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[PMID]:29045497
[Au] Autor:Krzyzanowska W; Pomierny B; Bystrowska B; Pomierny-Chamiolo L; Filip M; Budziszewska B; Pera J
[Ad] Endereço:Department of Biochemical Toxicology, Faculty of Pharmacy, Jagiellonian University Medical College, Kraków, Poland.
[Ti] Título:Ceftriaxone- and N-acetylcysteine-induced brain tolerance to ischemia: Influence on glutamate levels in focal cerebral ischemia.
[So] Source:PLoS One;12(10):e0186243, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:One of the major players in the pathophysiology of cerebral ischemia is disrupted homeostasis of glutamatergic neurotransmission, resulting in elevated extracellular glutamate (Glu) concentrations and excitotoxicity-related cell death. In the brain, Glu concentrations are regulated by Glu transporters, including Glu transporter-1 (GLT-1) and cystine/Glu antiporter (system xc-). Modulation of these transporters by administration of ceftriaxone (CEF, 200 mg/kg, i.p.) or N-acetylcysteine (NAC, 150 mg/kg, i.p.) for 5 days before focal cerebral ischemia may induce brain tolerance to ischemia by significantly limiting stroke-related damage and normalizing Glu concentrations. In the present study, focal cerebral ischemia was induced by 90-minute middle cerebral artery occlusion (MCAO). We compared the effects of CEF and NAC pretreatment on Glu concentrations in extracellular fluid and cellular-specific expression of GLT-1 and xCT with the effects of two reference preconditioning methods, namely, ischemic preconditioning and chemical preconditioning in rats. Both CEF and NAC significantly reduced Glu levels in the frontal cortex and hippocampus during focal cerebral ischemia, and this decrease was comparable with the Glu level achieved with the reference preconditioning strategies. The results of immunofluorescence staining of GLT-1 and xCT on astrocytes, neurons and microglia accounted for the observed changes in extracellular Glu levels to a certain extent. Briefly, after MCAO, the expression of GLT-1 on astrocytes decreased, but pretreatment with CEF seemed to prevent this downregulation. In addition, every intervention used in this study seemed to reduce xCT expression on astrocytes and neurons. The results of this study indicate that modulation of Glu transporter expression may restore Glu homeostasis. Moreover, our results suggest that CEF and NAC may induce brain tolerance to ischemia by influencing GLT-1 and system xc- expression levels. These transporters are presumably good targets for the development of novel therapies for brain ischemia.
[Mh] Termos MeSH primário: Sistemas de Transporte de Aminoácidos Acídicos/genética
Isquemia Encefálica/tratamento farmacológico
Transportador 2 de Aminoácido Excitatório/genética
Ácido Glutâmico/metabolismo
[Mh] Termos MeSH secundário: Acetilcisteína/administração & dosagem
Animais
Astrócitos/efeitos dos fármacos
Astrócitos/metabolismo
Isquemia Encefálica/genética
Isquemia Encefálica/patologia
Ceftriaxona/administração & dosagem
Lobo Frontal/efeitos dos fármacos
Lobo Frontal/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Hipocampo/efeitos dos fármacos
Hipocampo/metabolismo
Seres Humanos
Infarto da Artéria Cerebral Média
Ratos
Transmissão Sináptica/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Transport Systems, Acidic); 0 (Excitatory Amino Acid Transporter 2); 0 (Slc1a2 protein, rat); 0 (xCT protein, rat); 3KX376GY7L (Glutamic Acid); 75J73V1629 (Ceftriaxone); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186243


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[PMID]:28931644
[Au] Autor:Hamilton EMC; Bertini E; Kalaydjieva L; Morar B; Dojcáková D; Liu J; Vanderver A; Curiel J; Persoon CM; Diodato D; Pinelli L; van der Meij NL; Plecko B; Blaser S; Wolf NI; Waisfisz Q; Abbink TEM; van der Knaap MS; Recessive H-ABC Research Group
[Ad] Endereço:From the Department of Child Neurology (E.M.C.H., N.I.W., T.E.M.A., M.S.v.d.K.), Amsterdam Neuroscience (E.M.C.H., N.I.W., T.E.M.A., M.S.v.d.K.), Department of Clinical Genetics (C.M.P., Q.W.), Department of Functional Genomics, Center for Neurogenomics and Cognitive Research (M.S.v.d.K.), VU Univer
[Ti] Título: founder mutation in the Roma population causes recessive variant of H-ABC.
[So] Source:Neurology;89(17):1821-1828, 2017 Oct 24.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To identify the gene defect in patients with hypomyelination with atrophy of the basal ganglia and cerebellum (H-ABC) who are negative for mutations. METHODS: We performed homozygosity mapping and whole exome sequencing (WES) to detect the disease-causing variant. We used a Taqman assay for population screening. We developed a luciferase reporter construct to investigate the effect of the promoter mutation on expression. RESULTS: Sixteen patients from 14 families from different countries fulfilling the MRI criteria for H-ABC exhibited a similar, severe clinical phenotype, including lack of development and a severe epileptic encephalopathy. The majority of patients had a known Roma ethnic background. Single nucleotide polymorphism array analysis in 5 patients identified one large overlapping homozygous region on chromosome 13. WES in 2 patients revealed a homozygous deletion in the promoter region of . Sanger sequencing confirmed homozygosity for this variant in all 16 patients. All patients shared a common haplotype, indicative of a founder effect. Screening of 1,000 controls from different European Roma panels demonstrated an overall carrier rate of the mutation of 3%-25%. Transfection assays showed that the deletion significantly reduced expression in specific CNS cell lines. CONCLUSIONS: encodes ubiquitin-fold modifier 1 (UFM1), a member of the ubiquitin-like family involved in posttranslational modification of proteins. Its exact biological role is unclear. This study associates a gene defect with a disease and sheds new light on possible UFM1 functional networks.
[Mh] Termos MeSH primário: Sistemas de Transporte de Aminoácidos Acídicos/deficiência
Antiporters/deficiência
Gânglios da Base/patologia
Cerebelo/patologia
Doenças Desmielinizantes Hereditárias do Sistema Nervoso Central/genética
Doenças Mitocondriais/genética
Polimorfismo de Nucleotídeo Único/genética
Proteínas/genética
Transtornos Psicomotores/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Sistemas de Transporte de Aminoácidos Acídicos/genética
Antiporters/genética
Atrofia/etiologia
Gânglios da Base/diagnóstico por imagem
Linhagem Celular Tumoral/patologia
Cerebelo/diagnóstico por imagem
Criança
Pré-Escolar
Análise Mutacional de DNA
Saúde da Família
Feminino
Células HeLa
Doenças Desmielinizantes Hereditárias do Sistema Nervoso Central/complicações
Doenças Desmielinizantes Hereditárias do Sistema Nervoso Central/diagnóstico por imagem
Seres Humanos
Processamento de Imagem Assistida por Computador
Itália
Imagem por Ressonância Magnética
Masculino
Doenças Mitocondriais/complicações
Doenças Mitocondriais/diagnóstico por imagem
Transtornos Psicomotores/complicações
Transtornos Psicomotores/diagnóstico por imagem
Transfecção
Tubulina (Proteína)/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Transport Systems, Acidic); 0 (Antiporters); 0 (Proteins); 0 (TUBB4A protein, human); 0 (Tubulin); 0 (UFM1 protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171105
[Lr] Data última revisão:
171105
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000004578


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[PMID]:28575651
[Au] Autor:Chelban V; Patel N; Vandrovcova J; Zanetti MN; Lynch DS; Ryten M; Botía JA; Bello O; Tribollet E; Efthymiou S; Davagnanam I; Bashiri FA; Wood NW; Rothman JE; Alkuraya FS; Houlden H; SYNAPSE Study Group
[Ad] Endereço:Department of Molecular Neuroscience, University College London, London WC1N 3BG, UK; Department of Neurology and Neurosurgery, Institute of Emergency Medicine, Toma Ciorba 1, 2052 Chisinau, Republic of Moldova. Electronic address: v.chelban@ucl.ac.uk.
[Ti] Título:Mutations in NKX6-2 Cause Progressive Spastic Ataxia and Hypomyelination.
[So] Source:Am J Hum Genet;100(6):969-977, 2017 Jun 01.
[Is] ISSN:1537-6605
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Progressive limb spasticity and cerebellar ataxia are frequently found together in clinical practice and form a heterogeneous group of degenerative disorders that are classified either as pure spastic ataxia or as complex spastic ataxia with additional neurological signs. Inheritance is either autosomal dominant or autosomal recessive. Hypomyelinating features on MRI are sometimes seen with spastic ataxia, but this is usually mild in adults and severe and life limiting in children. We report seven individuals with an early-onset spastic-ataxia phenotype. The individuals come from three families of different ethnic backgrounds. Affected members of two families had childhood onset disease with very slow progression. They are still alive in their 30s and 40s and show predominant ataxia and cerebellar atrophy features on imaging. Affected members of the third family had a similar but earlier-onset presentation associated with brain hypomyelination. Using a combination of homozygozity mapping and exome sequencing, we mapped this phenotype to deleterious nonsense or homeobox domain missense mutations in NKX6-2. NKX6-2 encodes a transcriptional repressor with early high general and late focused CNS expression. Deficiency of its mouse ortholog results in widespread hypomyelination in the brain and optic nerve, as well as in poor motor coordination in a pattern consistent with the observed human phenotype. In-silico analysis of human brain expression and network data provides evidence that NKX6-2 is involved in oligodendrocyte maturation and might act within the same pathways of genes already associated with central hypomyelination. Our results support a non-redundant developmental role of NKX6-2 in humans and imply that NKX6-2 mutations should be considered in the differential diagnosis of spastic ataxia and hypomyelination.
[Mh] Termos MeSH primário: Sistemas de Transporte de Aminoácidos Acídicos/deficiência
Antiporters/deficiência
Doenças Desmielinizantes Hereditárias do Sistema Nervoso Central/complicações
Doenças Desmielinizantes Hereditárias do Sistema Nervoso Central/genética
Proteínas de Homeodomínio/genética
Deficiência Intelectual/complicações
Deficiência Intelectual/genética
Doenças Mitocondriais/complicações
Doenças Mitocondriais/genética
Espasticidade Muscular/complicações
Espasticidade Muscular/genética
Mutação/genética
Atrofia Óptica/complicações
Atrofia Óptica/genética
Transtornos Psicomotores/complicações
Transtornos Psicomotores/genética
Ataxias Espinocerebelares/complicações
Ataxias Espinocerebelares/genética
[Mh] Termos MeSH secundário: Adulto
Sequência de Aminoácidos
Sistemas de Transporte de Aminoácidos Acídicos/genética
Antiporters/genética
Encéfalo/embriologia
Encéfalo/metabolismo
Criança
Feminino
Redes Reguladoras de Genes
Proteínas de Homeodomínio/química
Seres Humanos
Lactente
Masculino
Linhagem
Fenótipo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Transport Systems, Acidic); 0 (Antiporters); 0 (Homeodomain Proteins); 0 (NKX6-2 protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE


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[PMID]:28495973
[Au] Autor:LaCrosse AL; O'Donovan SM; Sepulveda-Orengo MT; McCullumsmith RE; Reissner KJ; Schwendt M; Knackstedt LA
[Ad] Endereço:Psychology Department, University of Florida, Gainesville, Florida 32611.
[Ti] Título:Contrasting the Role of xCT and GLT-1 Upregulation in the Ability of Ceftriaxone to Attenuate the Cue-Induced Reinstatement of Cocaine Seeking and Normalize AMPA Receptor Subunit Expression.
[So] Source:J Neurosci;37(24):5809-5821, 2017 Jun 14.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Long-term treatment with ceftriaxone attenuates the reinstatement of cocaine seeking while increasing the function of the glutamate transporter 1 (GLT-1) and system xC- (Sxc) in the nucleus accumbens core (NAc). Sxc contributes the majority of nonsynaptic extracellular glutamate in the NAc, while GLT-1 is responsible for the majority of glutamate uptake. Here we used antisense to decrease the expression of GLT-1 and xCT (a catalytic subunit of Sxc) to determine the relative importance of both proteins in mediating the ability of ceftriaxone to prevent cue-induced reinstatement of cocaine seeking and normalize glutamatergic proteins in the NAc of rats. Intra-NAc xCT knockdown prevented ceftriaxone from attenuating reinstatement and from upregulating GLT-1 and resulted in increased surface expression of AMPA receptor subunits GluA1 and GluA2. Intra-NAc GLT-1 knockdown also prevented ceftriaxone from attenuating reinstatement and from upregulating xCT expression, without affecting GluA1 and GluA2 expression. In the absence of cocaine or ceftriaxone treatment, xCT knockdown in the NAc increased the expression of both GluA1 and GluA2 without affecting GLT-1 expression while GLT-1 knockdown had no effect. PCR and immunoprecipitation of GLT-1 revealed that ceftriaxone does not upregulate GLT-1 and xCT through a transcriptional mechanism, and their coregulation by ceftriaxone is not mediated by physical interaction. These data support important and distinct roles for xCT and GLT-1 in the actions of ceftriaxone and add to a body of literature finding evidence for coregulation of these transporters. Our results also point to xCT expression and subsequent basal glutamate levels as being a key mediator of AMPA receptor expression in the NAc. Ceftriaxone attenuates the reinstatement of cocaine, alcohol, and heroin seeking. The mechanism of action of this behavioral effect has been attributed to glutamate transporter 1 (GLT-1) and xCT (a catalytic subunit of Sxc)/Sxc upregulation in the nucleus accumbens core. Here we used an antisense strategy to knock down GLT-1 or xCT in the nucleus accumbens core and examined the behavioral and molecular consequences. While upregulation of both xCT and GLT-1 are essential to the ability of ceftriaxone to attenuate cue-induced reinstatement of cocaine seeking, each protein uniquely affects the expression of other glutamate receptor and transporter proteins. We also report that reducing basal glutamate levels through the manipulation of xCT expression increases the surface expression of AMPA receptor subunits, providing insight to the mechanism by which cocaine alters AMPA surface expression.
[Mh] Termos MeSH primário: Sistemas de Transporte de Aminoácidos Acídicos/metabolismo
Ceftriaxona/administração & dosagem
Transtornos Relacionados ao Uso de Cocaína/metabolismo
Transtornos Relacionados ao Uso de Cocaína/prevenção & controle
Transportador 2 de Aminoácido Excitatório/metabolismo
Núcleo Accumbens/metabolismo
Receptores de AMPA/metabolismo
[Mh] Termos MeSH secundário: Animais
Comportamento de Procura de Droga/efeitos dos fármacos
Masculino
Núcleo Accumbens/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Recidiva
Resultado do Tratamento
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Transport Systems, Acidic); 0 (Excitatory Amino Acid Transporter 2); 0 (Receptors, AMPA); 0 (Slc1a2 protein, rat); 0 (xCT protein, rat); 75J73V1629 (Ceftriaxone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170513
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3717-16.2017


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[PMID]:28436981
[Au] Autor:Cheng L; Duan B; Huang T; Zhang Y; Chen Y; Britz O; Garcia-Campmany L; Ren X; Vong L; Lowell BB; Goulding M; Wang Y; Ma Q
[Ad] Endereço:Institute of Brain Science, the State Key Laboratory of Medical Neurobiology and the Collaborative Innovation Center for Brain Science, Fudan University, Shanghai, China.
[Ti] Título:Identification of spinal circuits involved in touch-evoked dynamic mechanical pain.
[So] Source:Nat Neurosci;20(6):804-814, 2017 Jun.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mechanical hypersensitivity is a debilitating symptom for millions of chronic pain patients. It exists in distinct forms, including brush-evoked dynamic and filament-evoked punctate hypersensitivities. We reduced dynamic mechanical hypersensitivity induced by nerve injury or inflammation in mice by ablating a group of adult spinal neurons defined by developmental co-expression of VGLUT3 and Lbx1 (VT3 neurons): the mice lost brush-evoked nocifensive responses and conditional place aversion. Electrophysiological recordings show that VT3 neurons form morphine-resistant polysynaptic pathways relaying inputs from low-threshold Aß mechanoreceptors to lamina I output neurons. The subset of somatostatin-lineage neurons preserved in VT3 -neuron-ablated mice is largely sufficient to mediate morphine-sensitive and morphine-resistant forms of von Frey filament-evoked punctate mechanical hypersensitivity. Furthermore, acute silencing of VT3 neurons attenuated pre-established dynamic mechanical hypersensitivity induced by nerve injury, suggesting that these neurons may be a cellular target for treating this form of neuropathic pain.
[Mh] Termos MeSH primário: Sistemas de Transporte de Aminoácidos Acídicos/fisiologia
Neurônios/fisiologia
Medula Espinal/fisiologia
Tato/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Potenciais de Ação/fisiologia
Sistemas de Transporte de Aminoácidos Acídicos/biossíntese
Sistemas de Transporte de Aminoácidos Acídicos/genética
Animais
Aprendizagem da Esquiva/fisiologia
Clozapina/farmacologia
Toxina Diftérica/farmacologia
Feminino
Técnicas de Introdução de Genes
Fator de Crescimento Semelhante a EGF de Ligação à Heparina/genética
Hiperalgesia/fisiopatologia
Masculino
Camundongos
Camundongos Transgênicos
Morfina/farmacologia
Proteínas Musculares/biossíntese
Fibras Nervosas Amielínicas/fisiologia
Vias Neurais/efeitos dos fármacos
Vias Neurais/fisiologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Medição da Dor/efeitos dos fármacos
Somatostatina/fisiologia
Medula Espinal/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Transport Systems, Acidic); 0 (Diphtheria Toxin); 0 (Heparin-binding EGF-like Growth Factor); 0 (Lbx1h protein, mouse); 0 (Muscle Proteins); 0 (vesicular glutamate transporter 3, mouse); 51110-01-1 (Somatostatin); 76I7G6D29C (Morphine); J60AR2IKIC (Clozapine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE
[do] DOI:10.1038/nn.4549


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[PMID]:28429368
[Au] Autor:Juaristi I; García-Martín ML; Rodrigues TB; Satrústegui J; Llorente-Folch I; Pardo B
[Ad] Endereço:Departamento de Biología Molecular, Centro de Biología Molecular Severo Ochoa, Universidad Autónoma de Madrid-Consejo Superior de Investigaciones Científicas, Madrid, Spain.
[Ti] Título:ARALAR/AGC1 deficiency, a neurodevelopmental disorder with severe impairment of neuronal mitochondrial respiration, does not produce a primary increase in brain lactate.
[So] Source:J Neurochem;142(1):132-139, 2017 Jul.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:ARALAR/AGC1 (aspartate-glutamate mitochondrial carrier 1) is an important component of the NADH malate-aspartate shuttle (MAS). AGC1-deficiency is a rare disease causing global cerebral hypomyelination, developmental arrest, hypotonia, and epilepsy (OMIM ID #612949); the aralar-KO mouse recapitulates the major findings in humans. This study was aimed at understanding the impact of ARALAR-deficiency in brain lactate levels as a biomarker. We report that lactate was equally abundant in wild-type and aralar-KO mouse brain in vivo at postnatal day 17. We find that lactate production upon mitochondrial blockade depends on up-regulation of lactate formation in astrocytes rather than in neurons. However, ARALAR-deficiency decreased cell respiration in neurons, not astrocytes, which maintained unchanged respiration and lactate production. As the primary site of ARALAR-deficiency is neuronal, this explains the lack of accumulation of brain lactate in ARALAR-deficiency in humans and mice. On the other hand, we find that the cytosolic and mitochondrial components of the glycerol phosphate shuttle are present in astrocytes with similar activities. This suggests that glycerol phosphate shuttle is the main NADH shuttle in astrocytes and explains the absence of effects of ARALAR-deficiency in these cells.
[Mh] Termos MeSH primário: Agrecanas/genética
Agrecanas/metabolismo
Sistemas de Transporte de Aminoácidos Acídicos/deficiência
Antiporters/deficiência
Doenças Desmielinizantes Hereditárias do Sistema Nervoso Central/genética
Ácido Láctico/metabolismo
Mitocôndrias/genética
Mitocôndrias/metabolismo
Doenças Mitocondriais/genética
Doenças do Sistema Nervoso/genética
Doenças do Sistema Nervoso/metabolismo
Neurônios/metabolismo
Transtornos Psicomotores/genética
[Mh] Termos MeSH secundário: Sistemas de Transporte de Aminoácidos Acídicos/genética
Animais
Antiporters/genética
Astrócitos/metabolismo
Química Encefálica/genética
Glucose/metabolismo
Glucosefosfato Desidrogenase/genética
Glucosefosfato Desidrogenase/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Consumo de Oxigênio/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Agc1 protein, mouse); 0 (Aggrecans); 0 (Amino Acid Transport Systems, Acidic); 0 (Antiporters); 33X04XA5AT (Lactic Acid); EC 1.1.1.49 (Glucosephosphate Dehydrogenase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170422
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.14047


  7 / 213 MEDLINE  
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[PMID]:28394324
[Au] Autor:Del Pino I; Brotons-Mas JR; Marques-Smith A; Marighetto A; Frick A; Marín O; Rico B
[Ad] Endereço:Centre for Developmental Neurobiology, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London SE1 1UL, United Kingdom.
[Ti] Título:Abnormal wiring of CCK basket cells disrupts spatial information coding.
[So] Source:Nat Neurosci;20(6):784-792, 2017 Jun.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The function of cortical GABAergic interneurons is largely determined by their integration into specific neural circuits, but the mechanisms controlling the wiring of these cells remain largely unknown. This is particularly true for a major population of basket cells that express the neuropeptide cholecystokinin (CCK). Here we found that the tyrosine kinase receptor ErbB4 was required for the normal integration into cortical circuits of basket cells expressing CCK and vesicular glutamate transporter 3 (VGlut3). The number of inhibitory synapses made by CCK VGlut3 basket cells and the inhibitory drive they exerted on pyramidal cells were reduced in conditional mice lacking ErbB4. Developmental disruption of the connectivity of these cells diminished the power of theta oscillations during exploratory behavior, disrupted spatial coding by place cells, and caused selective alterations in spatial learning and memory in adult mice. These results suggest that normal integration of CCK basket cells in cortical networks is key to support spatial coding in the hippocampus.
[Mh] Termos MeSH primário: Córtex Cerebral/fisiologia
Colecistocinina/fisiologia
Neurônios GABAérgicos/fisiologia
Aprendizagem Espacial/fisiologia
Memória Espacial/fisiologia
[Mh] Termos MeSH secundário: Sistemas de Transporte de Aminoácidos Acídicos/metabolismo
Animais
Região CA1 Hipocampal/metabolismo
Região CA1 Hipocampal/fisiologia
Córtex Cerebral/metabolismo
Colecistocinina/genética
Colecistocinina/metabolismo
Comportamento Exploratório/fisiologia
Neurônios GABAérgicos/metabolismo
Interneurônios/metabolismo
Interneurônios/fisiologia
Locomoção/fisiologia
Masculino
Aprendizagem em Labirinto/fisiologia
Camundongos
Camundongos Transgênicos
Inibição Neural/fisiologia
Vias Neurais/fisiologia
Células de Lugar/fisiologia
Inibição Pré-Pulso/fisiologia
Células Piramidais/fisiologia
Receptor ErbB-4/biossíntese
Receptor ErbB-4/genética
Receptor ErbB-4/fisiologia
Ritmo Teta/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Transport Systems, Acidic); 0 (vesicular glutamate transporter 3, mouse); 9011-97-6 (Cholecystokinin); EC 2.7.10.1 (Receptor, ErbB-4)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170411
[St] Status:MEDLINE
[do] DOI:10.1038/nn.4544


  8 / 213 MEDLINE  
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[PMID]:28259708
[Au] Autor:Saheki T; Inoue K; Ono H; Fujimoto Y; Furuie S; Yamamura KI; Kuroda E; Ushikai M; Asakawa A; Inui A; Eto K; Kadowaki T; Moriyama M; Sinasac DS; Yamamoto T; Furukawa T; Kobayashi K
[Ad] Endereço:Laboratory of Yamamura Project, Institute of Resource Development and Analysis, Kumamoto University, Kumamoto 860-0811, Japan; Institute for Health Sciences, Tokushima Bunri University, Tokushima 770-8514, Japan; Department of Molecular Oncology, Kagoshima University Graduate School of Medical and D
[Ti] Título:Oral aversion to dietary sugar, ethanol and glycerol correlates with alterations in specific hepatic metabolites in a mouse model of human citrin deficiency.
[So] Source:Mol Genet Metab;120(4):306-316, 2017 Apr.
[Is] ISSN:1096-7206
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mice carrying simultaneous homozygous mutations in the genes encoding citrin, the mitochondrial aspartate-glutamate carrier 2 (AGC2) protein, and mitochondrial glycerol-3-phosphate dehydrogenase (mGPD), are a phenotypically representative model of human citrin (a.k.a., AGC2) deficiency. In this study, we investigated the voluntary oral intake and preference for sucrose, glycerol or ethanol solutions by wild-type, citrin (Ctrn)-knockout (KO), mGPD-KO, and Ctrn/mGPD double-KO mice; all substances that are known or suspected precipitating factors in the pathogenesis of human citrin deficiency. The double-KO mice showed clear suppressed intake of sucrose, consuming less with progressively higher concentrations compared to the other mice. Similar observations were made when glycerol or ethanol were given. The preference of Ctrn-KO and mGPD-KO mice varied with the different treatments; essentially no differences were observed for sucrose, while an intermediate intake or similar to that of the double-KO mice was observed for glycerol and ethanol. We next examined the hepatic glycerol 3-phosphate, citrate, citrulline, lysine, glutamate and adenine nucleotide levels following forced enteral administration of these solutions. A strong correlation between the simultaneous increased hepatic glycerol 3-phosphate and decreased ATP or total adenine nucleotide content and observed aversion of the mice during evaluation of their voluntary preferences was found. Overall, our results suggest that the aversion observed in the double-KO mice to these solutions is initiated and/or mediated by hepatic metabolic perturbations, resulting in a behavioral response to increased hepatic cytosolic NADH and a decreased cellular adenine nucleotide pool. These findings may underlie the dietary predilections observed in human citrin deficient patients.
[Mh] Termos MeSH primário: Citrulinemia/metabolismo
Sacarose na Dieta/administração & dosagem
Etanol/administração & dosagem
Glicerol/administração & dosagem
Fígado/química
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Sistemas de Transporte de Aminoácidos Acídicos/genética
Animais
Antiporters/genética
Modelos Animais de Doenças
Glicerolfosfato Desidrogenase/genética
Glicerofosfatos/metabolismo
Seres Humanos
Camundongos
Camundongos Knockout
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Transport Systems, Acidic); 0 (Antiporters); 0 (Dietary Sucrose); 0 (Glycerophosphates); 0 (aspartate-glutamate carrier); 3K9958V90M (Ethanol); 8L70Q75FXE (Adenosine Triphosphate); 9NTI6P3O4X (alpha-glycerophosphoric acid); EC 1.1.- (Glycerolphosphate Dehydrogenase); PDC6A3C0OX (Glycerol)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170306
[St] Status:MEDLINE


  9 / 213 MEDLINE  
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[PMID]:27044051
[Au] Autor:Sos KE; Mayer MI; Cserép C; Takács FS; Szonyi A; Freund TF; Nyiri G
[Ad] Endereço:Laboratory of Cerebral Cortex Research, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, 1083, Hungary.
[Ti] Título:Cellular architecture and transmitter phenotypes of neurons of the mouse median raphe region.
[So] Source:Brain Struct Funct;222(1):287-299, 2017 Jan.
[Is] ISSN:1863-2661
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The median raphe region (MRR, which consist of MR and paramedian raphe regions) plays a crucial role in regulating cortical as well as subcortical network activity and behavior, while its malfunctioning may lead to disorders, such as schizophrenia, major depression, or anxiety. Mouse MRR neurons are classically identified on the basis of their serotonin (5-HT), vesicular glutamate transporter type 3 (VGLUT3), and gamma-aminobutyric acid (GABA) contents; however, the exact cellular composition of MRR regarding transmitter phenotypes is still unknown. Using an unbiased stereological method, we found that in the MR, 8.5 % of the neurons were 5-HT, 26 % were VGLUT3, and 12.8 % were 5-HT and VGLUT3 positive; whereas 37.2 % of the neurons were GABAergic, and 14.4 % were triple negative. In the whole MRR, 2.1 % of the neurons were 5-HT, 7 % were VGLUT3, and 3.6 % were 5-HT and VGLUT3 positive; whereas 61 % of the neurons were GABAergic. Surprisingly, 25.4 % of the neurons were triple negative and were only positive for the neuronal marker NeuN. PET-1/ePET-Cre transgenic mouse lines are widely used to specifically manipulate only 5-HT containing neurons. Interestingly, however, using the ePET-Cre transgenic mice, we found that far more VGLUT3 positive cells expressed ePET than 5-HT positive cells, and about 38 % of the ePET cells contained only VGLUT3, while more than 30 % of 5-HT cells were ePET negative. These data should facilitate the reinterpretation of PET-1/ePET related data in the literature and the identification of the functional role of a putatively new type of triple-negative neuron in the MRR.
[Mh] Termos MeSH primário: Núcleo Dorsal da Rafe/fisiologia
Neurônios/fisiologia
[Mh] Termos MeSH secundário: Sistemas de Transporte de Aminoácidos Acídicos/metabolismo
Animais
Contagem de Células
Núcleo Dorsal da Rafe/química
Núcleo Dorsal da Rafe/citologia
Neurônios GABAérgicos/citologia
Neurônios GABAérgicos/metabolismo
Neurônios GABAérgicos/fisiologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Neurônios/citologia
Neurônios/metabolismo
Fenótipo
Neurônios Serotoninérgicos/citologia
Neurônios Serotoninérgicos/metabolismo
Neurônios Serotoninérgicos/fisiologia
Serotonina/metabolismo
Fatores de Transcrição/metabolismo
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Transport Systems, Acidic); 0 (Transcription Factors); 0 (vesicular glutamate transporter 3, mouse); 333DO1RDJY (Serotonin); 56-12-2 (gamma-Aminobutyric Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160405
[St] Status:MEDLINE
[do] DOI:10.1007/s00429-016-1217-x


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[PMID]:27789623
[Au] Autor:Haugas M; Tikker L; Achim K; Salminen M; Partanen J
[Ad] Endereço:Department of Biosciences, P.O. Box 56, Viikinkaari 9, FIN00014-University of Helsinki, Helsinki, Finland.
[Ti] Título:Gata2 and Gata3 regulate the differentiation of serotonergic and glutamatergic neuron subtypes of the dorsal raphe.
[So] Source:Development;143(23):4495-4508, 2016 12 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Serotonergic and glutamatergic neurons of the dorsal raphe regulate many brain functions and are important for mental health. Their functional diversity is based on molecularly distinct subtypes; however, the development of this heterogeneity is poorly understood. We show that the ventral neuroepithelium of mouse anterior hindbrain is divided into specific subdomains giving rise to serotonergic neurons as well as other types of neurons and glia. The newly born serotonergic precursors are segregated into distinct subpopulations expressing vesicular glutamate transporter 3 (Vglut3) or serotonin transporter (Sert). These populations differ in their requirements for transcription factors Gata2 and Gata3, which are activated in the post-mitotic precursors. Gata2 operates upstream of Gata3 as a cell fate selector in both populations, whereas Gata3 is important for the differentiation of the Sert precursors and for the serotonergic identity of the Vglut3 precursors. Similar to the serotonergic neurons, the Vglut3-expressing glutamatergic neurons, located in the central dorsal raphe, are derived from neural progenitors in the ventral hindbrain and express Pet1 Furthermore, both Gata2 and Gata3 are redundantly required for their differentiation. Our study demonstrates lineage relationships of the dorsal raphe neurons and suggests that functionally significant heterogeneity of these neurons is established early during their differentiation.
[Mh] Termos MeSH primário: Núcleo Dorsal da Rafe/citologia
Fator de Transcrição GATA2/genética
Fator de Transcrição GATA3/genética
Neurogênese/genética
Rombencéfalo/embriologia
Neurônios Serotoninérgicos/citologia
[Mh] Termos MeSH secundário: Sistemas de Transporte de Aminoácidos Acídicos/metabolismo
Animais
Camundongos
Camundongos Knockout
Células-Tronco Neurais/citologia
Neurogênese/fisiologia
Neuroglia/citologia
Rombencéfalo/fisiologia
Proteínas da Membrana Plasmática de Transporte de Serotonina/metabolismo
Inibidores da Recaptação de Serotonina e Norepinefrina/farmacologia
Fatores de Transcrição/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amino Acid Transport Systems, Acidic); 0 (Fev protein, mouse); 0 (GATA2 Transcription Factor); 0 (GATA3 Transcription Factor); 0 (Gata2 protein, mouse); 0 (Gata3 protein, mouse); 0 (Serotonin Plasma Membrane Transport Proteins); 0 (Serotonin and Noradrenaline Reuptake Inhibitors); 0 (Slc6a4 protein, mouse); 0 (Transcription Factors); 0 (vesicular glutamate transporter 3, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161102
[St] Status:MEDLINE



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