Neuronal signaling最新文献

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Extracellular microRNAs as messengers in the central and peripheral nervous system. 细胞外微rna在中枢和外周神经系统中的信使作用。
Neuronal signaling Pub Date : 2017-11-02 eCollection Date: 2017-12-01 DOI: 10.1042/NS20170112
Hannah Scott
{"title":"Extracellular microRNAs as messengers in the central and peripheral nervous system.","authors":"Hannah Scott","doi":"10.1042/NS20170112","DOIUrl":"https://doi.org/10.1042/NS20170112","url":null,"abstract":"<p><p>MicroRNAs are small post-transcriptional regulators that play an important role in nervous system development, function and disease. More recently, microRNAs have been detected extracellularly and circulating in blood and other body fluids, where they are protected from degradation by encapsulation in vesicles, such as exosomes, or by association with proteins. These microRNAs are thought to be released from cells selectively through active processes and taken up by specific target cells within the same or in remote tissues where they are able to exert their repressive function. These characteristics make extracellular microRNAs ideal candidates for intercellular communication over short and long distances. This review aims to explore the potential mechanisms underlying microRNA communication within the nervous system and between the nervous system and other tissues. The suggested roles of extracellular microRNAs in the healthy and the diseased nervous system will be reviewed.</p>","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":"1 4","pages":"NS20170112"},"PeriodicalIF":0.0,"publicationDate":"2017-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/NS20170112","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38203077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 13
SUMOylation and calcium signalling: potential roles in the brain and beyond. sumo酰化和钙信号传导:在大脑内外的潜在作用。
Neuronal signaling Pub Date : 2017-07-19 eCollection Date: 2017-08-01 DOI: 10.1042/NS20160010
Leticia Coelho-Silva, Gary J Stephens, Helena Cimarosti
{"title":"SUMOylation and calcium signalling: potential roles in the brain and beyond.","authors":"Leticia Coelho-Silva,&nbsp;Gary J Stephens,&nbsp;Helena Cimarosti","doi":"10.1042/NS20160010","DOIUrl":"https://doi.org/10.1042/NS20160010","url":null,"abstract":"<p><p>Small ubiquitin-like modifier (SUMO) conjugation (or SUMOylation) is a post-translational protein modification implicated in alterations to protein expression, localization and function. Despite a number of nuclear roles for SUMO being well characterized, this process has only started to be explored in relation to membrane proteins, such as ion channels. Calcium ion (Ca<sup>2+</sup>) signalling is crucial for the normal functioning of cells and is also involved in the pathophysiological mechanisms underlying relevant neurological and cardiovascular diseases. Intracellular Ca<sup>2+</sup> levels are tightly regulated; at rest, most Ca<sup>2+</sup> is retained in organelles, such as the sarcoplasmic reticulum, or in the extracellular space, whereas depolarization triggers a series of events leading to Ca<sup>2+</sup> entry, followed by extrusion and reuptake. The mechanisms that maintain Ca<sup>2+</sup> homoeostasis are candidates for modulation at the post-translational level. Here, we review the effects of protein SUMOylation, including Ca<sup>2+</sup> channels, their proteome and other proteins associated with Ca<sup>2+</sup> signalling, on vital cellular functions, such as neurotransmission within the central nervous system (CNS) and in additional systems, most prominently here, in the cardiac system.</p>","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":"1 3","pages":"NS20160010"},"PeriodicalIF":0.0,"publicationDate":"2017-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/NS20160010","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38203075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 7
Stochastic, structural and functional factors influencing AMPA and NMDA synaptic response variability: a review. 影响AMPA和NMDA突触反应变异性的随机、结构和功能因素综述。
Neuronal signaling Pub Date : 2017-06-14 eCollection Date: 2017-08-01 DOI: 10.1042/NS20160051
Vito Di Maio, Francesco Ventriglia, Silvia Santillo
{"title":"Stochastic, structural and functional factors influencing AMPA and NMDA synaptic response variability: a review.","authors":"Vito Di Maio,&nbsp;Francesco Ventriglia,&nbsp;Silvia Santillo","doi":"10.1042/NS20160051","DOIUrl":"https://doi.org/10.1042/NS20160051","url":null,"abstract":"<p><p>Synaptic transmission is the basic mechanism of information transfer between neurons not only in the brain, but along all the nervous system. In this review we will briefly summarize some of the main parameters that produce stochastic variability in the synaptic response. This variability produces different effects on important brain phenomena, like learning and memory, and, alterations of its basic factors can cause brain malfunctioning.</p>","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":"1 3","pages":"NS20160051"},"PeriodicalIF":0.0,"publicationDate":"2017-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/NS20160051","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38203076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 7
Conventional protein kinase C in the brain: 40 years later. 脑中的常规蛋白激酶C: 40年后。
Neuronal signaling Pub Date : 2017-04-10 eCollection Date: 2017-04-01 DOI: 10.1042/NS20160005
Julia A Callender, Alexandra C Newton
{"title":"Conventional protein kinase C in the brain: 40 years later.","authors":"Julia A Callender, Alexandra C Newton","doi":"10.1042/NS20160005","DOIUrl":"10.1042/NS20160005","url":null,"abstract":"<p><p>Protein kinase C (PKC) is a family of enzymes whose members transduce a large variety of cellular signals instigated by the receptor-mediated hydrolysis of membrane phospholipids. While PKC has been widely implicated in the pathology of diseases affecting all areas of physiology including cancer, diabetes, and heart disease-it was discovered, and initially characterized, in the brain. PKC plays a key role in controlling the balance between cell survival and cell death. Its loss of function is generally associated with cancer, whereas its enhanced activity is associated with neurodegeneration. This review presents an overview of signaling by diacylglycerol (DG)-dependent PKC isozymes in the brain, and focuses on the role of the Ca<sup>2+</sup>-sensitive conventional PKC isozymes in neurodegeneration.</p>","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":"1 2","pages":"NS20160005"},"PeriodicalIF":0.0,"publicationDate":"2017-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/NS20160005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38203073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 56
Targeting bone morphogenetic protein signalling in midbrain dopaminergic neurons as a therapeutic approach in Parkinson's disease. 靶向中脑多巴胺能神经元骨形态发生蛋白信号作为帕金森病的治疗方法。
Neuronal signaling Pub Date : 2017-03-31 eCollection Date: 2017-04-01 DOI: 10.1042/NS20170027
Gerard W O'Keeffe, Shane V Hegarty, Aideen M Sullivan
{"title":"Targeting bone morphogenetic protein signalling in midbrain dopaminergic neurons as a therapeutic approach in Parkinson's disease.","authors":"Gerard W O'Keeffe,&nbsp;Shane V Hegarty,&nbsp;Aideen M Sullivan","doi":"10.1042/NS20170027","DOIUrl":"https://doi.org/10.1042/NS20170027","url":null,"abstract":"<p><p>Parkinson's disease (PD) is the second most common neurodegenerative disease, characterized by the degeneration of midbrain dopaminergic (mDA) neurons and their axons, and aggregation of α-synuclein, which leads to motor and late-stage cognitive impairments. As the motor symptoms of PD are caused by the degeneration of a specific population of mDA neurons, PD lends itself to neurotrophic factor therapy. The goal of this therapy is to apply a neurotrophic factor that can slow down, halt or even reverse the progressive degeneration of mDA neurons. While the best known neurotrophic factors are members of the glial cell line-derived neurotrophic factor (GDNF) family, their lack of clinical efficacy to date means that it is important to continue to study other neurotrophic factors. Bone morphogenetic proteins (BMPs) are naturally secreted proteins that play critical roles during nervous system development and in the adult brain. In this review, we provide an overview of the BMP ligands, BMP receptors (BMPRs) and their intracellular signalling effectors, the Smad proteins. We review the available evidence that BMP-Smad signalling pathways play an endogenous role in mDA neuronal survival <i>in vivo</i>, before outlining how exogenous application of BMPs exerts potent effects on mDA neuron survival and axon growth <i>in vitro</i> and <i>in vivo</i>. We discuss the molecular mechanisms that mediate these effects, before highlighting the potential of targeting the downstream effectors of BMP-Smad signalling as a novel neuroprotective approach to slow or stop the degeneration of mDA neurons in PD.</p>","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":"1 2","pages":"NS20170027"},"PeriodicalIF":0.0,"publicationDate":"2017-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/NS20170027","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38203074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 14
AMPK: keeping the (power)house in order? AMPK:让(电力)房子井然有序?
Neuronal signaling Pub Date : 2017-03-24 eCollection Date: 2017-04-01 DOI: 10.1042/NS20160020
Claire Thornton
{"title":"AMPK: keeping the (power)house in order?","authors":"Claire Thornton","doi":"10.1042/NS20160020","DOIUrl":"10.1042/NS20160020","url":null,"abstract":"<p><p>Metabolically energetic organs, such as the brain, require a reliable source of ATP, the majority of which is provided by oxidative phosphorylation in the mitochondrial matrix. Maintaining mitochondrial integrity is therefore of paramount importance in highly specialized cells such as neurons. Beyond acting as cellular 'power stations' and initiators of apoptosis, neuronal mitochondria are highly mobile, transported to pre- and post-synaptic sites for rapid, localized ATP production, serve to buffer physiological and pathological calcium and contribute to dendritic arborization. Given such roles, it is perhaps unsurprising that recent studies implicate AMP-activated protein kinase (AMPK), a cellular energy-sensitive metabolic regulator, in triggering mitochondrial fission, potentially balancing mitochondrial dynamics, biogenesis and mitophagy.</p>","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":"1 2","pages":"NS20160020"},"PeriodicalIF":0.0,"publicationDate":"2017-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7373243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38203072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Retrograde apoptotic signaling by the p75 neurotrophin receptor. p75神经营养因子受体的逆行凋亡信号。
Neuronal signaling Pub Date : 2017-02-24 eCollection Date: 2017-02-01 DOI: 10.1042/NS20160007
Amrita Pathak, Bruce D Carter
{"title":"Retrograde apoptotic signaling by the p75 neurotrophin receptor.","authors":"Amrita Pathak,&nbsp;Bruce D Carter","doi":"10.1042/NS20160007","DOIUrl":"https://doi.org/10.1042/NS20160007","url":null,"abstract":"<p><p>Neurotrophins are target-derived factors necessary for mammalian nervous system development and maintenance. They are typically produced by neuronal target tissues and interact with their receptors at axonal endings. Therefore, locally generated neurotrophin signals must be conveyed from the axon back to the cell soma. Retrograde survival signaling by neurotrophin binding to Trk receptors has been extensively studied. However, neurotrophins also bind to the p75 receptor, which can induce apoptosis in a variety of contexts. Selective activation of p75 at distal axon ends has been shown to generate a retrograde apoptotic signal, although the mechanisms involved are poorly understood. The present review summarizes the available evidence for retrograde proapoptotic signaling in general and the role of the p75 receptor in particular, with discussion of unanswered questions in the field. In-depth knowledge of the mechanisms of retrograde apoptotic signaling is essential for understanding the etiology of neurodegeneration in many diseases and injuries.</p>","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":"1 1","pages":"NS20160007"},"PeriodicalIF":0.0,"publicationDate":"2017-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/NS20160007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38203092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 8
Trafficking of neuronal calcium channels. 神经元钙通道的运输。
Neuronal signaling Pub Date : 2017-02-20 eCollection Date: 2017-02-01 DOI: 10.1042/NS20160003
Norbert Weiss, Gerald W Zamponi
{"title":"Trafficking of neuronal calcium channels.","authors":"Norbert Weiss,&nbsp;Gerald W Zamponi","doi":"10.1042/NS20160003","DOIUrl":"https://doi.org/10.1042/NS20160003","url":null,"abstract":"<p><p>Neuronal voltage-gated calcium channels (VGCCs) serve complex yet essential physiological functions via their pivotal role in translating electrical signals into intracellular calcium elevations and associated downstream signalling pathways. There are a number of regulatory mechanisms to ensure a dynamic control of the number of channels embedded in the plasma membrane, whereas alteration of the surface expression of VGCCs has been linked to various disease conditions. Here, we provide an overview of the mechanisms that control the trafficking of VGCCs to and from the plasma membrane, and discuss their implication in pathophysiological conditions and their potential as therapeutic targets.</p>","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":"1 1","pages":"NS20160003"},"PeriodicalIF":0.0,"publicationDate":"2017-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/NS20160003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38203093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 22
Neuronal Signaling: an introduction. 神经元信号:导论。
Neuronal signaling Pub Date : 2016-10-18 eCollection Date: 2017-02-01 DOI: 10.1042/NS20160025
Aideen M Sullivan
{"title":"<i>Neuronal Signaling</i>: an introduction.","authors":"Aideen M Sullivan","doi":"10.1042/NS20160025","DOIUrl":"https://doi.org/10.1042/NS20160025","url":null,"abstract":"<p><p>There have been a number of advances in our knowledge of neuronal communication in processes involved in development, functioning and disorders of the nervous system. This progress has prompted the Biochemical Society to launch <i>Neuronal Signaling</i>, a new open access journal that aims to expand on the existing knowledge about signaling within and between neurons.</p>","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":"1 1","pages":"NS20160025"},"PeriodicalIF":0.0,"publicationDate":"2016-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1042/NS20160025","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38203071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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