Frontiers in Synaptic Neuroscience最新文献

筛选
英文 中文
Healthy cardiac myocytes can decrease sympathetic hyperexcitability in the early stages of hypertension. 健康的心肌细胞可以降低高血压早期的交感神经兴奋性。
IF 2.8 4区 医学
Frontiers in Synaptic Neuroscience Pub Date : 2022-08-04 eCollection Date: 2022-01-01 DOI: 10.3389/fnsyn.2022.949150
Harvey Davis, Kun Liu, Ni Li, Dan Li, David J Paterson
{"title":"Healthy cardiac myocytes can decrease sympathetic hyperexcitability in the early stages of hypertension.","authors":"Harvey Davis, Kun Liu, Ni Li, Dan Li, David J Paterson","doi":"10.3389/fnsyn.2022.949150","DOIUrl":"10.3389/fnsyn.2022.949150","url":null,"abstract":"<p><p>Sympathetic neurons are powerful drivers of cardiac excitability. In the early stages of hypertension, sympathetic hyperactivity is underpinned by down regulation of M current and increased activity of Cav<sub>2.2</sub> that is associated with greater intracellular calcium transients and enhanced neurotransmission. Emerging evidence suggests that retrograde signaling from the myocyte itself can modulate synaptic plasticity. Here we tested the hypothesis that cross culturing healthy myocytes onto diseased stellate neurons could influence sympathetic excitability. We employed neuronal mono-cultures, co-cultures of neonatal ventricular myocytes and sympathetic stellate neurons, and mono-cultures of sympathetic neurons with media conditioned by myocytes from normal (Wistar) and pre-hypertensive (SHR) rats, which have heightened sympathetic responsiveness. Neuronal firing properties were measured by current-clamp as a proxy for neuronal excitability. SHR neurons had a maximum higher firing rate, and reduced rheobase compared to Wistar neurons. There was no difference in firing rate or other biophysical properties in Wistar neurons when they were co-cultured with healthy myocytes. However, the firing rate decreased, phenocopying the Wistar response when either healthy myocytes or media in which healthy myocytes were grown was cross-cultured with SHR neurons. This supports the idea of a paracrine signaling pathway from the healthy myocyte to the diseased neuron, which can act as a modulator of sympathetic excitability.</p>","PeriodicalId":12650,"journal":{"name":"Frontiers in Synaptic Neuroscience","volume":"14 ","pages":"949150"},"PeriodicalIF":2.8,"publicationDate":"2022-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9386373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9163176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
rTg(TauP301L)4510 mice exhibit increased VGlut1 in hippocampal presynaptic glutamatergic vesicles and increased extracellular glutamate release. rTg(TauP301L)4510小鼠在海马突触前谷氨酸能小泡中表现出VGlut1增加和细胞外谷氨酸释放增加。
IF 3.7 4区 医学
Frontiers in Synaptic Neuroscience Pub Date : 2022-08-03 eCollection Date: 2022-01-01 DOI: 10.3389/fnsyn.2022.925546
Erika Taipala, Jeremiah C Pfitzer, Morgan Hellums, Miranda N Reed, Michael W Gramlich
{"title":"rTg(Tau<sub>P301L</sub>)4510 mice exhibit increased VGlut1 in hippocampal presynaptic glutamatergic vesicles and increased extracellular glutamate release.","authors":"Erika Taipala,&nbsp;Jeremiah C Pfitzer,&nbsp;Morgan Hellums,&nbsp;Miranda N Reed,&nbsp;Michael W Gramlich","doi":"10.3389/fnsyn.2022.925546","DOIUrl":"https://doi.org/10.3389/fnsyn.2022.925546","url":null,"abstract":"<p><p>The molecular pathways that contribute to the onset of symptoms in tauopathy models, including Alzheimer's disease (AD), are difficult to distinguish because multiple changes can happen simultaneously at different stages of disease progression. Understanding early synaptic alterations and their supporting molecular pathways is essential to develop better pharmacological targets to treat AD. Here, we focus on an early onset rTg(Tau<sub>P301<i>L</i></sub> )4510 tauopathy mouse model that exhibits hyperexcitability in hippocampal neurons of adult mice that is correlated with presynaptic changes and increased extracellular glutamate levels. However, it is not clear if increased extracellular glutamate is caused by presynaptic changes alone, or if presynaptic changes are a contributing factor among other factors. To determine whether pathogenic tau alters presynaptic function and glutamate release, we studied cultured hippocampal neurons at 14-18 days <i>in vitro</i> (DIV) from animals of both sexes to measure presynaptic changes in tau<sub>P301L</sub> positive mice. We observed that presynaptic vesicles exhibit increased vesicular glutamate transporter 1 (VGlut1) using immunohistochemistry of fixed cells and an established pH-sensitive green fluorescent protein approach. We show that tau<sub>P301L</sub> positive neurons exhibit a 40% increase in VGlut1 per vesicle compared to tau<sub>P301L</sub> negative littermates. Further, we use the extracellular glutamate reporter iGluSnFR to show that increased VGlut1 per vesicle directly translates into a 40% increase in extracellular glutamate. Together, these results show that increased extracellular glutamate levels observed in tau<sub>P301L</sub> mice are not caused by increased vesicle exocytosis probability but rather are directly related to increased VGlut1 transporters per synaptic vesicle.</p>","PeriodicalId":12650,"journal":{"name":"Frontiers in Synaptic Neuroscience","volume":" ","pages":"925546"},"PeriodicalIF":3.7,"publicationDate":"2022-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9383415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40713294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Glucagon-like peptide 1 and glucose-dependent insulinotropic peptide hormones and novel receptor agonists protect synapses in Alzheimer's and Parkinson's diseases. 胰高血糖素样肽1和葡萄糖依赖性胰岛素肽激素和新型受体激动剂保护阿尔茨海默病和帕金森病的突触。
IF 3.7 4区 医学
Frontiers in Synaptic Neuroscience Pub Date : 2022-07-27 eCollection Date: 2022-01-01 DOI: 10.3389/fnsyn.2022.955258
Christian Hölscher
{"title":"Glucagon-like peptide 1 and glucose-dependent insulinotropic peptide hormones and novel receptor agonists protect synapses in Alzheimer's and Parkinson's diseases.","authors":"Christian Hölscher","doi":"10.3389/fnsyn.2022.955258","DOIUrl":"https://doi.org/10.3389/fnsyn.2022.955258","url":null,"abstract":"<p><p>Glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) are peptide hormones and growth factors. A major pathological feature of both Alzheimer's dis-ease (AD) and Parkinson's disease (PD) is the loss of synaptic transmission in the cortex in AD and the loss of dopaminergic synapses in the nigra-striatal dopaminergic projection. Several studies demonstrate that GLP-1 and GIP receptor agonists protect synapses and synaptic transmission from the toxic events that underlie AD and PD. In a range of AD animal models, treatment with GLP-1, GIP, or dual-GLP-1/GIP receptor agonists effectively protected cognition, synaptic trans-mission, long-term potentiation (LTP), and prevented the loss of synapses and neurons. In PD models, dopaminergic production resumed and synapses became functional again. Importantly, the GLP-1 receptor agonists exendin-4 and liraglutide have shown good protective effects in clinical trials in AD and PD patients. Studies show that growth factors and peptide drugs that can cross the blood-brain barrier (BBB) better are more potent than those that do not cross the BBB. We therefore developed dual-GLP-1/GIP receptor agonists that can cross the BBB at an enhanced rate and showed superior protective properties on synapses in animal models of AD and PD.</p>","PeriodicalId":12650,"journal":{"name":"Frontiers in Synaptic Neuroscience","volume":" ","pages":"955258"},"PeriodicalIF":3.7,"publicationDate":"2022-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9363704/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40696435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 5
Editorial: Regulation of AMPA Receptors, From the Genetic to the Functional Level. 编辑:AMPA受体的调控,从遗传到功能水平。
IF 3.7 4区 医学
Frontiers in Synaptic Neuroscience Pub Date : 2022-07-12 eCollection Date: 2022-01-01 DOI: 10.3389/fnsyn.2022.952564
Alberto Ouro, Tak Pan Wong, Laura Jiménez-Sánchez
{"title":"Editorial: Regulation of AMPA Receptors, From the Genetic to the Functional Level.","authors":"Alberto Ouro,&nbsp;Tak Pan Wong,&nbsp;Laura Jiménez-Sánchez","doi":"10.3389/fnsyn.2022.952564","DOIUrl":"https://doi.org/10.3389/fnsyn.2022.952564","url":null,"abstract":"the central and peripheral systems. They are in postsynaptic cells, but can also be found in pre-synaptic sites and glia processes. glutamate the postsynaptic AMPARs mediate the fast excitatory synaptic transmission which can be changed in an activity dependent manner and involve a minority of Ca 2 + permeable AMPARs. This Research Topic describes several new mechanisms that regulate AMPAR trafficking and plasticity;","PeriodicalId":12650,"journal":{"name":"Frontiers in Synaptic Neuroscience","volume":" ","pages":"952564"},"PeriodicalIF":3.7,"publicationDate":"2022-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9319205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40556119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Corrigendum: Editorial: Activated Synapses. 更正:编辑:激活突触。
IF 3.7 4区 医学
Frontiers in Synaptic Neuroscience Pub Date : 2022-06-23 eCollection Date: 2022-01-01 DOI: 10.3389/fnsyn.2022.932503
F Javier Rubio, Emmanuel Valjent, Bruce T Hope
{"title":"Corrigendum: Editorial: Activated Synapses.","authors":"F Javier Rubio,&nbsp;Emmanuel Valjent,&nbsp;Bruce T Hope","doi":"10.3389/fnsyn.2022.932503","DOIUrl":"https://doi.org/10.3389/fnsyn.2022.932503","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fnsyn.2022.875904.].</p>","PeriodicalId":12650,"journal":{"name":"Frontiers in Synaptic Neuroscience","volume":" ","pages":"932503"},"PeriodicalIF":3.7,"publicationDate":"2022-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9260674/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40580741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Astrocyte: A Foe or a Friend in Intellectual Disability-Related Diseases. 星形胶质细胞:智力残疾相关疾病的敌人还是朋友。
IF 3.7 4区 医学
Frontiers in Synaptic Neuroscience Pub Date : 2022-06-23 eCollection Date: 2022-01-01 DOI: 10.3389/fnsyn.2022.877928
Busong Wang, Lu Zou, Min Li, Liang Zhou
{"title":"Astrocyte: A Foe or a Friend in Intellectual Disability-Related Diseases.","authors":"Busong Wang,&nbsp;Lu Zou,&nbsp;Min Li,&nbsp;Liang Zhou","doi":"10.3389/fnsyn.2022.877928","DOIUrl":"https://doi.org/10.3389/fnsyn.2022.877928","url":null,"abstract":"<p><p>Intellectual disabilities are a type of neurodevelopmental disease caused by neurological dysfunction. Their incidence is largely associated with neural development. Astrocytes are the most widely distributed cells in the mammalian brain. Previous studies have reported that astrocytes only supported and separated the neurons in the brain. However, recent studies have found that they also play an important role in neural development. Understanding the astrocyte mechanism in intellectual development disorder-related diseases will help provide new therapeutic targets for the treatment of intellectual disability-related diseases. This mini-review introduced the association between astrocyte and intellectual disabilities. Furthermore, recent advances in genetic and environmental factors causing intellectual disability and different pharmaceutical effects of intellectual disability-related drugs on astrocytes have been summarised. Finally, we discussed future perspectives of astrocyte-based therapy for intellectual disability.</p>","PeriodicalId":12650,"journal":{"name":"Frontiers in Synaptic Neuroscience","volume":" ","pages":"877928"},"PeriodicalIF":3.7,"publicationDate":"2022-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9259964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40603771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Regulation of Inhibitory Signaling at the Receptor and Cellular Level; Advances in Our Understanding of GABAergic Neurotransmission and the Mechanisms by Which It Is Disrupted in Epilepsy. 抑制信号在受体和细胞水平上的调控gaba能神经传递及其在癫痫中的破坏机制的研究进展。
IF 3.7 4区 医学
Frontiers in Synaptic Neuroscience Pub Date : 2022-06-15 eCollection Date: 2022-01-01 DOI: 10.3389/fnsyn.2022.914374
Allison E Tipton, Shelley J Russek
{"title":"Regulation of Inhibitory Signaling at the Receptor and Cellular Level; Advances in Our Understanding of GABAergic Neurotransmission and the Mechanisms by Which It Is Disrupted in Epilepsy.","authors":"Allison E Tipton,&nbsp;Shelley J Russek","doi":"10.3389/fnsyn.2022.914374","DOIUrl":"https://doi.org/10.3389/fnsyn.2022.914374","url":null,"abstract":"<p><p>Inhibitory signaling in the brain organizes the neural circuits that orchestrate how living creatures interact with the world around them and how they build representations of objects and ideas. Without tight control at multiple points of cellular engagement, the brain's inhibitory systems would run down and the ability to extract meaningful information from excitatory events would be lost leaving behind a system vulnerable to seizures and to cognitive decline. In this review, we will cover many of the salient features that have emerged regarding the dynamic regulation of inhibitory signaling seen through the lens of cell biology with an emphasis on the major building blocks, the ligand-gated ion channel receptors that are the first transduction point when the neurotransmitter GABA is released into the synapse. Epilepsy association will be used to indicate importance of key proteins and their pathways to brain function and to introduce novel areas for therapeutic intervention.</p>","PeriodicalId":12650,"journal":{"name":"Frontiers in Synaptic Neuroscience","volume":" ","pages":"914374"},"PeriodicalIF":3.7,"publicationDate":"2022-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9302637/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40645333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Microphysiological Modeling of the Structure and Function of Neuromuscular Transmitter Release Sites. 神经肌肉递质释放位点结构和功能的微生理建模。
IF 3.7 4区 医学
Frontiers in Synaptic Neuroscience Pub Date : 2022-06-13 eCollection Date: 2022-01-01 DOI: 10.3389/fnsyn.2022.917285
Rozita Laghaei, Stephen D Meriney
{"title":"Microphysiological Modeling of the Structure and Function of Neuromuscular Transmitter Release Sites.","authors":"Rozita Laghaei,&nbsp;Stephen D Meriney","doi":"10.3389/fnsyn.2022.917285","DOIUrl":"https://doi.org/10.3389/fnsyn.2022.917285","url":null,"abstract":"<p><p>The general mechanism of calcium-triggered chemical transmitter release from neuronal synapses has been intensely studied, is well-known, and highly conserved between species and synapses across the nervous system. However, the structural and functional details within each transmitter release site (or active zone) are difficult to study in living tissue using current experimental approaches owing to the small spatial compartment within the synapse where exocytosis occurs with a very rapid time course. Therefore, computer simulations offer the opportunity to explore these microphysiological environments of the synapse at nanometer spatial scales and on a sub-microsecond timescale. Because biological reactions and physiological processes at synapses occur under conditions where stochastic behavior is dominant, simulation approaches must be driven by such stochastic processes. MCell provides a powerful simulation approach that employs particle-based stochastic simulation tools to study presynaptic processes in realistic and complex (3D) geometries using optimized Monte Carlo algorithms to track finite numbers of molecules as they diffuse and interact in a complex cellular space with other molecules in solution and on surfaces (representing membranes, channels and binding sites). In this review we discuss MCell-based spatially realistic models of the mammalian and frog neuromuscular active zones that were developed to study presynaptic mechanisms that control transmitter release. In particular, these models focus on the role of presynaptic voltage-gated calcium channels, calcium sensors that control the probability of synaptic vesicle fusion, and the effects of action potential waveform shape on presynaptic calcium entry. With the development of these models, they can now be used in the future to predict disease-induced changes to the active zone, and the effects of candidate therapeutic approaches.</p>","PeriodicalId":12650,"journal":{"name":"Frontiers in Synaptic Neuroscience","volume":" ","pages":"917285"},"PeriodicalIF":3.7,"publicationDate":"2022-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9236679/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40405537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Editorial: Perineuronal Nets as Therapeutic Targets for the Treatment of Neuropsychiatric Disorders. 社论:神经神经元周围网络作为治疗神经精神疾病的治疗靶点。
IF 3.7 4区 医学
Frontiers in Synaptic Neuroscience Pub Date : 2022-06-10 eCollection Date: 2022-01-01 DOI: 10.3389/fnsyn.2022.889800
Caroline A Browne, Katherine Conant, Amy W Lasek, Juan Nacher
{"title":"Editorial: Perineuronal Nets as Therapeutic Targets for the Treatment of Neuropsychiatric Disorders.","authors":"Caroline A Browne,&nbsp;Katherine Conant,&nbsp;Amy W Lasek,&nbsp;Juan Nacher","doi":"10.3389/fnsyn.2022.889800","DOIUrl":"https://doi.org/10.3389/fnsyn.2022.889800","url":null,"abstract":"","PeriodicalId":12650,"journal":{"name":"Frontiers in Synaptic Neuroscience","volume":" ","pages":"889800"},"PeriodicalIF":3.7,"publicationDate":"2022-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9240763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40467351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Editorial: Molecular Nanomachines of the Presynaptic Terminal, Volume II. 编辑:突触前末端的分子纳米机器,第二卷。
IF 3.7 4区 医学
Frontiers in Synaptic Neuroscience Pub Date : 2022-06-07 eCollection Date: 2022-01-01 DOI: 10.3389/fnsyn.2022.941339
Lucia Tabares, Silvio O Rizzoli
{"title":"Editorial: Molecular Nanomachines of the Presynaptic Terminal, Volume II.","authors":"Lucia Tabares,&nbsp;Silvio O Rizzoli","doi":"10.3389/fnsyn.2022.941339","DOIUrl":"https://doi.org/10.3389/fnsyn.2022.941339","url":null,"abstract":"","PeriodicalId":12650,"journal":{"name":"Frontiers in Synaptic Neuroscience","volume":" ","pages":"941339"},"PeriodicalIF":3.7,"publicationDate":"2022-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9211065/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40391178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信