH increases the excitability of medial prefrontal cortex neurons by regulating TEA-sensitive IK channels as well as other TEA-insensitive K＋ channels, probably ID and inward-rectifier Kir channels. This effect of CPH may explain its apparent clinical efficacy as an antidepressant and antipsychotic.

关键词： Cyproheptadine Neuronal excitability Te-traethylammonium-sensitive Ik cortical neurons Sigma-1 receptor

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

Protein Kinase C Controls the Excitability of Cortical Pyramidal Neurons by Regulating Kv2.2 Channel Activity

引用

Neuroscience Bulletin 2022年第2期38卷 135-148页

作者： Zhaoyang Li Wenhao Dong Xinyuan Zhang Jun-mei Lu yan-ai mei Changlong Hu State Key Laboratory of Medical Neurobiology Institutes of Brain Science and School of Life SciencesFudan UniversityShanghai 200438China

The family of voltage-gated potassium Kv2 channels consists of the Kv2.1 and Kv2.2 ***2.1 is constitutively highly phosphorylated in neurons and its function relies on its phosphorylation *** the function of Kv2.2 is also dependent on its phosphorylation state remains ***,we investigated whether Kv2.2 channels can be phosphorylated by protein kinase C(PKC)and examined the effects of PKC-induced phosphorylation on their activity and *** of PKC inhibited Kv2.2 currents and altered their steadystate activation in HEK293 *** mutations and specific antibodies against phosphorylated S481 or S488 demonstrated the importance of these residues for the PKC-dependent modulation of *** layer Ⅱ pyramidal neurons in cortical slices,activation of PKC similarly regulated native Kv2.2 channels and simultaneously reduced the frequency of action *** conclusion,this study provides the first evidence to our knowledge that PKC-induced phosphorylation of the Kv2.2 channel controls the excitability of cortical pyramidal neurons.

关键词： Kv2.2 PKC Phosphorylation Pyramidal neurons Excitability

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

Protective effect of oat bran extracts on human dermal fibroblast injury induced by hydrogen peroxide

引用

Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2013年第2期14卷 97-105页

作者： Bing FENG Lai-ji MA Jin-jing YAO Yun FANG yan-ai mei Shao-min WEI School of Chemical and Material Engineering Jiangnan University R&D Center Shanghai Jahwa United Co.Ltd. Department of Physiology and Biophysics School of Life SciencesFudan University

Oat contains different components that possess antioxidant properties; no study to date has addressed the antioxidant effect of the extract of oat bran on the cellular level. Therefore, the present study focuses on the investi- gation of the protective effect of oat bran extract by enzymatic hydrolysates on human dermal fibroblast injury induced by hydrogen peroxide （H2O2）. Kjeldahl determination, phenol-sulfuric acid method, and high-performance liquid chromatography （HPLC） analysis indicated that the enzymatic products of oat bran contain a protein amount of 71.93%, of which 97.43% are peptides with a molecular range from 438.56 to 1301.01 Da. Assays for 1,1-diphenyl-2-picrylhydrazyl （DPPH） radical scavenging activity indicate that oat peptide-dch extract has a direct and concentration-dependent antioxidant activity. 3-（4,5-Dimethylthiazol-2-yl）-2,5-diphenyl tetrazolium bromide （MTT） colorimetric assay and the TdT-mediated digoxigenin-dUTP nick-end labeling （TUNEL） assay for apoptosis showed that administration of H2O2 in human dermal fibroblasts caused cell damage and apoptosis. Pre-incubation of human dermal fibroblasts with the Oatp for 24 h markedly inhibited human dermal fibroblast injury induced by H2O2, but ap- plication oat peptides with H2O2 at same time did not. Pre-treatment of human dermal fibroblasts with Oatp significantly reversed the H2O2-induced decrease of superoxide dismutase （SOD） and the inhibition of malondialdehyde （MDA）. The results demonstrate that oat peptides possess antioxidant activity and are effective against H2O2-induced human dermal fibroblast injury by the enhanced activity of SOD and decrease in MDA level. Our results suggest that oat bran will have the potential to be further explored as an antioxidant functional food in the prevention of aging-related skin injury.

关键词： Oat bran Extraction Antioxidant Human dermal fibroblasts Cell injury

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

Melatonin protected against extremely low-frequency electromagnetic fields-induced Na+ currents increase in rat cerebellar granule cells through intracellular Ca2+ release

Melatonin protected against extremely low-frequency electrom...

引用

中国神经科学学会第十届全国学术会议

作者： Dong-Dong LIU yan-ai mei Institutes of Brain Science School of Life Sciences and State Key Laboratory of Medical NeurobiologyFudan University

Although melatonin(MEL) has been reported being able to protect cells against oxidative damage induced by electromagnetic radiation,few reports have addressed whether there are other protective ***,we investigated the effects of MEL on ELF-EMF-induced *** in rat cerebellar granule cells(GCs).Our results reveal that exposing cerebellar GCs to ELF-EMF for 60 min significantly increased ***(J by 62.5%,MEL(5 μM) could protect GCs against ELF-EMF-induced Na currents *** inhibitory effect of MEL is mimicked by IIK-7,the agonist of MT2 receptor,and eliminated by 4P-PDOT(10 μM),an antagonist of MT2 *** Na channel steady-state activation curve was significantly shifted(by 5.5 mV) towards hyperpolarization by ELF-EMF stimulation,but MEL did not modified the Na channel steady-state activation property in control group or GCs following ELF-EMF *** GCs to ELF-EMF significantly enhanced the intracellular phosphorylated PKA levels by 21.5%,bother of MEL and IIK-7 did not reduce ELF-EMF-induced increase in phosphorylated *** contrary,bother of MEL or IIK-7 itself was able to increase phosphorylated PKA levels in cerebellar *** inhibitory effects of MEL on ELF-EMF-induced Nav activity was abolished after application of U-73122(5 μM),the phospholipase C(PLC) blockers and was greatly reduced by the calmodulin inhibitors *** imaging showed that MEL could increase the elevation of intracellular calcium evoked by high concentration potassium chloride(HK)both the cell exposed to EMF or *** the MEL-induced intracellular Ca increase was reduced by ryanodine-sensitive receptors’ blocker,ruthenium *** data show for the first time that MEL protected against neuronal I enhanced by ELF-EMF exposure through the intracellular Ca,which probably occurred through the MT2receptor/PLC pathway.

关键词： melatonin extremely low-frequency electromagnetic fields Na+ currents MT2 receptors intracellular Ca2+ rat cerebellar granule cells

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

GDF-15 regulates Kv2.1-mediated outward K+ current on cerebellar granule neurons through the Akt/mTOR pathway

GDF-15 regulates Kv2.1-mediated outward K+ current on cerebe...

引用

中国神经科学学会第十届全国学术会议

作者： Chang-Ying WANG An-Qi HUANG yan-ai mei State Key Laboratory of Medical Neurobiology School of Life Sciences and Institutes of Brain ScienceFudan University

GDF-15,known as a novel member of die transforming growth factor-p(TGF-p) superfamily,can supply critical roles in the central and peripheral nervous system,but the signal transduction and receptor subtypes involved are not well ***,we report that GDF-15 specifically increases the delay rectified outward K currents(I) in rat cerebellar granule neurons(CGNs) in a time and concentration dependent ***-15-induced amplification of I is mediated by increasing the expression and reduced lysosome-dependent degradation of Kv2.1 protein,the mainα-subunit of *** of CGNs to GDF-15 markedly induces phosphorylation of ERK,Akt and mTOR,but GDF-15-induced I densities and increased expression of Kv2.1 are only attenuated by Akt or mTOR inhibitors,not by ERK *** blockade of Src mediated phosphorylation of TβRH abrogates the effect of GDF-15 on I amplification and Kv2.1 induction,rather than the TpRI *** assays showed GDF-15increased phosphorylation of Tyr on TβRII in CGN *** data reveal,for the first time,effect of GDF-15 on Kv2.1 expression might channeled through TpRII to activate Src kinase and Akt/mTOR pathway,an unanticipated role of non-Smad-dependent pathway in previously unrecognized GDF-15-mediated signaling.

关键词： Keywards:GDF-15 Akt/mTOR IK Kv2.1 CGNs

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

确定总应变寿命方程中指数的一种方法

引用

航空动力学报 2017年第1期32卷 105-113页

作者：刘香王延荣田爱梅北京航空航天大学能源与动力工程学院北京100191 先进航空发动机协同创新中心北京100191 北京航空航天大学宇航学院北京100191

在由材料的单调拉伸强度极限和断面收缩率确定总应变寿命方程中疲劳强度系数和疲劳延性系数的基础上,考查了利用材料在两个不同应力幅下的疲劳试验数据和单调拉伸延伸率来确定总应变寿命方程中疲劳强度指数和疲劳延性指数的一种方法,给... 详细信息

在由材料的单调拉伸强度极限和断面收缩率确定总应变寿命方程中疲劳强度系数和疲劳延性系数的基础上,考查了利用材料在两个不同应力幅下的疲劳试验数据和单调拉伸延伸率来确定总应变寿命方程中疲劳强度指数和疲劳延性指数的一种方法,给出了只需较少的疲劳试验数据和单调拉伸力学性能参数即可确定材料的总应变寿命方程中全部4个参数的分析流程,并利用航空发动机中常用的钛合金和镍基合金材料的疲劳试验数据对该方法进行了验证,结果表明该方法所确定的总应变寿命方程对所考查的材料大多数情形的疲劳寿命预测结果较为理想,基本在3倍分散带以内.

关键词：总应变寿命方程疲劳强度系数疲劳延性系数疲劳强度指数疲劳延性指数寿命预测

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

Overexpression of sigma-1 receptor inhibits ADAM10 and ADAM17 mediated shedding in vitro

引用

Protein & Cell 2012年第2期3卷 400-400页

作者： Juan Li Bin Liu Xiaofei Gao Zhixing Ma Tianyi CaoSong yan-ai mei Yufang Zheng School of Life Sciences Fudan UniversityShanghai 200433China

Erratum to:Protein Cell 2012,3(2):153-159 DOI 10.1007/s13238-012-2006-9 Two mistakes in Fig.3A and 4A,respectively,were made due to typesetting *** 3A,on the left column of page 156,should be cor-rected as *** 4A,on t... 详细信息

关键词： Figure cor ADAM10

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

Neuritin enhances synaptic transmission in medial prefrontal cortex in mice by increasing Cav3.3 surface expression

Neuritin enhances synaptic transmission in medial prefrontal...

引用

中国神经科学学会第十二届全国学术会议

作者： Jun-mei Lu Dong-Dong Liu Zhao-yang Li Chen Ling yan-ai mei Institutes of Brain Science State Key Laboratory of Medical Neurobiology and School of Life Sciences Fudan University

Neuritin is a neurotrophic factor involved in neural development and synaptic plasticity. However, its role in modulating synaptic transmission remains unclear. Here, we investigated the effects of neuritin on miniature excitatory post-synaptic currents（m EPSCs） and glutamate release in the medial prefrontal cortex（mPFC） in mice. Incubation of mPFC slices with neuritin for 45 min significantly increased m EPSC frequency and glutamate release as measured by HPLC, which was mimicked by insulin and abrogated by an insulin receptor inhibitor. Neuritin-induced up-regulation of synaptic transmission was correlated with activation of ERK, and inhibition of MEK/ERK activity attenuated the neuritin-induced increase in m EPSC frequency and glutamate release. T-type calcium channel inhibitors but not the L-type inhibitor abolished the inward calcium current and the effects of neuritin on m EPSC frequency and glutamate release. Western blotting of membrane proteins showed that neuritin promoted surface expression of Cav3.3 α-subunit, which was also eliminated by inhibition of insulin receptor or MEK/ERK activity. The effects of neuritin on m EPSC frequency, glutamate release, and Cav3.3 α-subunit expression were inhibited by an intracellular protein transport inhibitor. These results confirm involvement of the insulinreceptor and ERK signaling pathway, and provide novel insights into the mechanisms ofneuritin function in synaptic transmission.

关键词： Cav3.3 mEPSCs neuritin prefrontal cortex transmitter release

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

考虑尺寸效应的缺口疲劳寿命预测方法

引用

航空动力学报 2017年第2期32卷 429-437页

作者：刘香王延荣田爱梅石亮北京航空航天大学能源与动力工程学院北京100191 先进航空发动机协同创新中心北京100191 北京航空航天大学宇航学院北京100191

利用试样缺口根部归一化应力的分布规律,在考虑应力梯度的缺口疲劳寿命预测方法的基础上,着重考虑尺寸效应对缺口疲劳寿命的影响,构建了综合考虑平均应力、应力梯度和尺寸效应的缺口疲劳寿命预测方法.利用已有的TC4合金缺口疲劳试验数... 详细信息

利用试样缺口根部归一化应力的分布规律,在考虑应力梯度的缺口疲劳寿命预测方法的基础上,着重考虑尺寸效应对缺口疲劳寿命的影响,构建了综合考虑平均应力、应力梯度和尺寸效应的缺口疲劳寿命预测方法.利用已有的TC4合金缺口疲劳试验数据对所发展的方法进行了验证,并与常用的几种局部应力应变法的寿命预测结果进行了对比分析.结果表明:所对比的几种局部应力应变法的寿命预测结果过于保守,而所发展的缺口疲劳寿命预测方法的预测结果几乎全在3倍分散带以内,且大多数预测结果在2倍分散带以内.

关键词：缺口疲劳平均应力应力梯度尺寸效应局部应力应变法寿命预测

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

The calcineurin-NFATc4 pathway is critical for neuritin to promote Kv4.2 transcription

The calcineurin-NFATc4 pathway is critical for neuritin to p...

引用

中国神经科学学会第十届全国学术会议

作者： Jin-Jing YAO Xiao-Qin ZHAN Qian-Ru ZHAO yan-ai mei Institutes of Brain Science School of Life Sciences and State Key Laboratory of Medical NeurobiologyFudan University

Objective Neuritin is a new neurotrophic factor discovered in a screen to identify genes involved in activity-dependent synaptic *** also plays multiple roles in the process of neural development and synaptic *** previous work had reported that Neuritin increases Kv4.2-mediated I in rat cerebellar granule neurons by activating insulin receptor pathway and up-regulated the transcription and translation of ***,the mechanisms how Neuritin could promote Kv4.2 transcription is still not ***,we try to fig out whether the calcineurin-NFATc4 pathway is involved in the function of *** By using specific chemical inhibitors against Calcineurin,Cyclosporin A(CsA) and FK520,to block Calcineurin-NFATc4 pathway to find out whether it could offset the increase of Kv4.2 expression and I density caused by *** using NFATc4 mice,we found whether this transcription factor is important for Neuritin to regulate Kv4.2 ***,we isolated Kv4.2promoter and cloned it into the pGL3-Enhancer Vector to study whether Neuritin could increase the activation of ***(1)Calcineurin inhibitors could block Neuritin’s function on up-regulating Kv4.2 expression(CsA:from 45.5±5.7%to 5.1±3.2%;FK520:from 45.5±5.7%to 10.7±4.1%) and I density(CsA:from 53.8±6.7%to7.1±3.9%;FK520:from 53.8±6.7%to 16.9±5.3%).(2) In NFATC4" mice’s cerebellar granule cells Neuritin could not increase Kv4.2 expression and I *** incubating with Neuritin,Kv4.2 expression was increased 3.01+1.8%,I density was increased 5.89+3.1%,there is no significant difference compared with control group.(3) The Kv4.2promoter sequence has been *** The Calcineurin-NFATc4 pathway is critical for Neuritin to promote Kv4.2 *** are trying to find out the mechanism under this modulation.

关键词： calcineurin-NFATc4 pathway neuritin Kv4.2 IA cerebellar granule cells

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

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：