Base de dados : MEDLINE
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  1 / 10969 MEDLINE  
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[PMID]:28471021
[Au] Autor:Spessott WA; Sanmillan ML; Kulkarni VV; McCormick ME; Giraudo CG
[Ad] Endereço:Department of Pathology and Laboratory Medicine, University of Pennsylvania - The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania.
[Ti] Título:Syntaxin 4 mediates endosome recycling for lytic granule exocytosis in cytotoxic T-lymphocytes.
[So] Source:Traffic;18(7):442-452, 2017 Jul.
[Is] ISSN:1600-0854
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Adaptive and innate immunity utilize the perforin-killing pathway to eliminate virus-infected or cancer cells. Cytotoxic T-lymphocytes (CTLs) and natural killer cells mediate this process by releasing toxic proteins at the contact area with target cells known as immunological synapse (IS). Formation of a stable IS and exocytosis of toxic proteins requires persistent fusion of Rab11a recycling endosomes with the plasma membrane (PM) that may assure the delivery of key effector proteins. Despite the importance of the recycling endosomal compartment, the membrane fusion proteins that control this process at the IS remain elusive. Here, by performing knockdown experiments we found that syntaxin 4 (STX4) is necessary for cytotoxic activity and CD107a degranulation against target cells in a similar fashion to syntaxin 11, which is involved in lytic granule (LG) exocytosis and immunodeficiency when it is mutated. Using total internal reflection fluorescent microscopy we identified that STX4 mediates fusion of EGFP-Rab11a vesicles at the IS. Immunoprecipitation experiments in lysates of activated CTLs indicate that endogenous STX4 may drive this fusion step by interacting with cognate proteins: Munc18-3/SNAP23/VAMP7 and/or VAMP8. These results reveal the role of STX4 in mediating fusion of Rab11a endosomes upstream of lytic granules (LGs) exocytosis and further demonstrate the importance of this pathway in controlling CTL-mediated cytotoxicity.
[Mh] Termos MeSH primário: Grânulos Citoplasmáticos/metabolismo
Endossomos/metabolismo
Exocitose/imunologia
Proteínas Qa-SNARE/metabolismo
Linfócitos T Citotóxicos/metabolismo
[Mh] Termos MeSH secundário: Degranulação Celular
Linhagem Celular
Grânulos Citoplasmáticos/imunologia
Citotoxicidade Imunológica
Técnicas de Silenciamento de Genes
Seres Humanos
Proteína 1 de Membrana Associada ao Lisossomo/metabolismo
Transporte Proteico
Proteínas Qa-SNARE/genética
Linfócitos T Citotóxicos/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lysosomal-Associated Membrane Protein 1); 0 (Qa-SNARE Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1111/tra.12490


  2 / 10969 MEDLINE  
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[PMID]:29326040
[Au] Autor:Noh MR; Jang HS; Song DK; Lee SR; Lipschutz JH; Park KM; Kim JI
[Ad] Endereço:Department of Anatomy and BK21 Plus, Kyungpook National University School of Medicine, Daegu, Republic of Korea.
[Ti] Título:Downregulation of exocyst Sec10 accelerates kidney tubule cell recovery through enhanced cell migration.
[So] Source:Biochem Biophys Res Commun;496(2):309-315, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Migration of surviving kidney tubule cells after sub-lethal injury, for example ischemia/reperfusion (I/R), plays a critical role in recovery. Exocytosis is known to be involved in cell migration, and a key component in exocytosis is the highly-conserved eight-protein exocyst complex. We investigated the expression of a central exocyst complex member, Sec10, in kidneys following I/R injury, as well as the role of Sec10 in wound healing following scratch injury of cultured Madin-Darby canine kidney (MDCK) cells. Sec10 overexpression and knockdown (KD) in MDCK cells were used to investigate the speed of wound healing and the mechanisms underlying recovery. In mice, Sec10 decreased after I/R injury, and increased during the recovery period. In cell culture, Sec10 OE inhibited ruffle formation and wound healing, while Sec10 KD accelerated it. Sec10 OE cells had higher amounts of diacylglycerol kinase (DGK) gamma at the leading edge than did control cells. A DGK inhibitor reversed the inhibition of wound healing and ruffle formation in Sec10 OE cells. Conclusively, downregulation of Sec10 following I/R injury appears to accelerate recovery of kidney tubule cells through activated ruffle formation and enhanced cell migration.
[Mh] Termos MeSH primário: Diacilglicerol Quinase/antagonistas & inibidores
Túbulos Renais/metabolismo
Traumatismo por Reperfusão/prevenção & controle
Proteínas de Transporte Vesicular/genética
[Mh] Termos MeSH secundário: Animais
Bioensaio
Linhagem Celular
Movimento Celular/efeitos dos fármacos
Diacilglicerol Quinase/genética
Diacilglicerol Quinase/metabolismo
Cães
Inibidores Enzimáticos/farmacologia
Exocitose
Regulação da Expressão Gênica
Túbulos Renais/patologia
Células Madin Darby de Rim Canino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Piperidinas/farmacologia
Quinazolinonas/farmacologia
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Traumatismo por Reperfusão/genética
Traumatismo por Reperfusão/metabolismo
Traumatismo por Reperfusão/patologia
Proteínas de Transporte Vesicular/agonistas
Proteínas de Transporte Vesicular/antagonistas & inibidores
Proteínas de Transporte Vesicular/metabolismo
Cicatrização/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (EXOC5 protein, mouse); 0 (Enzyme Inhibitors); 0 (Piperidines); 0 (Quinazolinones); 0 (RNA, Small Interfering); 0 (Vesicular Transport Proteins); 120166-69-0 (R 59949); EC 2.7.1.107 (Diacylglycerol Kinase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE


  3 / 10969 MEDLINE  
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[PMID]:29247648
[Au] Autor:Deng B; Zhu X; Zhao Y; Zhang D; Pannu A; Chen L; Niu W
[Ad] Endereço:Department of Immunology, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Metabolic Diseases Hospital, Tianjin Medical University, Tianjin, 300070, China.
[Ti] Título:PKC and Rab13 mediate Ca signal-regulated GLUT4 traffic.
[So] Source:Biochem Biophys Res Commun;495(2):1956-1963, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Exercise/muscle contraction increases cell surface glucose transporter 4 (GLUT4), leading to glucose uptake to regulate blood glucose level. Elevating cytosolic Ca mediates this effect, but the detailed mechanism is not clear yet. We used calcium ionophore ionomycin to raise intracellular cytosolic Ca level to explore the underlying mechanism. We showed that in L6 myoblast muscle cells stably expressing GLUT4myc, ionomycin increased cell surface GLUT4myc levels and the phosphorylation of AS160, TBC1D1. siPKCα and siPKCθ but not siPKCδ and siPKCε inhibited the ionomycin-increased cell surface GLUT4myc level. siPKCα, siPKCθ inhibited the phosphorylation of AS160 and TBC1D1 induced by ionomycin. siPKCα and siPKCθ prevented ionomycin-inhibited endocytosis of GLUT4myc. siPKCθ, but not siPKCα inhibited ionomycin-stimulated exocytosis of GLUT4myc. siRab13 but not siRab8a, siRab10 and siRab14 inhibited the exocytosis of GLUT4myc promoted by ionomycin. In summary, ionomycin-promoted exocytosis of GLUT4 is partly reversed by siPKCθ, whereas ionomycin-inhibited endocytosis of GLUT4 requires both siPKCα and siPKCθ. PKCα and PKCθ contribute to ionomycin-induced phosphorylation of AS160 and TBC1D1. Rab13 is required for ionomycin-regulated GLUT4 exocytosis.
[Mh] Termos MeSH primário: Sinalização do Cálcio/fisiologia
Endocitose/fisiologia
Exocitose/fisiologia
GTP Fosfo-Hidrolases/metabolismo
Transportador de Glucose Tipo 4/metabolismo
Mioblastos/fisiologia
Proteína Quinase C/metabolismo
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Ionóforos de Cálcio/administração & dosagem
Sinalização do Cálcio/efeitos dos fármacos
Linhagem Celular
Endocitose/efeitos dos fármacos
Exocitose/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/fisiologia
Ionomicina/administração & dosagem
Mioblastos/efeitos dos fármacos
Transporte Proteico/fisiologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Calcium Ionophores); 0 (Glucose Transporter Type 4); 0 (Slc2a4 protein, rat); 56092-81-0 (Ionomycin); EC 2.7.11.13 (Protein Kinase C); EC 3.6.1.- (GTP Phosphohydrolases); EC 3.6.1.- (Rab13 protein, rat); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE


  4 / 10969 MEDLINE  
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[PMID]:28456985
[Au] Autor:Andrews NW
[Ad] Endereço:Department of Cell Biology and Molecular Genetics, University of Maryland at College Park, 2134 Bioscience Research Building, College Park, MD, 20742-5815, USA. andrewsn@umd.edu.
[Ti] Título:Detection of Lysosomal Exocytosis by Surface Exposure of Lamp1 Luminal Epitopes.
[So] Source:Methods Mol Biol;1594:205-211, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Elevation in the cytosolic Ca concentration triggers exocytosis of lysosomes in many cell types. This chapter describes a method to detect lysosomal exocytosis in mammalian cells, which takes advantage of the presence of an abundant glycoprotein, Lamp1, on the membrane of lysosomes. Lamp1 is a transmembrane protein with a large, heavily glycosylated region that faces the lumen of lysosomes. When lysosomes fuse with the plasma membrane, epitopes present on the luminal domain of Lamp1 are exposed on the cell surface. The Lamp1 luminal epitopes can then be detected on the surface of live, unfixed cells using highly specific monoclonal antibodies and fluorescence microscopy. The main advantage of this method is its sensitivity, and the fact that it provides spatial information on lysosomal exocytosis at the single cell level.
[Mh] Termos MeSH primário: Lisossomos/metabolismo
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Membrana Celular/metabolismo
Epitopos/análise
Exocitose/genética
Exocitose/fisiologia
Seres Humanos
Proteína 1 de Membrana Associada ao Lisossomo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epitopes); 0 (Lysosomal-Associated Membrane Protein 1); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6934-0_13


  5 / 10969 MEDLINE  
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[PMID]:28456984
[Au] Autor:Södergren AL; Ramström S
[Ad] Endereço:Clinical Chemistry, Department of Clinical and Experimental Medicine, Linköping University, SE-58185, Linköping, Sweden. anna.sodergren@liu.se.
[Ti] Título:Detection of Lysosomal Exocytosis in Platelets by Flow Cytometry.
[So] Source:Methods Mol Biol;1594:191-203, 2017.
[Is] ISSN:1940-6029
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Flow cytometry is a method that allows high throughput analysis of individual cells in suspension. By inclusion of fluorescently labelled antibodies, it is possible to analyze the abundance of one or more surface antigens, such as LAMP-1, without prior lysis of cells. Here we describe the special considerations required for the investigation of lysosomal exocytosis from platelets analyzed with flow cytometry.
[Mh] Termos MeSH primário: Exocitose/fisiologia
Lisossomos/metabolismo
[Mh] Termos MeSH secundário: Plaquetas/metabolismo
Citometria de Fluxo
Seres Humanos
Proteína 1 de Membrana Associada ao Lisossomo/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lysosomal-Associated Membrane Protein 1)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE
[do] DOI:10.1007/978-1-4939-6934-0_12


  6 / 10969 MEDLINE  
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[PMID]:29212789
[Au] Autor:Rorsman P; Ashcroft FM
[Ad] Endereço:Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford, United Kingdom; Department of Neuroscience and Physiology, Metabolic Research Unit, Göteborg, Sweden; and Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
[Ti] Título:Pancreatic ß-Cell Electrical Activity and Insulin Secretion: Of Mice and Men.
[So] Source:Physiol Rev;98(1):117-214, 2018 Jan 01.
[Is] ISSN:1522-1210
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The pancreatic ß-cell plays a key role in glucose homeostasis by secreting insulin, the only hormone capable of lowering the blood glucose concentration. Impaired insulin secretion results in the chronic hyperglycemia that characterizes type 2 diabetes (T2DM), which currently afflicts >450 million people worldwide. The healthy ß-cell acts as a glucose sensor matching its output to the circulating glucose concentration. It does so via metabolically induced changes in electrical activity, which culminate in an increase in the cytoplasmic Ca concentration and initiation of Ca -dependent exocytosis of insulin-containing secretory granules. Here, we review recent advances in our understanding of the ß-cell transcriptome, electrical activity, and insulin exocytosis. We highlight salient differences between mouse and human ß-cells, provide models of how the different ion channels contribute to their electrical activity and insulin secretion, and conclude by discussing how these processes become perturbed in T2DM.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/metabolismo
Homeostase/fisiologia
Células Secretoras de Insulina/metabolismo
Insulina/metabolismo
[Mh] Termos MeSH secundário: Animais
Canais de Cálcio/metabolismo
Exocitose/fisiologia
Seres Humanos
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Calcium Channels); 0 (Insulin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171214
[Lr] Data última revisão:
171214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1152/physrev.00008.2017


  7 / 10969 MEDLINE  
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[PMID]:29096080
[Au] Autor:Biederer T; Kaeser PS; Blanpied TA
[Ad] Endereço:Department of Neuroscience, Tufts University School of Medicine, Boston, MA 02111, USA. Electronic address: thomas.biederer@tufts.edu.
[Ti] Título:Transcellular Nanoalignment of Synaptic Function.
[So] Source:Neuron;96(3):680-696, 2017 Nov 01.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:At each of the brain's vast number of synapses, the presynaptic nerve terminal, synaptic cleft, and postsynaptic specialization form a transcellular unit to enable efficient transmission of information between neurons. While we know much about the molecular machinery within each compartment, we are only beginning to understand how these compartments are structurally registered and functionally integrated with one another. This review will describe the organization of each compartment and then discuss their alignment across pre- and postsynaptic cells at a nanometer scale. We propose that this architecture may allow for precise synaptic information exchange and may be modulated to contribute to the remarkable plasticity of brain function.
[Mh] Termos MeSH primário: Comunicação Celular/fisiologia
Exocitose/fisiologia
Plasticidade Neuronal/fisiologia
Sinapses/fisiologia
Transmissão Sináptica/fisiologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Terminações Pré-Sinápticas/fisiologia
Terminações Pré-Sinápticas/ultraestrutura
Sinapses/ultraestrutura
Vesículas Sinápticas/fisiologia
Vesículas Sinápticas/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171103
[St] Status:MEDLINE


  8 / 10969 MEDLINE  
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[PMID]:28893927
[Au] Autor:Hong Y; Zhao T; Li XJ; Li S
[Ad] Endereço:Department of Human Genetics, Emory University School of Medicine, Atlanta, Georgia 30322.
[Ti] Título:Mutant Huntingtin Inhibits αB-Crystallin Expression and Impairs Exosome Secretion from Astrocytes.
[So] Source:J Neurosci;37(39):9550-9563, 2017 Sep 27.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the brain, astrocytes secrete diverse substances that regulate neuronal function and viability. Exosomes, which are vesicles produced through the formation of multivesicular bodies and their subsequent fusion with the plasma membrane, are also released from astrocytes via exocytotic secretion. Astrocytic exosomes carry heat shock proteins that can reduce the cellular toxicity of misfolded proteins and prevent neurodegeneration. Although mutant huntingtin (mHtt) affects multiple functions of astrocytes, it remains unknown whether mHtt impairs the production of exosomes from astrocytes. We found that mHtt is not present in astrocytic exosomes, but can decrease exosome secretion from astrocytes in HD140Q knock-in (KI) mice. N-terminal mHtt accumulates in the nuclei and forms aggregates, causing decreased secretion of exosomes from cultured astrocytes. Consistently, there is a significant decrease in secreted exosomes in both female and male HD KI mouse striatum in which abundant nuclear mHtt aggregates are present. Conversely, injection of astrocytic exosomes into the striatum of HD140Q KI mice reduces the density of mHtt aggregates. Further, mHtt in astrocytes decreased the expression of αB-crystallin, a small heat shock protein that is enriched in astrocytes and mediates exosome secretion, by reducing the association of Sp1 with the enhancer of the α gene. Importantly, overexpression of αB-crystallin rescues defective exosome release from HD astrocytes as well as mHtt aggregates in the striatum of HD140Q KI mice. Our results demonstrate that mHtt reduces the expression of αB-crystallin in astrocytes to decrease exosome secretion in the HD brains, contributing to non-cell-autonomous neurotoxicity in HD. Huntington's disease (HD) is characterized by selective neurodegeneration that preferentially occurs in the striatal medium spiny neurons. Recent studies in different HD mouse models demonstrated that dysfunction of astrocytes, a major type of glial cell, leads to neuronal vulnerability. Emerging evidence shows that exosomes secreted from astrocytes contain neuroprotective cargoes that could support the survival of neighboring neurons. We found that mHtt in astrocytes impairs exosome secretion by decreasing αB-crystallin, a protein that is expressed mainly in glial cells and mediates exosome secretion. Overexpression of αB-crystallin could alleviate the deficient exosome release and neuropathology in HD mice. Our results revealed a new pathological pathway that affects the critical support of glial cells to neurons in the HD brain.
[Mh] Termos MeSH primário: Astrócitos/secreção
Exossomos/secreção
Proteína Huntingtina/genética
Doença de Huntington/metabolismo
Cadeia B de alfa-Cristalina/metabolismo
[Mh] Termos MeSH secundário: Animais
Astrócitos/metabolismo
Células Cultivadas
Corpo Estriado/metabolismo
Exocitose
Feminino
Proteína Huntingtina/metabolismo
Masculino
Camundongos
Mutação
Cadeia B de alfa-Cristalina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Htt protein, mouse); 0 (Huntingtin Protein); 0 (alpha-Crystallin B Chain)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171015
[Lr] Data última revisão:
171015
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1418-17.2017


  9 / 10969 MEDLINE  
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[PMID]:28867551
[Au] Autor:Reddy-Alla S; Böhme MA; Reynolds E; Beis C; Grasskamp AT; Mampell MM; Maglione M; Jusyte M; Rey U; Babikir H; McCarthy AW; Quentin C; Matkovic T; Bergeron DD; Mushtaq Z; Göttfert F; Owald D; Mielke T; Hell SW; Sigrist SJ; Walter AM
[Ad] Endereço:Institute for Biology/Genetics, Freie Universität Berlin, 14195 Berlin, Germany.
[Ti] Título:Stable Positioning of Unc13 Restricts Synaptic Vesicle Fusion to Defined Release Sites to Promote Synchronous Neurotransmission.
[So] Source:Neuron;95(6):1350-1364.e12, 2017 Sep 13.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neural information processing depends on precisely timed, Ca -activated synaptic vesicle exocytosis from release sites within active zones (AZs), but molecular details are unknown. Here, we identify that the (M)Unc13-family member Unc13A generates release sites and show the physiological relevance of their restrictive AZ targeting. Super-resolution and intravital imaging of Drosophila neuromuscular junctions revealed that (unlike the other release factors Unc18 and Syntaxin-1A) Unc13A was stably and precisely positioned at AZs. Local Unc13A levels predicted single AZ activity. Different Unc13A portions selectively affected release site number, position, and functionality. An N-terminal fragment stably localized to AZs, displaced endogenous Unc13A, and reduced the number of release sites, while a C-terminal fragment generated excessive sites at atypical locations, resulting in reduced and delayed evoked transmission that displayed excessive facilitation. Thus, release site generation by the Unc13A C terminus and their specific AZ localization via the N terminus ensure efficient transmission and prevent ectopic, temporally imprecise release.
[Mh] Termos MeSH primário: Proteínas de Transporte/metabolismo
Drosophila
Exocitose/fisiologia
Transmissão Sináptica/fisiologia
Vesículas Sinápticas/metabolismo
[Mh] Termos MeSH secundário: Animais
Junção Neuromuscular/metabolismo
Junção Neuromuscular/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (phorbol ester binding protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170905
[St] Status:MEDLINE


  10 / 10969 MEDLINE  
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[PMID]:28847813
[Au] Autor:Moore LA; Trussell LO
[Ad] Endereço:Neuroscience Graduate Program and moorlu@ohsu.edu.
[Ti] Título:Corelease of Inhibitory Neurotransmitters in the Mouse Auditory Midbrain.
[So] Source:J Neurosci;37(39):9453-9464, 2017 Sep 27.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The central nucleus of the inferior colliculus (ICC) of the auditory midbrain, which integrates most ascending auditory information from lower brainstem regions, receives prominent long-range inhibitory input from the ventral nucleus of the lateral lemniscus (VNLL), a region thought to be important for temporal pattern discrimination. Histological evidence suggests that neurons in the VNLL release both glycine and GABA in the ICC, but functional evidence for their corelease is lacking. We took advantage of the mouse line (both male and female) to target expression of ChR2 to glycinergic afferents in the ICC and made whole-cell recordings while exciting glycinergic fibers with light. Using this approach, it was clear that a significant fraction of glycinergic boutons corelease GABA in the ICC. Viral injections were used to target ChR2 expression specifically to glycinergic fibers ascending from the VNLL, allowing for activation of fibers from a single source of ascending input in a way that has not been previously possible in the ICC. We then investigated aspects of the glycinergic versus GABAergic current components to probe functional consequences of corelease. Surprisingly, the time course and short-term plasticity of synaptic signaling were nearly identical for the two transmitters. We therefore conclude that the two neurotransmitters may be functionally interchangeable and that multiple receptor subtypes subserving inhibition may offer diverse mechanisms for maintaining inhibitory homeostasis. Corelease of neurotransmitters is a common feature of the brain. GABA and glycine corelease is particularly common in the spinal cord and brainstem, but its presence in the midbrain is unknown. We show corelease of GABA and glycine for the first time in the central nucleus of the inferior colliculus of the auditory midbrain. Glycine and GABA are both inhibitory neurotransmitters involved in fast synaptic transmission, so we explored differences between the currents to establish a physiological foundation for functional differences In contrast to the auditory brainstem, coreleased GABAergic and glycinergic currents in the midbrain are strikingly similar. This apparent redundancy may ensure homeostasis if one neurotransmitter system is compromised.
[Mh] Termos MeSH primário: Potenciais Pós-Sinápticos Excitadores
Glicina/metabolismo
Colículos Inferiores/metabolismo
Ácido gama-Aminobutírico/metabolismo
[Mh] Termos MeSH secundário: Animais
Channelrhodopsins
Exocitose
Feminino
Proteínas da Membrana Plasmática de Transporte de Glicina/genética
Proteínas da Membrana Plasmática de Transporte de Glicina/metabolismo
Homeostase
Colículos Inferiores/citologia
Colículos Inferiores/fisiologia
Masculino
Camundongos
Neurônios Aferentes/metabolismo
Neurônios Aferentes/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Channelrhodopsins); 0 (Glycine Plasma Membrane Transport Proteins); 0 (Slc6a5 protein, mouse); 56-12-2 (gamma-Aminobutyric Acid); TE7660XO1C (Glycine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1125-17.2017



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