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[PMID]:29248581
[Au] Autor:Zhang T; Hou L; Chen DT; McMahon FJ; Wang JC; Rice JP
[Ad] Endereço:Department of Epidemiology and Biostatistics, School of Public Health, Xi'an Jiaotong University, Shaanxi, China.
[Ti] Título:Exome sequencing of a large family identifies potential candidate genes contributing risk to bipolar disorder.
[So] Source:Gene;645:119-123, 2018 Mar 01.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Bipolar disorder is a mental illness with lifetime prevalence of about 1%. Previous genetic studies have identified multiple chromosomal linkage regions and candidate genes that might be associated with bipolar disorder. The present study aimed to identify potential susceptibility variants for bipolar disorder using 6 related case samples from a four-generation family. A combination of exome sequencing and linkage analysis was performed to identify potential susceptibility variants for bipolar disorder. Our study identified a list of five potential candidate genes for bipolar disorder. Among these five genes, GRID1(Glutamate Receptor Delta-1 Subunit), which was previously reported to be associated with several psychiatric disorders and brain related traits, is particularly interesting. Variants with functional significance in this gene were identified from two cousins in our bipolar disorder pedigree. Our findings suggest a potential role for these genes and the related rare variants in the onset and development of bipolar disorder in this one family. Additional research is needed to replicate these findings and evaluate their patho-biological significance.
[Mh] Termos MeSH primário: Transtorno Bipolar/genética
Polimorfismo de Nucleotídeo Único
Sequenciamento Completo do Exoma/métodos
[Mh] Termos MeSH secundário: Caderinas/genética
Feminino
Redes Reguladoras de Genes
Ligação Genética
Predisposição Genética para Doença
Seres Humanos
Masculino
Proteínas do Tecido Nervoso/genética
Linhagem
Monoéster Fosfórico Hidrolases/genética
Receptores de Glutamato/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDHR1 protein, human); 0 (Cadherins); 0 (Nerve Tissue Proteins); 0 (Receptors, Glutamate); 0 (glutamate receptor delta 1); EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.62 (multiple inositol-polyphosphate phosphatase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180203
[Lr] Data última revisão:
180203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE


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[PMID]:29207948
[Au] Autor:Ali Z; Zulfiqar S; Klar J; Wikström J; Ullah F; Khan A; Abdullah U; Baig S; Dahl N
[Ad] Endereço:Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, BMC Box815, 751 08, Uppsala, Sweden.
[Ti] Título:Homozygous GRID2 missense mutation predicts a shift in the D-serine binding domain of GluD2 in a case with generalized brain atrophy and unusual clinical features.
[So] Source:BMC Med Genet;18(1):144, 2017 12 06.
[Is] ISSN:1471-2350
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Spinocerebellar ataxias comprise a large and heterogeneous group of disorders that may present with isolated ataxia, or ataxia in combination with other neurologic or non-neurologic symptoms. Monoallelic or biallelic GRID2 mutations were recently reported in rare cases with cerebellar syndrome and variable degree of ataxia, ocular symptoms, hypotonia and developmental delay. CASE PRESENTATION: We report on a consanguineous family with autosomal recessive childhood onset of slowly progressive cerebellar ataxia and delayed psychomotor development in three siblings. MRI of an adult and affected family member revealed slightly widened cerebral and cerebellar sulci, suggesting generalized brain atrophy, and mild cerebellar atrophy. Using whole exome sequencing we identified a novel homozygous missense variant [c.2128C > T, p.(Arg710Trp)] in GRID2 that segregates with the disease. The missense variant is located in a conserved region encoding the extracellular serine-binding domain of the GluD2 protein and predicts a change in conformation of the protein. CONCLUSION: The widespread supratentorial brain abnormalities, absence of oculomotor symptoms, increased peripheral muscle tone and the novel missense mutation add to the clinical and genetic variability in GRID2 associated cerebellar syndrome. The neuroradiological findings in our family indicate a generalized neurodegenerative process to be taken into account in other families segregating complex clinical features and GRID2 mutations.
[Mh] Termos MeSH primário: Encéfalo/patologia
Mutação de Sentido Incorreto
Receptores de Glutamato/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Sequência de Aminoácidos
Atrofia
Sequência de Bases
Sítios de Ligação
Encéfalo/diagnóstico por imagem
Ataxia Cerebelar/genética
Cerebelo/diagnóstico por imagem
Cerebelo/patologia
Consanguinidade
Deficiências do Desenvolvimento/genética
Feminino
Homozigoto
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Modelos Moleculares
Linhagem
Conformação Proteica
Domínios Proteicos
Receptores de Glutamato/química
Receptores de Glutamato/metabolismo
Serina/metabolismo
Sequenciamento Completo do Exoma
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Glutamate); 0 (glutamate receptor delta 2); 452VLY9402 (Serine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171231
[Lr] Data última revisão:
171231
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE
[do] DOI:10.1186/s12881-017-0504-6


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[PMID]:28667061
[Au] Autor:Alsharafi WA; Luo Z; Long X; Xie Y; Xiao B
[Ad] Endereço:Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
[Ti] Título:MicroRNA in glutamate receptor-dependent neurological diseases.
[So] Source:Clin Sci (Lond);131(14):1591-1604, 2017 Jul 15.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glutamate-mediated excitotoxicity is the major neuropathological process contributing to numerous neurological diseases. Recently, emerging evidence indicates that microRNAs (miRNAs) play essential roles in the pathophysiology of a wide range of neurological diseases. Notably, there have been significant developments in understanding the biogenesis of miRNAs, their regulatory mechanisms, and their potential as effective biomarkers and therapies. In the present review, we summarize the recent literature that highlights the versatile roles played by miRNAs in glutamate receptor (GluR)-dependent neurological diseases. Based on the reported studies to date, modulation of miRNAs could emerge as a promising therapeutic target for a variety of neurological diseases that were discussed in this review.
[Mh] Termos MeSH primário: MicroRNAs/genética
Doenças do Sistema Nervoso/genética
Receptores de Glutamato/genética
[Mh] Termos MeSH secundário: Biomarcadores/metabolismo
Regulação da Expressão Gênica
Terapia Genética/métodos
Seres Humanos
Terapia de Alvo Molecular/métodos
Doenças do Sistema Nervoso/terapia
Receptores de Glutamato/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (MicroRNAs); 0 (Receptors, Glutamate)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170702
[St] Status:MEDLINE
[do] DOI:10.1042/CS20170964


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[PMID]:28630145
[Au] Autor:Goo MS; Sancho L; Slepak N; Boassa D; Deerinck TJ; Ellisman MH; Bloodgood BL; Patrick GN
[Ad] Endereço:Section of Neurobiology, Division of Biological Sciences, University of California, San Diego, La Jolla, CA.
[Ti] Título:Activity-dependent trafficking of lysosomes in dendrites and dendritic spines.
[So] Source:J Cell Biol;216(8):2499-2513, 2017 Aug 07.
[Is] ISSN:1540-8140
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In neurons, lysosomes, which degrade membrane and cytoplasmic components, are thought to primarily reside in somatic and axonal compartments, but there is little understanding of their distribution and function in dendrites. Here, we used conventional and two-photon imaging and electron microscopy to show that lysosomes traffic bidirectionally in dendrites and are present in dendritic spines. We find that lysosome inhibition alters their mobility and also decreases dendritic spine number. Furthermore, perturbing microtubule and actin cytoskeletal dynamics has an inverse relationship on the distribution and motility of lysosomes in dendrites. We also find trafficking of lysosomes is correlated with synaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type glutamate receptors. Strikingly, lysosomes traffic to dendritic spines in an activity-dependent manner and can be recruited to individual spines in response to local activation. These data indicate the position of lysosomes is regulated by synaptic activity and thus plays an instructive role in the turnover of synaptic membrane proteins.
[Mh] Termos MeSH primário: Dendritos/metabolismo
Espinhas Dendríticas/metabolismo
Hipocampo/metabolismo
Lisossomos/metabolismo
Proteínas de Membrana/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Membranas Sinápticas/metabolismo
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/metabolismo
Animais
Animais Recém-Nascidos
Dendritos/ultraestrutura
Espinhas Dendríticas/ultraestrutura
Feminino
Células HEK293
Hipocampo/ultraestrutura
Seres Humanos
Lisossomos/ultraestrutura
Masculino
Microscopia Eletrônica
Microscopia de Fluorescência por Excitação Multifotônica
Microscopia de Vídeo
Microtúbulos/metabolismo
Desnaturação Proteica
Ratos Sprague-Dawley
Receptores de Glutamato/metabolismo
Receptores de N-Metil-D-Aspartato/metabolismo
Fatores de Tempo
Imagem com Lapso de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Nerve Tissue Proteins); 0 (Receptors, Glutamate); 0 (Receptors, N-Methyl-D-Aspartate); 0 (alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid subtype glutamate receptor, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1083/jcb.201704068


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[PMID]:28628100
[Au] Autor:Geisheker MR; Heymann G; Wang T; Coe BP; Turner TN; Stessman HAF; Hoekzema K; Kvarnung M; Shaw M; Friend K; Liebelt J; Barnett C; Thompson EM; Haan E; Guo H; Anderlid BM; Nordgren A; Lindstrand A; Vandeweyer G; Alberti A; Avola E; Vinci M; Giusto S; Pramparo T; Pierce K; Nalabolu S; Michaelson JJ; Sedlacek Z; Santen GWE; Peeters H; Hakonarson H; Courchesne E; Romano C; Kooy RF; Bernier RA; Nordenskjöld M; Gecz J; Xia K; Zweifel LS; Eichler EE
[Ad] Endereço:Department of Genome Sciences, University of Washington, Seattle, Washington, USA.
[Ti] Título:Hotspots of missense mutation identify neurodevelopmental disorder genes and functional domains.
[So] Source:Nat Neurosci;20(8):1043-1051, 2017 Aug.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although de novo missense mutations have been predicted to account for more cases of autism than gene-truncating mutations, most research has focused on the latter. We identified the properties of de novo missense mutations in patients with neurodevelopmental disorders (NDDs) and highlight 35 genes with excess missense mutations. Additionally, 40 amino acid sites were recurrently mutated in 36 genes, and targeted sequencing of 20 sites in 17,688 patients with NDD identified 21 new patients with identical missense mutations. One recurrent site substitution (p.A636T) occurs in a glutamate receptor subunit, GRIA1. This same amino acid substitution in the homologous but distinct mouse glutamate receptor subunit Grid2 is associated with Lurcher ataxia. Phenotypic follow-up in five individuals with GRIA1 mutations shows evidence of specific learning disabilities and autism. Overall, we find significant clustering of de novo mutations in 200 genes, highlighting specific functional domains and synaptic candidate genes important in NDD pathology.
[Mh] Termos MeSH primário: Sequência de Aminoácidos/genética
Transtorno Autístico/genética
Exoma/genética
Predisposição Genética para Doença
Mutação de Sentido Incorreto/genética
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
Receptores de AMPA/genética
Receptores de Glutamato/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, AMPA); 0 (Receptors, Glutamate); 0 (glutamate receptor ionotropic, AMPA 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE
[do] DOI:10.1038/nn.4589


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[PMID]:28606925
[Au] Autor:Gu Y; Jukkola P; Wang Q; Esparza T; Zhao Y; Brody D; Gu C
[Ad] Endereço:Department of Biological Chemistry and Pharmacology, The Ohio State University, Columbus, OH.
[Ti] Título:Polarity of varicosity initiation in central neuron mechanosensation.
[So] Source:J Cell Biol;216(7):2179-2199, 2017 Jul 03.
[Is] ISSN:1540-8140
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Little is known about mechanical regulation of morphological and functional polarity of central neurons. In this study, we report that mechanical stress specifically induces varicosities in the axons but not the dendrites of central neurons by activating TRPV4, a Ca /Na -permeable mechanosensitive channel. This process is unexpectedly rapid and reversible, consistent with the formation of axonal varicosities in vivo induced by mechanical impact in a mouse model of mild traumatic brain injury. In contrast, prolonged stimulation of glutamate receptors induces varicosities in dendrites but not in axons. We further show that axonal varicosities are induced by persistent Ca increase, disassembled microtubules (MTs), and subsequently reversible disruption of axonal transport, and are regulated by stable tubulin-only polypeptide, an MT-associated protein. Finally, axonal varicosity initiation can trigger action potentials to antidromically propagate to the soma in retrograde signaling. Therefore, our study demonstrates a new feature of neuronal polarity: axons and dendrites preferentially respond to physical and chemical stresses, respectively.
[Mh] Termos MeSH primário: Lesões Encefálicas Traumáticas/metabolismo
Polaridade Celular
Hipocampo/metabolismo
Mecanotransdução Celular
Neurônios/metabolismo
Canais de Cátion TRPV/metabolismo
[Mh] Termos MeSH secundário: Potenciais de Ação
Animais
Axônios/metabolismo
Lesões Encefálicas Traumáticas/patologia
Lesões Encefálicas Traumáticas/fisiopatologia
Sinalização do Cálcio
Dendritos/metabolismo
Modelos Animais de Doenças
Células HEK293
Hipocampo/embriologia
Hipocampo/patologia
Hipocampo/fisiopatologia
Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Microtúbulos/metabolismo
Plasticidade Neuronal
Neurônios/patologia
Estimulação Física
Interferência de RNA
Ratos
Receptores de Glutamato/metabolismo
Estresse Mecânico
Canais de Cátion TRPV/genética
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Nm] Nome de substância:
0 (Receptors, Glutamate); 0 (TRPV Cation Channels); 0 (TRPV4 protein, human); 0 (Trpv4 protein, mouse); 0 (Trpv4 protein, rat)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE
[do] DOI:10.1083/jcb.201606065


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[PMID]:28582391
[Au] Autor:Mesbahi-Vasey S; Veras L; Yonkunas M; Johnson JW; Kurnikova MG
[Ad] Endereço:Department of Chemistry, Carnegie Mellon University, Pittsburgh, Pennsylvania, United States of America.
[Ti] Título:All atom NMDA receptor transmembrane domain model development and simulations in lipid bilayers and water.
[So] Source:PLoS One;12(6):e0177686, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:N-methyl-d-aspartate receptors (NMDARs) are members of the ionotropic glutamate receptor family that mediate excitatory synaptic transmission in the central nervous system. The channels of NMDARs are permeable to Ca2+ but blocked by Mg2+, distinctive properties that underlie essential brain processes such as induction of synaptic plasticity. However, due to limited structural information about the NMDAR transmembrane ion channel forming domain, the mechanism of divalent cation permeation and block is understood poorly. In this paper we developed an atomistic model of the transmembrane domain (TMD) of NMDARs composed of GluN1 and GluN2A subunits (GluN1/2A receptors). The model was generated using (a) a homology model based on the structure of the NaK channel and a partially resolved structure of an AMPA receptor (AMPAR), and (b) a partially resolved X-ray structure of GluN1/2B NMDARs. Refinement and extensive Molecular Dynamics (MD) simulations of the NMDAR TMD model were performed in explicit lipid bilayer membrane and water. Targeted MD with simulated annealing was introduced to promote structure refinement. Putative positions of the Mg2+ and Ca2+ ions in the ion channel divalent cation binding site are proposed. Differences in the structural and dynamic behavior of the channel protein in the presence of Mg2+ or Ca2+ are analyzed. NMDAR protein conformational flexibility was similar with no ion bound to the divalent cation binding site and with Ca2+ bound, whereas Mg2+ binding reduced protein fluctuations. While bound at the binding site both ions retained their preferred ligand coordination numbers: 6 for Mg2+, and 7-8 for Ca2+. Four asparagine side chain oxygens, a back-bone oxygen, and a water molecule participated in binding a Mg2+ ion. The Ca2+ ion first coordination shell ligands typically included four to five side-chain oxygen atoms of the binding site asparagine residues, two water molecules and zero to two backbone oxygens of the GluN2B subunits. These results demonstrate the importance of high-resolution channel structures for elucidation of mechanisms of NMDAR permeation and block.
[Mh] Termos MeSH primário: Asparagina/química
Bicamadas Lipídicas/química
Proteínas do Tecido Nervoso/química
Receptores de N-Metil-D-Aspartato/química
Água/química
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Asparagina/metabolismo
Sítios de Ligação
Cálcio/química
Cálcio/metabolismo
Cátions Bivalentes
Cristalografia por Raios X
Seres Humanos
Bicamadas Lipídicas/metabolismo
Magnésio/química
Magnésio/metabolismo
Camundongos
Simulação de Dinâmica Molecular
Proteínas do Tecido Nervoso/metabolismo
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Multimerização Proteica
Estrutura Secundária de Proteína
Receptores de Glutamato/química
Receptores de Glutamato/metabolismo
Receptores de N-Metil-D-Aspartato/metabolismo
Alinhamento de Sequência
ATPase Trocadora de Sódio-Potássio/química
ATPase Trocadora de Sódio-Potássio/metabolismo
Homologia Estrutural de Proteína
Termodinâmica
Água/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cations, Divalent); 0 (Gprin1 protein, mouse); 0 (Lipid Bilayers); 0 (N-methyl D-aspartate receptor subtype 2A); 0 (Nerve Tissue Proteins); 0 (Receptors, Glutamate); 0 (Receptors, N-Methyl-D-Aspartate); 0 (alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid subtype glutamate receptor, human); 059QF0KO0R (Water); 7006-34-0 (Asparagine); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase); I38ZP9992A (Magnesium); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177686


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[PMID]:28577822
[Au] Autor:Deters KD; Nho K; Risacher SL; Kim S; Ramanan VK; Crane PK; Apostolova LG; Saykin AJ; Alzheimer's Disease Neuroimaging Initiative
[Ad] Endereço:Center for Neuroimaging, Department of Radiology and Imaging Sciences, Indiana University School of Medicine, Indianapolis, IN, USA; Indiana Alzheimer Disease Center, Indiana University School of Medicine, Indianapolis, IN, USA; Program in Medical Neuroscience, Paul and Carole Stark Neurosciences Re
[Ti] Título:Genome-wide association study of language performance in Alzheimer's disease.
[So] Source:Brain Lang;172:22-29, 2017 Sep.
[Is] ISSN:1090-2155
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Language impairment is common in prodromal stages of Alzheimer's disease (AD) and progresses over time. However, the genetic architecture underlying language performance is poorly understood. To identify novel genetic variants associated with language performance, we analyzed brain MRI and performed a genome-wide association study (GWAS) using a composite measure of language performance from the Alzheimer's Disease Neuroimaging Initiative (ADNI; n=1560). The language composite score was associated with brain atrophy on MRI in language and semantic areas. GWAS identified GLI3 (GLI family zinc finger 3) as significantly associated with language performance (p<5×10 ). Enrichment of GWAS association was identified in pathways related to nervous system development and glutamate receptor function and trafficking. Our results, which warrant further investigation in independent and larger cohorts, implicate GLI3, a developmental transcription factor involved in patterning brain structures, as a putative gene associated with language dysfunction in AD.
[Mh] Termos MeSH primário: Doença de Alzheimer/genética
Estudo de Associação Genômica Ampla
Linguagem
[Mh] Termos MeSH secundário: Idoso
Doença de Alzheimer/patologia
Doença de Alzheimer/fisiopatologia
Encéfalo/metabolismo
Encéfalo/patologia
Encéfalo/fisiopatologia
Feminino
Seres Humanos
Fatores de Transcrição Kruppel-Like/genética
Imagem por Ressonância Magnética
Masculino
Proteínas do Tecido Nervoso/genética
Neuroimagem
Sintomas Prodrômicos
Receptores de Glutamato/metabolismo
Proteína Gli3 com Dedos de Zinco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GLI3 protein, human); 0 (Kruppel-Like Transcription Factors); 0 (Nerve Tissue Proteins); 0 (Receptors, Glutamate); 0 (Zinc Finger Protein Gli3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170605
[St] Status:MEDLINE


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[PMID]:28565929
[Au] Autor:Gökçek-Saraç Ç; Er H; Kencebay Manas C; Kantar Gok D; Özen S; Derin N
[Ad] Endereço:a Faculty of Engineering, Department of Biomedical Engineering , Akdeniz University , Antalya , Turkey.
[Ti] Título:Effects of acute and chronic exposure to both 900 MHz and 2100 MHz electromagnetic radiation on glutamate receptor signaling pathway.
[So] Source:Int J Radiat Biol;93(9):980-989, 2017 Sep.
[Is] ISSN:1362-3095
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To demonstrate the molecular effects of acute and chronic exposure to both 900 and 2100 MHz radiofrequency electromagnetic radiation (RF-EMR) on the hippocampal level/activity of some of the enzymes - including PKA, CaMKIIα, CREB, and p44/42 MAPK - from N-methyl-D-aspartate receptor (NMDAR)-related signaling pathways. MATERIALS AND METHODS: Rats were divided into the following groups: sham rats, and rats exposed to 900 and 2100 MHz RF-EMR for 2 h/day for acute (1 week) or chronic (10 weeks), respectively. Western blotting and activity measurement assays were used to assess the level/activity of the selected enzymes. RESULTS: The obtained results revealed that the hippocampal level/activity of selected enzymes was significantly higher in the chronic groups as compared to the acute groups at both 900 and 2100 MHz RF-EMR exposure. In addition, hippocampal level/activity of selected enzymes was significantly higher at 2100 MHz RF-EMR than 900 MHz RF-EMR in both acute and chronic groups. CONCLUSIONS: The present study provides experimental evidence that both exposure duration (1 week versus 10 weeks) and different carrier frequencies (900 vs. 2100 MHz) had different effects on the protein expression of hippocampus in Wistar rats, which might encourage further research on protection against RF-EMR exposure.
[Mh] Termos MeSH primário: Campos Eletromagnéticos
Hipocampo/metabolismo
Hipocampo/efeitos da radiação
Micro-Ondas
Receptores de Glutamato/metabolismo
Transdução de Sinais/efeitos da radiação
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta à Radiação
Masculino
Dose de Radiação
Exposição à Radiação
Ratos
Ratos Wistar
Transdução de Sinais/fisiologia
Fatores de Tempo
Irradiação Corporal Total/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Glutamate)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM; S
[Da] Data de entrada para processamento:170602
[St] Status:MEDLINE
[do] DOI:10.1080/09553002.2017.1337279


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[PMID]:28554889
[Au] Autor:Siu CR; Beshara SP; Jones DG; Murphy KM
[Ad] Endereço:McMaster Integrative Neuroscience Discovery and Study Program, McMaster University, Hamilton, Ontario L8S 4K1, Canada.
[Ti] Título:Development of Glutamatergic Proteins in Human Visual Cortex across the Lifespan.
[So] Source:J Neurosci;37(25):6031-6042, 2017 Jun 21.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Traditionally, human primary visual cortex (V1) has been thought to mature within the first few years of life, based on anatomical studies of synapse formation, and establishment of intracortical and intercortical connections. Human vision, however, develops well beyond the first few years. Previously, we found prolonged development of some GABAergic proteins in human V1 (Pinto et al., 2010). Yet as >80% of synapses in V1 are excitatory, it remains unanswered whether the majority of synapses regulating experience-dependent plasticity and receptive field properties develop late, like their inhibitory counterparts. To address this question, we used Western blotting of postmortem tissue from human V1 (12 female, 18 male) covering a range of ages. Then we quantified a set of postsynaptic glutamatergic proteins (PSD-95, GluA2, GluN1, GluN2A, GluN2B), calculated indices for functional pairs that are developmentally regulated (GluA2:GluN1; GluN2A:GluN2B), and determined interindividual variability. We found early loss of GluN1, prolonged development of PSD-95 and GluA2 into late childhood, protracted development of GluN2A until ∼40 years, and dramatic loss of GluN2A in aging. The GluA2:GluN1 index switched at ∼1 year, but the GluN2A:GluN2B index continued to shift until ∼40 year before changing back to GluN2B in aging. We also identified young childhood as a stage of heightened interindividual variability. The changes show that human V1 develops gradually through a series of five orchestrated stages, making it likely that V1 participates in visual development and plasticity across the lifespan. Anatomical structure of human V1 appears to mature early, but vision changes across the lifespan. This discrepancy has fostered two hypotheses: either other aspects of V1 continue changing, or later changes in visual perception depend on extrastriate areas. Previously, we showed that some GABAergic synaptic proteins change across the lifespan, but most synapses in V1 are excitatory leaving unanswered how they change. So we studied expression of glutamatergic proteins in human V1 to determine their development. Here we report prolonged maturation of glutamatergic proteins, with five stages that map onto life-long changes in human visual perception. Thus, the apparent discrepancy between development of structure and function may be explained by life-long synaptic changes in human V1.
[Mh] Termos MeSH primário: Glutamatos/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Córtex Visual/crescimento & desenvolvimento
Córtex Visual/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Envelhecimento/fisiologia
Criança
Pré-Escolar
Proteína 4 Homóloga a Disks-Large
Feminino
Seres Humanos
Lactente
Recém-Nascido
Peptídeos e Proteínas de Sinalização Intracelular
Masculino
Proteínas de Membrana
Meia-Idade
Rede Nervosa/crescimento & desenvolvimento
Rede Nervosa/metabolismo
Plasticidade Neuronal/fisiologia
Receptores de Glutamato/metabolismo
Sinapses/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DLG4 protein, human); 0 (Disks Large Homolog 4 Protein); 0 (Glutamates); 0 (Intracellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (Nerve Tissue Proteins); 0 (Receptors, Glutamate)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170531
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2304-16.2017



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