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Pesquisa : D12.776.157.530.400.875.750.800 [Categoria DeCS]
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[PMID]:28464817
[Au] Autor:Sigurdsson MI; Saddic L; Heydarpour M; Chang TW; Shekar P; Aranki S; Couper GS; Shernan SK; Muehlschlegel JD; Body SC
[Ad] Endereço:Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital/Harvard Medical School, 75 Francis Street, Boston, MA, 02115, USA. martiningi@gmail.com.
[Ti] Título:Post-operative atrial fibrillation examined using whole-genome RNA sequencing in human left atrial tissue.
[So] Source:BMC Med Genomics;10(1):25, 2017 May 02.
[Is] ISSN:1755-8794
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Both ambulatory atrial fibrillation (AF) and post-operative AF (poAF) are associated with substantial morbidity and mortality. Analyzing the tissue-specific gene expression in the left atrium (LA) can identify novel genes associated with AF and further the understanding of the mechanism by which previously identified genetic variants associated with AF mediate their effects. METHODS: LA free wall samples were obtained intraoperatively immediately prior to mitral valve surgery in 62 Caucasian individuals. Gene expression was quantified on mRNA harvested from these samples using RNA sequencing. An expression quantitative trait loci (eQTL) analysis was performed, comparing gene expression between different genotypes of 1.0 million genetic markers, emphasizing genomic regions and genes associated with AF. RESULTS: Comparison of whole-genome expression between patients who later developed poAF and those who did not identified 23 differentially expressed genes. These included genes associated with the resting membrane potential modified by potassium currents, as well as genes within Wnt signaling and cyclic GMP metabolism. The eQTL analysis identified 16,139 cis eQTL relationships in the LA, including several involving genes and single nucleotide polymorphisms (SNPs) linked to AF. A previous relationship between rs3744029 and MYOZ1 expression was confirmed, and a novel relationship between rs6795970 and the expression of the SCN10A gene was identified. CONCLUSIONS: The current study is the first analysis of the human LA expression landscape using high-throughput RNA sequencing. Several novel genes and variants likely involved in AF pathogenesis were identified, thus furthering the understanding of how variants associated with AF mediate their effects via altered gene expression. TRIAL REGISTRATION: ClinicalTrials.gov ID: NCT00833313 , registered 5. January 2009.
[Mh] Termos MeSH primário: Fibrilação Atrial/genética
Regulação da Expressão Gênica
Predisposição Genética para Doença
Átrios do Coração/metabolismo
Polimorfismo de Nucleotídeo Único
Locos de Características Quantitativas
[Mh] Termos MeSH secundário: Idoso
Fibrilação Atrial/metabolismo
Fibrilação Atrial/fisiopatologia
Proteínas de Transporte/genética
Proteínas de Transporte/metabolismo
GMP Cíclico/metabolismo
Grupo com Ancestrais do Continente Europeu/genética
Feminino
Estudos de Associação Genética
Átrios do Coração/fisiopatologia
Sequenciamento de Nucleotídeos em Larga Escala
Seres Humanos
Masculino
Potenciais da Membrana/genética
Meia-Idade
Proteínas Musculares/genética
Proteínas Musculares/metabolismo
Canal de Sódio Disparado por Voltagem NAV1.8/genética
Canal de Sódio Disparado por Voltagem NAV1.8/metabolismo
Período Pós-Operatório
Análise de Sequência de RNA
Transdução de Sinais/genética
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (MYOZ1 protein, human); 0 (Muscle Proteins); 0 (NAV1.8 Voltage-Gated Sodium Channel); 0 (SCN10A protein, human); H2D2X058MU (Cyclic GMP)
[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:170504
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1186/s12920-017-0270-5


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[PMID]:28510137
[Au] Autor:Dick OE; Krylov BV; Nozdrachev AD
[Ad] Endereço:Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg, 199034, Russia. glazov.holo@mail.ioffe.ru.
[Ti] Título:Possible mechanism of bursting suppression in nociceptive neurons.
[So] Source:Dokl Biochem Biophys;473(1):137-140, 2017 Mar.
[Is] ISSN:1608-3091
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng
[Ab] Resumo:The use of the mathematical model of rat nociceptive neuron membrane allowed us to predict a new mechanism of suppression of ectopic bursting discharges, which arise in neurons of dorsal root ganglia and are one of the causes of neuropathic pain. The treatment with comenic acid leads to switching off the ectopic bursting discharges due to a decrease in the effective charge transferring via the activation gating structure of the slow sodium channels (Na 1.8a). Comenic acid is a drug substance of a new non-opioid analgesic [1] Thus, this analgesic not only reduces the frequency of rhythmic discharges of nociceptive neuron membrane [2] but also it suppresses its ectopic bursting discharges.
[Mh] Termos MeSH primário: Modelos Neurológicos
Nociceptores/citologia
[Mh] Termos MeSH secundário: Ácidos Carboxílicos/farmacologia
Ativação do Canal Iônico/efeitos dos fármacos
Canal de Sódio Disparado por Voltagem NAV1.8/química
Canal de Sódio Disparado por Voltagem NAV1.8/metabolismo
Nociceptores/efeitos dos fármacos
Nociceptores/metabolismo
Pironas/farmacologia
Tetrodotoxina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carboxylic Acids); 0 (NAV1.8 Voltage-Gated Sodium Channel); 0 (Pyrones); 0 (comenic acid); 4368-28-9 (Tetrodotoxin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE
[do] DOI:10.1134/S1607672917020120


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[PMID]:28380690
[Au] Autor:Miller RE; Ishihara S; Bhattacharyya B; Delaney A; Menichella DM; Miller RJ; Malfait AM
[Ad] Endereço:Rush University Medical Center, Chicago, Illinois.
[Ti] Título:Chemogenetic Inhibition of Pain Neurons in a Mouse Model of Osteoarthritis.
[So] Source:Arthritis Rheumatol;69(7):1429-1439, 2017 Jul.
[Is] ISSN:2326-5205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To determine the ability of drugs that activate inhibitory G protein-coupled receptors (GPCRs) expressed in peripheral voltage-gated sodium channel 1.8 (Na 1.8)-positive sensory neurons to control osteoarthritis (OA)-associated pain. METHODS: We used designer receptors exclusively activated by a designer drug (DREADD) technology, which employs engineered GPCRs to activate or inhibit neurons upon binding the synthetic ligand clozapine N-oxide (CNO). Na 1.8-Pdi C57BL/6 mice were generated to express the inhibitory DREADD receptor Pdi in Na 1.8-expressing sensory neurons. Destabilization of the medial meniscus (DMM) surgery was performed in 10-week-old male mice. Four, 8, 12, or 16 weeks after surgery, knee hyperalgesia or hind paw mechanical allodynia was tested. Subsequently, CNO or vehicle was administered, and the effect on pain-related behaviors was measured by a blinded observer. Morphine was used as a control. RESULTS: Immunohistochemistry and electrophysiology confirmed functional expression of the inhibitory DREADD receptor Pdi by Na 1.8-positive sensory neurons. Acute inhibition of Na 1.8-expressing neurons in mice treated with CNO reduced knee hyperalgesia 4 weeks after DMM surgery and reduced mechanical allodynia 8 weeks after DMM surgery. Inhibition had no effect on pain-related behaviors 12 and 16 weeks after DMM surgery. Morphine, a drug that activates GPCRs in the peripheral and central nervous systems, was still effective in the later stage of experimental OA. CONCLUSION: Chemogenetic inhibition of Na 1.8-expressing neurons blocks knee hyperalgesia and mechanical allodynia in early experimental OA, but is no longer efficacious in the later stages. These data indicate that activation of inhibitory GPCRs located solely outside the central nervous system may be ineffective in treating chronic OA pain.
[Mh] Termos MeSH primário: Artralgia/fisiopatologia
Artrite Experimental/fisiopatologia
Comportamento Animal/efeitos dos fármacos
Clozapina/análogos & derivados
Hiperalgesia/fisiopatologia
Inibição Neural/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Osteoartrite do Joelho/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Artrite Experimental/patologia
Clozapina/farmacologia
Modelos Animais de Doenças
Imunofluorescência
Gânglios Espinais/citologia
Imuno-Histoquímica
Articulação do Joelho/patologia
Masculino
Meniscos Tibiais/cirurgia
Camundongos
Canal de Sódio Disparado por Voltagem NAV1.8/metabolismo
Neurônios/metabolismo
Neurônios/fisiologia
Osteoartrite do Joelho/patologia
Técnicas de Patch-Clamp
Receptores Acoplados a Proteínas-G/metabolismo
Medula Espinal/metabolismo
Medula Espinal/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NAV1.8 Voltage-Gated Sodium Channel); 0 (Receptors, G-Protein-Coupled); 0 (Scn10a protein, mouse); J60AR2IKIC (Clozapine); MZA8BK588J (clozapine N-oxide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.1002/art.40118


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[PMID]:28326938
[Au] Autor:Nencini S; Ringuet M; Kim DH; Chen YJ; Greenhill C; Ivanusic JJ
[Ad] Endereço:Department of Anatomy and Neuroscience, University of Melbourne, Melbourne, Australia.
[Ti] Título:Mechanisms of nerve growth factor signaling in bone nociceptors and in an animal model of inflammatory bone pain.
[So] Source:Mol Pain;13:1744806917697011, 2017 Jan.
[Is] ISSN:1744-8069
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sequestration of nerve growth factor has been used successfully in the management of pain in animal models of bone disease and in human osteoarthritis. However, the mechanisms of nerve growth factor-induced bone pain and its role in modulating inflammatory bone pain remain to be determined. In this study, we show that nerve growth factor receptors (TrkA and p75) and some other nerve growth factor-signaling molecules (TRPV1 and Nav1.8, but not Nav1.9) are expressed in substantial proportions of rat bone nociceptors. We demonstrate that nerve growth factor injected directly into rat tibia rapidly activates and sensitizes bone nociceptors and produces acute behavioral responses with a similar time course. The nerve growth factor-induced changes in the activity and sensitivity of bone nociceptors we report are dependent on signaling through the TrkA receptor, but are not affected by mast cell stabilization. We failed to show evidence for longer term changes in expression of TrkA, TRPV1, Nav1.8 or Nav1.9 in the soma of bone nociceptors in a rat model of inflammatory bone pain. Thus, retrograde transport of NGF/TrkA and increased expression of some of the common nerve growth factor signaling molecules do not appear to be important for the maintenance of inflammatory bone pain. The findings are relevant to understand the basis of nerve growth factor sequestration and other therapies directed at nerve growth factor signaling, in managing pain in bone disease.
[Mh] Termos MeSH primário: Osso e Ossos/metabolismo
Fator de Crescimento Neural/metabolismo
Nociceptores/metabolismo
Osteoartrite/complicações
Dor/etiologia
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Anticorpos/farmacologia
Osso e Ossos/patologia
Peptídeo Relacionado com Gene de Calcitonina/metabolismo
Modelos Animais de Doenças
Adjuvante de Freund/toxicidade
Masculino
Canal de Sódio Disparado por Voltagem NAV1.8/metabolismo
Canal de Sódio Disparado por Voltagem NAV1.9/metabolismo
Fator de Crescimento Neural/farmacologia
Osteoartrite/induzido quimicamente
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/efeitos dos fármacos
Substância P/metabolismo
Canais de Cátion TRPV/imunologia
Canais de Cátion TRPV/metabolismo
Ubiquitina Tiolesterase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (NAV1.8 Voltage-Gated Sodium Channel); 0 (NAV1.9 Voltage-Gated Sodium Channel); 0 (Scn10a protein, rat); 0 (Scn11a protein, rat); 0 (TRPV Cation Channels); 0 (Trpv1 protein, rat); 33507-63-0 (Substance P); 83652-28-2 (Calcitonin Gene-Related Peptide); 9007-81-2 (Freund's Adjuvant); 9061-61-4 (Nerve Growth Factor); EC 3.4.19.12 (UCHL1 protein, rat); EC 3.4.19.12 (Ubiquitin Thiolesterase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE
[do] DOI:10.1177/1744806917697011


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[PMID]:28166971
[Au] Autor:Chauhan DS; Swain DK; Shah N; Yadav HP; Nakade UP; Singh VK; Nigam R; Yadav S; Garg SK
[Ad] Endereço:College of Biotechnology, UP Pandit Deendayal Upadhayaya Pashu Chikitsa Vigyan Vishwavidyalaya Evam Go Anusandhan Sansthan, Mathura, 281001, Uttar Pradesh, India.
[Ti] Título:Functional and molecular characterization of voltage gated sodium channel Na 1.8 in bull spermatozoa.
[So] Source:Theriogenology;90:210-218, 2017 Mar 01.
[Is] ISSN:1879-3231
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of our study was to characterize the voltage gated sodium channel Na 1.8 in bull spermatozoa. Forty ejaculates were collected from four Hariana bulls and semen samples were pooled in view of the nonsignificant variations between different ejaculates. Functional characterization was undertaken using A-803467, a selective blocker of Na 1.8, and veratridine as an opener of the voltage gated sodium channels while molecular characterization was done using western blotting and indirect immunofluorescence assays. In vitro capacitation was induced using heparin, and to study the functional involvement of Na 1.8 in regulation of capacitation induced hyper sperm motility, A-803467 was used. Selective blocking of Na 1.8 by A-803467 at 6 and 8 µM concentration significantly (P < 0.05) decreased the forward progressive sperm motility in a time-dependent manner, while, blocking at higher concentrations (10 and 15 µM) resulted in fast forward motility in spermatozoa after 2 h of incubation and it was observed up to 3 h. Treatment of sperm cells with veratridine (6, 8, 10, 15, 20 µM) resulted in concentration- and time-dependent increase in forward progressive sperm motility and it persisted up to 4 h. However, hyperactive motility was induced by veratridine at higher concentrations (10 and 15 µM) after 2 h of incubation. In vitro capacitated spermatozoa treated with A-803467 revealed significant (P < 0.05) reduction in forward progressive motility after 2 h of incubation. Both A-803467 and veratridine altered the percentage of spermatozoa showing high mitochondrial transmembrane potential in concentration- and time-dependent manner. High concentrations (10 and 15 µM) of A-803467 and veratridine resulted in bent neck condition in spermatozoa along with significant (P < 0.05) reduction in membrane integrity (HOST negative). Immunoblot revealed the presence of a single protein band of 260 kDa molecular weight along with positive immunoreactivity (IR) in head, neck, middle piece and tail of the spermatozoa. Strongest IR was observed in the neck and middle piece whereas weak IR was observed in tail and acrosomal region of the spermatozoa. Results of our present study evidently revealed the presence of voltage gated sodium channel Na 1.8 in bull spermatozoa and its functional involvement in regulation of spermatozoa dynamics in terms of motility, membrane integrity, acrosome integrity, capacitation and mitochondrial transmembrane potential. Further studies are warranted to unravel their mechanistic pathways and/or their interaction with other ion channels in regulating sperm dynamics.
[Mh] Termos MeSH primário: Canal de Sódio Disparado por Voltagem NAV1.8/metabolismo
Espermatozoides/metabolismo
[Mh] Termos MeSH secundário: Compostos de Anilina/farmacologia
Animais
Western Blotting
Bovinos
Furanos/farmacologia
Masculino
Potenciais da Membrana
Mitocôndrias/fisiologia
Capacitação Espermática/efeitos dos fármacos
Motilidade Espermática/efeitos dos fármacos
Espermatozoides/efeitos dos fármacos
Veratridina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (A 803467); 0 (Aniline Compounds); 0 (Furans); 0 (NAV1.8 Voltage-Gated Sodium Channel); 71-62-5 (Veratridine)
[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:170208
[St] Status:MEDLINE


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[PMID]:28115479
[Au] Autor:Su C; Schwarz TL
[Ad] Endereço:The F.M. Kirby Neurobiology Center, Boston Children's Hospital, and.
[Ti] Título:-GlcNAc Transferase Is Essential for Sensory Neuron Survival and Maintenance.
[So] Source:J Neurosci;37(8):2125-2136, 2017 Feb 22.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:-GlcNAc transferase (OGT) regulates a wide range of cellular processes through the addition of the GlcNAc sugar moiety to thousands of protein substrates. Because nutrient availability affects the activity of OGT, its role has been broadly studied in metabolic tissues. OGT is enriched in the nervous system, but little is known about its importance in basic neuronal processes Here, we show that OGT is essential for sensory neuron survival and maintenance in mice. Sensory neuron-specific knock-out of OGT results in behavioral hyposensitivity to thermal and mechanical stimuli accompanied by decreased epidermal innervation and cell-body loss in the dorsal root ganglia. These effects are observed early in postnatal development and progress as animals age. Cultured sensory neurons lacking OGT also exhibit decreased axonal outgrowth. The effects on neuronal health are not solely due to disruption of developmental processes, because inducing OGT knock-out in the sensory neurons of adult mice results in a similar decrease in nerve fiber endings and cell bodies. Significant nerve-ending loss occurs before a decrease in cell bodies; this phenotype is indicative of axonal dieback that progresses to neuronal death. Our findings demonstrate that OGT is important in regulating axonal maintenance in the periphery and the overall health and survival of sensory neurons. We show the importance of -GlcNAc transferase (OGT) for sensory neuron health and survival This study is the first to find that loss of OGT results in neuronal cell death. Moreover, it suggests that aberrant GlcNAc signaling can contribute to the development of neuropathy. The sensory neurons lie outside of the blood-brain barrier and therefore, compared to central neurons, may have a greater need for mechanisms of metabolic sensing and compensation. Peripheral sensory neurons in particular are subject to degeneration in diabetes. Our findings provide a foundation for understanding the role of OGT under normal physiological conditions in the peripheral nervous system. This knowledge will be important for gaining greater insight into such disease states as diabetic neuropathy.
[Mh] Termos MeSH primário: N-Acetilglucosaminiltransferases/metabolismo
Células Receptoras Sensoriais/fisiologia
[Mh] Termos MeSH secundário: Animais
Peso Corporal/genética
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/genética
Células Cultivadas
Gânglios Espinais/citologia
Regulação da Expressão Gênica/genética
Teste de Tolerância a Glucose
Locomoção/genética
Masculino
Transtornos Mentais/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Força Muscular/genética
N-Acetilglucosaminiltransferases/deficiência
Canal de Sódio Disparado por Voltagem NAV1.8/genética
Canal de Sódio Disparado por Voltagem NAV1.8/metabolismo
Plasticidade Neuronal/genética
Sensação Térmica/genética
Fator de Transcrição Brn-3A/genética
Fator de Transcrição Brn-3A/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NAV1.8 Voltage-Gated Sodium Channel); 0 (Pou4f1 protein, mouse); 0 (Scn10a protein, mouse); 0 (Transcription Factor Brn-3A); EC 2.4.1.- (N-Acetylglucosaminyltransferases); EC 2.4.1.- (O-GlcNAc transferase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170125
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3384-16.2017


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[PMID]:27984182
[Au] Autor:Smith BJ; Côté PD; Tremblay F
[Ad] Endereço:Department of Biology, Dalhousie University, 1355 Oxford St., PO Box 15000, Halifax, NS B3H 4R2, Canada. Electronic address: BN948751@dal.ca.
[Ti] Título:Contribution of Na 1.8 sodium channels to retinal function.
[So] Source:Neuroscience;340:279-290, 2017 Jan 06.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We examined the contribution of the sodium channel isoform Na 1.8 to retinal function using the specific blocker A803467. We found that A803467 has little influence on the electroretinogram (ERG) a- and b-waves, but significantly reduces the oscillatory potentials (OPs) to 40-60% of their original amplitude, with significant changes in implicit time in the rod-driven range. To date, only two cell types were found in mouse to express Na 1.8; the starburst amacrine cells (SBACs), and a subtype of retinal ganglion cells (RGCs). When we recorded light responses from ganglion cells using a multielectrode array we found significant and opposing changes in two physiological groups of RGCs. ON-sustained cells showed significant decreases while transient ON-OFF cells showed significant increases. The effects on ON-OFF transient cells but not ON-sustained cells disappeared in the presence of an inhibitory cocktail. We have previously shown that RGCs have only a minor contribution to the OPs (Smith et al., 2014), therefore suggesting that SBACs might be a significant contributor to this ERG component. Targeting SBACs with the cholinergic neurotoxin ethylcholine mustard aziridinium (AF64A) caused a reduction in the amplitude of the OPs similar to A803467. Our results, both using the ERG and MEA recordings from RGCs, suggest that Na 1.8 plays a role in modulating specific aspects of the retinal physiology and that SBACs are a fundamental cellular contributor to the OPs in mice, a clear demonstration of the dichotomy between ERG b-wave and OPs.
[Mh] Termos MeSH primário: Canal de Sódio Disparado por Voltagem NAV1.8/metabolismo
Retina/metabolismo
Visão Ocular/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Potenciais de Ação/fisiologia
Compostos de Anilina/farmacologia
Animais
Aziridinas/farmacologia
Colina/análogos & derivados
Colina/farmacologia
Antagonistas Colinérgicos/farmacologia
Eletrorretinografia
Furanos/farmacologia
Glicinérgicos/farmacologia
Camundongos Endogâmicos C57BL
Microeletrodos
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Periodicidade
Estimulação Luminosa
Retina/efeitos dos fármacos
Bloqueadores dos Canais de Sódio/farmacologia
Estricnina/farmacologia
Técnicas de Cultura de Tecidos
Visão Ocular/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (A 803467); 0 (Aniline Compounds); 0 (Aziridines); 0 (Cholinergic Antagonists); 0 (Furans); 0 (Glycine Agents); 0 (NAV1.8 Voltage-Gated Sodium Channel); 0 (Scn10a protein, mouse); 0 (Sodium Channel Blockers); A668M9E227 (ethylcholine aziridinium); H9Y79VD43J (Strychnine); N91BDP6H0X (Choline)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161217
[St] Status:MEDLINE


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[PMID]:27272739
[Au] Autor:Zhang L; Zhou F; Huang L; Wu Q; Zheng J; Wu Y; Yin K; Cheng J
[Ad] Endereço:Department of Forensic Pathology, Zhongshan School of Medicine, Sun Yat-sen University, No. 74, Zhongshan 2nd Road, Guangzhou, Guangdong, 510080, China.
[Ti] Título:Association of common and rare variants of SCN10A gene with sudden unexplained nocturnal death syndrome in Chinese Han population.
[So] Source:Int J Legal Med;131(1):53-60, 2017 Jan.
[Is] ISSN:1437-1596
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Sudden unexplained nocturnal death syndrome (SUNDS) remains an autopsy negative entity with unknown etiology to both forensic pathologists and physicians. The electrocardiogram (ECG) characteristics and clinical phenotype of SUNDS survivors strongly suggest that SUNDS shares some similarities with Brugada syndrome (BrS). Recently, the variants of sodium channel Na 1.8 coding gene SCN10A were identified to be associated with BrS. Here, we investigated the association of SCN10A gene variants with 105 sporadic SUNDS victims and 22 BrS cases in the Chinese Han population. A total of 6 rare mutations and 16 polymorphisms were detected in SUNDS victims. Of the six rare mutations, two were putative pathogenic mutations (F386C and R1263*), one was a likely pathogenic mutation (R14H), and the other three were predicted as benign (R817Q, T1181M, and P1683S). As for the 16 polymorphisms, 1 was a novel polymorphism (c.4144-84G>A) located in intron 24, and the rest were reported previously including one polymorphism (c.2884A>G [I962V]) which showed a statistically significant difference in allele frequency (p = 0.044) between SUNDS and the control group. There were also 5 rare mutations and 15 polymorphisms detected in BrS cases. This is the first report of common and rare variants of SCN10A gene in SUNDS and BrS in the Chinese Han population, which provides the genetic epidemiological evidence that SCN10A may be a novel susceptibility gene for SUNDS and account for approximately 3 % of SUNDS in China.
[Mh] Termos MeSH primário: Códon sem Sentido
Morte Súbita/etiologia
Mutação de Sentido Incorreto
Canal de Sódio Disparado por Voltagem NAV1.8/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Adolescente
Adulto
Síndrome de Brugada/genética
China
Grupos Étnicos/genética
Frequência do Gene
Predisposição Genética para Doença
Genótipo
Seres Humanos
Meia-Idade
Reação em Cadeia da Polimerase
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Codon, Nonsense); 0 (NAV1.8 Voltage-Gated Sodium Channel); 0 (SCN10A protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160609
[St] Status:MEDLINE
[do] DOI:10.1007/s00414-016-1397-1


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[PMID]:27916453
[Au] Autor:Han Q; Kim YH; Wang X; Liu D; Zhang ZJ; Bey AL; Lay M; Chang W; Berta T; Zhang Y; Jiang YH; Ji RR
[Ad] Endereço:Department of Anesthesiology, Duke University Medical Center, Durham, NC 27710, USA.
[Ti] Título:SHANK3 Deficiency Impairs Heat Hyperalgesia and TRPV1 Signaling in Primary Sensory Neurons.
[So] Source:Neuron;92(6):1279-1293, 2016 Dec 21.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Abnormal pain sensitivity is commonly associated with autism spectrum disorders (ASDs) and affects the life quality of ASD individuals. SHANK3 deficiency was implicated in ASD and pain dysregulation. Here, we report functional expression of SHANK3 in mouse dorsal root ganglion (DRG) sensory neurons and spinal cord presynaptic terminals. Homozygous and heterozygous Shank3 complete knockout (Δe4-22) results in impaired heat hyperalgesia in inflammatory and neuropathic pain. Specific deletion of Shank3 in Nav1.8-expressing sensory neurons also impairs heat hyperalgesia in homozygous and heterozygous mice. SHANK3 interacts with transient receptor potential subtype V1 (TRPV1) via Proline-rich region and regulates TRPV1 surface expression. Furthermore, capsaicin-induced spontaneous pain, inward currents in DRG neurons, and synaptic currents in spinal cord neurons are all reduced after Shank3 haploinsufficiency. Finally, partial knockdown of SHANK3 expression in human DRG neurons abrogates TRPV1 function. Our findings reveal a peripheral mechanism of SHANK3, which may underlie pain deficits in SHANK3-related ASDs.
[Mh] Termos MeSH primário: Hiperalgesia/genética
Proteínas do Tecido Nervoso/genética
Dor/genética
Terminações Pré-Sinápticas/metabolismo
Células Receptoras Sensoriais/metabolismo
Canais de Cátion TRPV/metabolismo
[Mh] Termos MeSH secundário: Animais
Comportamento Animal
Western Blotting
Capsaicina/toxicidade
Gânglios Espinais/citologia
Seres Humanos
Hiperalgesia/metabolismo
Imuno-Histoquímica
Inflamação/genética
Inflamação/metabolismo
Camundongos
Camundongos Knockout
Canal de Sódio Disparado por Voltagem NAV1.8/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Neuralgia/genética
Neuralgia/metabolismo
Dor/induzido quimicamente
Dor/metabolismo
Técnicas de Patch-Clamp
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fármacos do Sistema Sensorial/toxicidade
Medula Espinal/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NAV1.8 Voltage-Gated Sodium Channel); 0 (Nerve Tissue Proteins); 0 (SHANK3 protein, human); 0 (Scn10a protein, mouse); 0 (Sensory System Agents); 0 (Shank3 protein, mouse); 0 (TRPV Cation Channels); 0 (TRPV1 protein, human); 0 (TRPV1 protein, mouse); S07O44R1ZM (Capsaicin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161206
[St] Status:MEDLINE


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[PMID]:27822503
[Au] Autor:Yuan X; Huang Y; Shah S; Wu H; Gautron L
[Ad] Endereço:Division of Hypothalamic Research and Department of Internal Medicine, The University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, Texas 75390; Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
[Ti] Título:Levels of Cocaine- and Amphetamine-Regulated Transcript in Vagal Afferents in the Mouse Are Unaltered in Response to Metabolic Challenges.
[So] Source:eNeuro;3(5), 2016 Sep-Oct.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cocaine- and amphetamine-regulated transcript (CART) is one of the most abundant neuropeptides in vagal afferents, including those involved in regulating feeding. Recent observations indicate that metabolic challenges dramatically alter the neuropeptidergic profile of CART-producing vagal afferents. Here, using confocal microscopy, we reassessed the distribution and regulation of CART(55-102) immunoreactivity in vagal afferents of the male mouse in response to metabolic challenges, including fasting and high-fat-diet feeding. Importantly, the perikarya and axons of vagal C-fibers were labeled using mice expressing channelrodhopsin-2 (ChR2-YFP) in Na 1.8-Cre-expressing neurons. In these mice, approximately 82% of the nodose ganglion neurons were labeled with ChR2-YFP. Furthermore, ChR2-YFP-labeled axons could easily be identified in the dorsovagal complex. CART(55-102) immunoreactivity was observed in 55% of the ChR2-YFP-labeled neurons in the nodose ganglion and 22% of the ChR2-YFP-labeled varicosities within the area postrema of fed, fasted, and obese mice. The distribution of positive profiles was also identical across the full range of CART staining in fed, fasted, and obese mice. In contrast to previous studies, fasting did not induce melanin-concentrating hormone (MCH) immunoreactivity in vagal afferents. Moreover, prepro-MCH mRNA was undetectable in the nodose ganglion of fasted mice. In summary, this study showed that the perikarya and central terminals of vagal afferents are invariably enriched in CART and devoid of MCH.
[Mh] Termos MeSH primário: Ingestão de Alimentos/fisiologia
Jejum/fisiologia
Proteínas do Tecido Nervoso/metabolismo
Neurônios Aferentes/metabolismo
Obesidade/metabolismo
Nervo Vago/metabolismo
[Mh] Termos MeSH secundário: Animais
Trato Gastrointestinal/inervação
Trato Gastrointestinal/metabolismo
Trato Gastrointestinal/patologia
Expressão Gênica
Hormônios Hipotalâmicos/metabolismo
Masculino
Melaninas/metabolismo
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Canal de Sódio Disparado por Voltagem NAV1.8/metabolismo
Neurônios Aferentes/patologia
Gânglio Nodoso/metabolismo
Gânglio Nodoso/patologia
Obesidade/patologia
Hormônios Hipofisários/metabolismo
RNA Mensageiro/metabolismo
Ratos Zucker
Nervo Vago/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypothalamic Hormones); 0 (Melanins); 0 (NAV1.8 Voltage-Gated Sodium Channel); 0 (Nerve Tissue Proteins); 0 (Pituitary Hormones); 0 (RNA, Messenger); 0 (Scn10a protein, mouse); 0 (cocaine- and amphetamine-regulated transcript protein); 67382-96-1 (melanin-concentrating hormone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161109
[St] Status:MEDLINE



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