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Pesquisa : B01.050.150.900.649.313.992.635.505.500.400.025 [Categoria DeCS]
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[PMID]:28453726
[Au] Autor:Li J; Yousefi K; Ding W; Singh J; Shehadeh LA
[Ad] Endereço:Department of Medicine, Division of Cardiology, University of Miami Leonard M. Miller School of Medicine, Miami, FL 33136, USA.
[Ti] Título:Osteopontin RNA aptamer can prevent and reverse pressure overload-induced heart failure.
[So] Source:Cardiovasc Res;113(6):633-643, 2017 May 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aims: Cardiac myocyte hypertrophy, the main compensatory response to chronic stress in the heart often progresses to a state of decompensation that can lead to heart failure. Osteopontin (OPN) is an effector for extracellular signalling that induces myocyte growth and fibrosis. Although increased OPN activity has been observed in stressed myocytes and fibroblasts, the detailed and long term effects of blocking OPN signalling on the heart remain poorly defined. Targeting cardiac OPN protein by an RNA aptamer may be beneficial for tuning down OPN pathologic signalling. We aimed to demonstrate the therapeutic effects of an OPN RNA aptamer on cardiac dysfunction. Methods and results: In vivo, we show that in a mouse model of pressure overload, treating at the time of surgeries with an OPN aptamer prevented cardiomyocyte hypertrophy and cardiac fibrosis, blocked OPN downstream signalling (PI3K and Akt phosphorylation), reduced expression of extracellular matrix (Lum, Col3a1, Fn1) and hypertrophy (Nppa, Nppb) genes, and prevented cardiac dysfunction. Treating at two months post-surgeries with the OPN aptamer reversed cardiac dysfunction and fibrosis and myocyte hypertrophy. While genetic homozygous deletion of OPN reduced myocardial wall thickness, surprisingly cardiac function and myocardial fibrosis, specifically collagen deposition and myofibroblast infiltration, were worse compared with wild type mice at three months of pressure overload. Conclusion: Taken together, these data demonstrate that tuning down cardiac OPN signalling by an OPN RNA aptamer is a novel and effective approach for preventing cardiac hypertrophy and fibrosis, improving cardiac function, and reversing pressure overload-induced heart failure.
[Mh] Termos MeSH primário: Aorta/fisiopatologia
Aptâmeros de Nucleotídeos/metabolismo
Pressão Arterial
Insuficiência Cardíaca/prevenção & controle
Hipertrofia Ventricular Esquerda/prevenção & controle
Miocárdio/metabolismo
Osteopontina/metabolismo
Disfunção Ventricular Esquerda/prevenção & controle
Função Ventricular Esquerda
Remodelação Ventricular
[Mh] Termos MeSH secundário: Animais
Aorta/cirurgia
Aptâmeros de Nucleotídeos/genética
Colágeno Tipo III/metabolismo
Citocinas/metabolismo
Modelos Animais de Doenças
Fibrose
Regulação da Expressão Gênica
Predisposição Genética para Doença
Insuficiência Cardíaca/genética
Insuficiência Cardíaca/metabolismo
Insuficiência Cardíaca/fisiopatologia
Hipertrofia Ventricular Esquerda/genética
Hipertrofia Ventricular Esquerda/metabolismo
Hipertrofia Ventricular Esquerda/fisiopatologia
Ligadura
Lumicana/metabolismo
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Knockout
Miocárdio/patologia
Osteopontina/deficiência
Osteopontina/genética
Fenótipo
Fosfatidilinositol 3-Quinase/metabolismo
Fosforilação
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
Fatores de Tempo
Disfunção Ventricular Esquerda/genética
Disfunção Ventricular Esquerda/metabolismo
Disfunção Ventricular Esquerda/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aptamers, Nucleotide); 0 (COL3A1 protein, mouse); 0 (Collagen Type III); 0 (Cytokines); 0 (Lum protein, mouse); 0 (Lumican); 0 (Spp1 protein, mouse); 106441-73-0 (Osteopontin); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvx016


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[PMID]:29339718
[Au] Autor:Parfejevs V; Debbache J; Shakhova O; Schaefer SM; Glausch M; Wegner M; Suter U; Riekstina U; Werner S; Sommer L
[Ad] Endereço:Institute of Anatomy, University of Zürich, 8057, Zürich, Switzerland.
[Ti] Título:Injury-activated glial cells promote wound healing of the adult skin in mice.
[So] Source:Nat Commun;9(1):236, 2018 01 16.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cutaneous wound healing is a complex process that aims to re-establish the original structure of the skin and its functions. Among other disorders, peripheral neuropathies are known to severely impair wound healing capabilities of the skin, revealing the importance of skin innervation for proper repair. Here, we report that peripheral glia are crucially involved in this process. Using a mouse model of wound healing, combined with in vivo fate mapping, we show that injury activates peripheral glia by promoting de-differentiation, cell-cycle re-entry and dissemination of the cells into the wound bed. Moreover, injury-activated glia upregulate the expression of many secreted factors previously associated with wound healing and promote myofibroblast differentiation by paracrine modulation of TGF-ß signalling. Accordingly, depletion of these cells impairs epithelial proliferation and wound closure through contraction, while their expansion promotes myofibroblast formation. Thus, injury-activated glia and/or their secretome might have therapeutic potential in human wound healing disorders.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Neuroglia/fisiologia
Pele/fisiopatologia
Cicatrização/fisiologia
[Mh] Termos MeSH secundário: Animais
Ciclo Celular/genética
Ciclo Celular/fisiologia
Diferenciação Celular/genética
Células Cultivadas
Perfilação da Expressão Gênica
Seres Humanos
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos DBA
Camundongos Knockout
Camundongos Transgênicos
Miofibroblastos/metabolismo
Miofibroblastos/fisiologia
Neuroglia/citologia
Neuroglia/metabolismo
Fatores de Transcrição SOXE/genética
Fatores de Transcrição SOXE/metabolismo
Transdução de Sinais/genética
Pele/lesões
Pele/inervação
Fator de Crescimento Transformador beta/genética
Fator de Crescimento Transformador beta/metabolismo
Cicatrização/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (SOXE Transcription Factors); 0 (Sox10 protein, mouse); 0 (Transforming Growth Factor beta)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-01488-2


  3 / 2558 MEDLINE  
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[PMID]:29360879
[Au] Autor:Henriques SF; Patissier C; Bourg N; Fecchio C; Sandona D; Marsolier J; Richard I
[Ad] Endereço:INTEGRARE, Genethon, Inserm, Univ Evry, Université Paris-Saclay, Evry, France.
[Ti] Título:Different outcome of sarcoglycan missense mutation between human and mouse.
[So] Source:PLoS One;13(1):e0191274, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sarcoglycanopathies are rare autosomic limb girdle muscular dystrophies caused by mutations in one of the genes coding for sarcoglycan (α, ß, δ, and γ-sarcoglycans). Sarcoglycans form a complex, which is an important part of the dystrophin-associated glycoprotein complex that protects sarcolemma against muscle contraction-induced damages. Absence of one of the sarcoglycan at the plasma membrane induces the disappearance of the whole complex and perturbs muscle fiber membrane integrity. We previously demonstrated that point mutations in the human sarcoglycan genes affects the folding of the corresponding protein, which is then retained in the endoplasmic reticulum by the protein quality control and prematurely degraded by the proteasome. Interestingly, modulation of the quality control using pharmacological compounds allowed the rescue of the membrane localization of the mutated sarcoglycan. Two previously generated mouse models, knock-in for the most common sarcoglycan mutant, R77C α-sarcoglycan, failed in reproducing the dystrophic phenotype observed in human patients. Based on these results and the need to test therapies for these fatal diseases, we decided to generate a new knock-in mouse model carrying the missense mutation T151R in the ß-sarcoglycan gene since this is the second sarcoglycan protein with the most frequently reported missense mutations. Muscle analysis, performed at the age of 4 and 9-months, showed the presence of the mutated ß-sarcoglycan protein and of the other components of the dystrophin-associated glycoprotein complex at the muscle membrane. In addition, these mice did not develop a dystrophic phenotype, even at a late stage or in condition of stress-inducing exercise. We can speculate that the absence of phenotype in mouse may be due to a higher tolerance of the endoplasmic reticulum quality control for amino-acid changes in mice compared to human.
[Mh] Termos MeSH primário: Distrofia Muscular do Cíngulo dos Membros/genética
Mutação de Sentido Incorreto
Sarcoglicanas/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Substituição de Aminoácidos
Animais
Modelos Animais de Doenças
Feminino
Seres Humanos
Masculino
Camundongos
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Músculo Esquelético/metabolismo
Músculo Esquelético/patologia
Distrofia Muscular do Cíngulo dos Membros/metabolismo
Distrofia Muscular do Cíngulo dos Membros/patologia
Proteólise
Sarcoglicanas/metabolismo
Especificidade da Espécie
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (SGCB protein, human); 0 (Sarcoglycans)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191274


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[PMID]:28464043
[Au] Autor:d'Anglemont de Tassigny X; Jayasena CN; Murphy KG; Dhillo WS; Colledge WH
[Ad] Endereço:Reproductive Physiology Group, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, United Kingdom.
[Ti] Título:Mechanistic insights into the more potent effect of KP-54 compared to KP-10 in vivo.
[So] Source:PLoS One;12(5):e0176821, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kisspeptins regulate the mammalian reproductive axis by stimulating release of gonadotrophin releasing hormone (GnRH). Different length kisspeptins (KP) are found of 54, 14, 13 or 10 amino-acids which share a common C-terminal 10-amino acid sequence. KP-54 and KP-10 have been widely used to stimulate the reproductive axis but data suggest that KP-54 and KP-10 are not equally effective at eliciting reproductive hormone secretion after peripheral delivery. To confirm this, we analysed the effect of systemic administration of KP-54 or KP-10 on luteinizing hormone (LH) secretion into the bloodstream of male mice. Plasma LH measurements 10 min or 2 hours after kisspeptin injection showed that KP-54 can sustain LH release far longer than KP-10, suggesting a differential mode of action of the two peptides. To investigate the mechanism for this, we evaluated the pharmacokinetics of the two peptides in vivo and their potential to cross the blood brain barrier (BBB). We found that KP-54 has a half-life of ~32 min in the bloodstream, while KP-10 has a half-life of ~4 min. To compensate for this difference in half-life, we repeated injections of KP-10 every 10 min over 1 hr but failed to reproduce the sustained rise in LH observed after a single KP-54 injection, suggesting that the failure of KP-10 to sustain LH release may not just be related to peptide clearance. We tested the ability of peripherally administered KP-54 and KP-10 to activate c-FOS in GnRH neurons behind the blood brain barrier (BBB) and found that only KP-54 could do this. These data are consistent with KP-54 being able to cross the BBB and suggest that KP10 may be less able to do so.
[Mh] Termos MeSH primário: Fármacos do Sistema Nervoso Central/farmacologia
Kisspeptinas/farmacologia
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Barreira Hematoencefálica/efeitos dos fármacos
Barreira Hematoencefálica/metabolismo
Permeabilidade Capilar/efeitos dos fármacos
Permeabilidade Capilar/fisiologia
Fármacos do Sistema Nervoso Central/farmacocinética
Relação Dose-Resposta a Droga
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Hipotálamo/citologia
Hipotálamo/efeitos dos fármacos
Hipotálamo/metabolismo
Imuno-Histoquímica
Kisspeptinas/farmacocinética
Hormônio Luteinizante/sangue
Hormônio Luteinizante/secreção
Masculino
Camundongos da Linhagem 129
Neurônios/citologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Proteínas Proto-Oncogênicas c-fos/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Central Nervous System Agents); 0 (KISS1 protein, human); 0 (Kisspeptins); 0 (Proto-Oncogene Proteins c-fos); 9002-67-9 (Luteinizing Hormone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180125
[Lr] Data última revisão:
180125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0176821


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[PMID]:28743859
[Au] Autor:Jiang X; Hawkins JS; Lee J; Lizama CO; Bos FL; Zape JP; Ghatpande P; Peng Y; Louie J; Lagna G; Zovein AC; Hata A
[Ad] Endereço:Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, 94143, USA.
[Ti] Título:Let-7 microRNA-dependent control of leukotriene signaling regulates the transition of hematopoietic niche in mice.
[So] Source:Nat Commun;8(1):128, 2017 07 25.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hematopoietic stem and progenitor cells arise from the vascular endothelium of the dorsal aorta and subsequently switch niche to the fetal liver through unknown mechanisms. Here we report that vascular endothelium-specific deletion of mouse Drosha (Drosha ), an enzyme essential for microRNA biogenesis, leads to anemia and death. A similar number of hematopoietic stem and progenitor cells emerge from Drosha-deficient and control vascular endothelium, but Drosha -derived hematopoietic stem and progenitor cells accumulate in the dorsal aorta and fail to colonize the fetal liver. Depletion of the let-7 family of microRNAs is a primary cause of this defect, as it leads to activation of leukotriene B4 signaling and induction of the α4ß1 integrin cell adhesion complex in hematopoietic stem and progenitor cells. Inhibition of leukotriene B4 or integrin rescues maturation and migration of Drosha hematopoietic stem and progenitor cells to the fetal liver, while it hampers hematopoiesis in wild-type animals. Our study uncovers a previously undefined role of innate leukotriene B4 signaling as a gatekeeper of the hematopoietic niche transition.Hematopoietic stem and progenitor cells are generated first from the vascular endothelium of the dorsal aorta and then the fetal liver but what regulates this switch is unknown. Here, the authors show that changing miRNA biogenesis and leukotriene B4 signaling in mice modulates this switch in the niche.
[Mh] Termos MeSH primário: Hematopoese/genética
Células-Tronco Hematopoéticas/metabolismo
Leucotrieno B4/metabolismo
MicroRNAs/genética
Nicho de Células-Tronco/genética
[Mh] Termos MeSH secundário: Animais
Aorta/metabolismo
Endotélio Vascular/metabolismo
Fígado/embriologia
Fígado/metabolismo
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Microscopia de Fluorescência
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Ribonuclease III/genética
Ribonuclease III/metabolismo
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MicroRNAs); 0 (mirnlet7 microRNA, mouse); 1HGW4DR56D (Leukotriene B4); EC 3.1.26.3 (Drosha protein, mouse); EC 3.1.26.3 (Ribonuclease III)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-00137-y


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[PMID]:29025768
[Au] Autor:Sirish P; Ledford HA; Timofeyev V; Thai PN; Ren L; Kim HJ; Park S; Lee JH; Dai G; Moshref M; Sihn CR; Chen WC; Timofeyeva MV; Jian Z; Shimkunas R; Izu LT; Chiamvimonvat N; Chen-Izu Y; Yamoah EN; Zhang XD
[Ad] Endereço:From the Division of Cardiovascular Medicine, Department of Internal Medicine (P.S., H.A.L., V.T., P.N.T., L.R., S.P., G.D., M.M., C.-R.S., W.C.C., M.V.T., N.C., Y.C.-I., X.-D.Z.), Center for Neuroscience (H.J.K.), Department of Pharmacology (Z.J., R.S., L.T.I., N.C., Y.C.-I.) and Department of Biom
[Ti] Título:Action Potential Shortening and Impairment of Cardiac Function by Ablation of .
[So] Source:Circ Arrhythm Electrophysiol;10(10), 2017 Oct.
[Is] ISSN:1941-3084
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Intracellular pH (pH ) is critical to cardiac excitation and contraction; uncompensated changes in pH impair cardiac function and trigger arrhythmia. Several ion transporters participate in cardiac pH regulation. Our previous studies identified several isoforms of a solute carrier Slc26a6 to be highly expressed in cardiomyocytes. We show that Slc26a6 mediates electrogenic Cl /HCO exchange activities in cardiomyocytes, suggesting the potential role of Slc26a6 in regulation of not only pH , but also cardiac excitability. METHODS AND RESULTS: To test the mechanistic role of Slc26a6 in the heart, we took advantage of knockout ( ) mice using both in vivo and in vitro analyses. Consistent with our prediction of its electrogenic activities, ablation of results in action potential shortening. There are reduced Ca transient and sarcoplasmic reticulum Ca load, together with decreased sarcomere shortening in cardiomyocytes. These abnormalities translate into reduced fractional shortening and cardiac contractility at the in vivo level. Additionally, pH is elevated in cardiomyocytes with slower recovery kinetics from intracellular alkalization, consistent with the Cl /HCO exchange activities of Slc26a6. Moreover, mice show evidence of sinus bradycardia and fragmented QRS complex, supporting the critical role of Slc26a6 in cardiac conduction system. CONCLUSIONS: Our study provides mechanistic insights into Slc26a6, a unique cardiac electrogenic Cl /HCO transporter in ventricular myocytes, linking the critical roles of Slc26a6 in regulation of pH , excitability, and contractility. pH is a critical regulator of other membrane and contractile proteins. Future studies are needed to investigate possible changes in these proteins in mice.
[Mh] Termos MeSH primário: Potenciais de Ação
Antiporters/deficiência
Acoplamento Excitação-Contração
Frequência Cardíaca
Contração Miocárdica
Miócitos Cardíacos/metabolismo
[Mh] Termos MeSH secundário: Animais
Antiporters/genética
Bradicardia/genética
Bradicardia/metabolismo
Bradicardia/fisiopatologia
Células CHO
Cricetulus
Genótipo
Concentração de Íons de Hidrogênio
Cinética
Proteínas de Membrana Transportadoras/genética
Proteínas de Membrana Transportadoras/metabolismo
Camundongos da Linhagem 129
Camundongos Knockout
Fenótipo
Sarcômeros/metabolismo
Retículo Sarcoplasmático/metabolismo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiporters); 0 (Membrane Transport Proteins); 0 (SLC26A6 protein, human); 0 (Slc26a6 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE


  7 / 2558 MEDLINE  
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[PMID]:29024668
[Au] Autor:Sheffield MEJ; Adoff MD; Dombeck DA
[Ad] Endereço:Department of Neurobiology, Northwestern University, Evanston, IL 60208, USA.
[Ti] Título:Increased Prevalence of Calcium Transients across the Dendritic Arbor during Place Field Formation.
[So] Source:Neuron;96(2):490-504.e5, 2017 Oct 11.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hippocampal place cell ensembles form a cognitive map of space during exposure to novel environments. However, surprisingly little evidence exists to support the idea that synaptic plasticity in place cells is involved in forming new place fields. Here we used high-resolution functional imaging to determine the signaling patterns in CA1 soma, dendrites, and axons associated with place field formation when mice are exposed to novel virtual environments. We found that putative local dendritic spikes often occur prior to somatic place field firing. Subsequently, the first occurrence of somatic place field firing was associated with widespread regenerative dendritic events, which decreased in prevalence with increased novel environment experience. This transient increase in regenerative events was likely facilitated by a reduction in dendritic inhibition. Since regenerative dendritic events can provide the depolarization necessary for Hebbian potentiation, these results suggest that activity-dependent synaptic plasticity underlies the formation of many CA1 place fields.
[Mh] Termos MeSH primário: Potenciais de Ação/fisiologia
Região CA1 Hipocampal/metabolismo
Cálcio/metabolismo
Dendritos/metabolismo
Locomoção/fisiologia
Plasticidade Neuronal/fisiologia
[Mh] Termos MeSH secundário: Animais
Região CA1 Hipocampal/química
Região CA1 Hipocampal/citologia
Dendritos/química
Masculino
Camundongos
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Técnicas de Cultura de Órgãos
Prevalência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE


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[PMID]:29024666
[Au] Autor:Beutler LR; Chen Y; Ahn JS; Lin YC; Essner RA; Knight ZA
[Ad] Endereço:Department of Medicine, University of California, San Francisco, San Francisco, CA 94158, USA; Kavli Center for Fundamental Neuroscience, University of California, San Francisco, San Francisco, CA 94158, USA.
[Ti] Título:Dynamics of Gut-Brain Communication Underlying Hunger.
[So] Source:Neuron;96(2):461-475.e5, 2017 Oct 11.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Communication between the gut and brain is critical for homeostasis, but how this communication is represented in the dynamics of feeding circuits is unknown. Here we describe nutritional regulation of key neurons that control hunger in vivo. We show that intragastric nutrient infusion rapidly and durably inhibits hunger-promoting AgRP neurons in awake, behaving mice. This inhibition is proportional to the number of calories infused but surprisingly independent of macronutrient identity or nutritional state. We show that three gastrointestinal signals-serotonin, CCK, and PYY-are necessary or sufficient for these effects. In contrast, the hormone leptin has no acute effect on dynamics of these circuits or their sensory regulation but instead induces a slow modulation that develops over hours and is required for inhibition of feeding. These findings reveal how layers of visceral signals operating on distinct timescales converge on hypothalamic feeding circuits to generate a central representation of energy balance.
[Mh] Termos MeSH primário: Química Encefálica/fisiologia
Encéfalo/fisiologia
Comportamento Alimentar/fisiologia
Trato Gastrointestinal/fisiologia
Fome/fisiologia
Rede Nervosa/fisiologia
[Mh] Termos MeSH secundário: Animais
Feminino
Trato Gastrointestinal/química
Trato Gastrointestinal/inervação
Masculino
Camundongos
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Obesos
Camundongos Transgênicos
Rede Nervosa/química
Vias Neurais/química
Vias Neurais/fisiologia
Optogenética/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171119
[Lr] Data última revisão:
171119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE


  9 / 2558 MEDLINE  
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[PMID]:28967909
[Au] Autor:Davis P; Zaki Y; Maguire J; Reijmers LG
[Ad] Endereço:Department of Neuroscience, Tufts University School of Medicine, Boston, Massachusetts, USA.
[Ti] Título:Cellular and oscillatory substrates of fear extinction learning.
[So] Source:Nat Neurosci;20(11):1624-1633, 2017 Nov.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mammalian brain contains dedicated circuits for both the learned expression and suppression of fear. These circuits require precise coordination to facilitate the appropriate expression of fear behavior, but the mechanisms underlying this coordination remain unclear. Using a combination of chemogenetics, activity-based neuronal-ensemble labeling and in vivo electrophysiology, we found that fear extinction learning confers on parvalbumin-expressing (PV) interneurons in the basolateral amygdala (BLA) a dedicated role in the selective suppression of a previously encoded fear memory and BLA fear-encoding neurons. In addition, following extinction learning, PV interneurons enable a competing interaction between a 6-12 Hz oscillation and a fear-associated 3-6 Hz oscillation within the BLA. Loss of this competition increases a 3-6 Hz oscillatory signature, with BLA→medial prefrontal cortex directionality signaling the recurrence of fear expression. The discovery of cellular and oscillatory substrates of fear extinction learning that critically depend on BLA PV interneurons could inform therapies aimed at preventing the pathological recurrence of fear following extinction learning.
[Mh] Termos MeSH primário: Complexo Nuclear Basolateral da Amígdala/fisiologia
Relógios Biológicos/fisiologia
Extinção Psicológica/fisiologia
Medo/fisiologia
Aprendizagem/fisiologia
Córtex Pré-Frontal/fisiologia
[Mh] Termos MeSH secundário: Animais
Complexo Nuclear Basolateral da Amígdala/citologia
Medo/psicologia
Feminino
Masculino
Camundongos
Camundongos da Linhagem 129
Camundongos Transgênicos
Córtex Pré-Frontal/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171003
[St] Status:MEDLINE
[do] DOI:10.1038/nn.4651


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[PMID]:28951447
[Au] Autor:Schecter RW; Maher EE; Welsh CA; Stevens B; Erisir A; Bear MF
[Ad] Endereço:Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139.
[Ti] Título:Experience-Dependent Synaptic Plasticity in V1 Occurs without Microglial CX3CR1.
[So] Source:J Neurosci;37(44):10541-10553, 2017 Nov 01.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brief monocular deprivation (MD) shifts ocular dominance and reduces the density of thalamic synapses in layer 4 of the mouse primary visual cortex (V1). We found that microglial lysosome content is also increased as a result of MD. Previous studies have shown that the microglial fractalkine receptor CX3CR1 is involved in synaptic development and hippocampal plasticity. We therefore tested the hypothesis that neuron-to-microglial communication via CX3CR1 is an essential component of visual cortical development and plasticity in male mice. Our data show that CX3CR1 is not required for normal development of V1 responses to visual stimulation, multiple forms of experience-dependent plasticity, or the synapse loss that accompanies MD in layer 4. By ruling out an essential role for fractalkine signaling, our study narrows the search for understanding how microglia respond to active synapse modification in the visual cortex. Microglia in the visual cortex respond to monocular deprivation with increased lysosome content, but signaling through the fractalkine receptor CX3CR1 is not an essential component in the mechanisms of visual cortical development or experience-dependent synaptic plasticity.
[Mh] Termos MeSH primário: Potenciais Evocados Visuais/fisiologia
Microglia/metabolismo
Plasticidade Neuronal/fisiologia
Receptores de Quimiocinas/deficiência
Córtex Visual/crescimento & desenvolvimento
Córtex Visual/metabolismo
[Mh] Termos MeSH secundário: Animais
Receptor 1 de Quimiocina CX3C
Comunicação Celular/fisiologia
Corpos Geniculados/crescimento & desenvolvimento
Corpos Geniculados/metabolismo
Masculino
Camundongos
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Técnicas de Cultura de Órgãos
Visão Monocular/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CX3C Chemokine Receptor 1); 0 (Cx3cr1 protein, mouse); 0 (Receptors, Chemokine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2679-16.2017



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