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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

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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

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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

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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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