Base de dados : MEDLINE
Pesquisa : A08.675 [Categoria DeCS]
Referências encontradas : 236160 [refinar]
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  1 / 236160 MEDLINE  
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[PMID]:29381757
[Au] Autor:Barnes RM; Johnston HM; MacKenzie N; Tobin SJ; Taglang CM
[Ad] Endereço:Psychology Department, Montana State University, Bozeman, Montana, United States of America.
[Ti] Título:The effect of ad hominem attacks on the evaluation of claims promoted by scientists.
[So] Source:PLoS One;13(1):e0192025, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Two experiments were conducted to determine the relative impact of direct and indirect (ad hominem) attacks on science claims. Four hundred and thirty-nine college students (Experiment 1) and 199 adults (Experiment 2) read a series of science claims and indicated their attitudes towards those claims. Each claim was paired with one of the following: A) a direct attack upon the empirical basis of the science claim B) an ad hominem attack on the scientist who made the claim or C) both. Results indicate that ad hominem attacks may have the same degree of impact as attacks on the empirical basis of the science claims, and that allegations of conflict of interest may be just as influential as allegations of outright fraud.
[Mh] Termos MeSH primário: Estimulação Elétrica
Neurônios/fisiologia
Medula Espinal/fisiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Animais
Gatos
Feminino
Seres Humanos
Masculino
Medula Espinal/citologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0192025


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[PMID]:29373584
[Au] Autor:Zhao X; Li R; Jin H; Jin H; Wang Y; Zhang W; Wang H; Chen W
[Ad] Endereço:Tianjin Institute of Health and Environmental Medicine, Tianjin, China.
[Ti] Título:Epigallocatechin-3-gallate confers protection against corticosterone-induced neuron injuries via restoring extracellular signal-regulated kinase 1/2 and phosphatidylinositol-3 kinase/protein kinase B signaling pathways.
[So] Source:PLoS One;13(1):e0192083, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Extensive studies suggested epigallocatechin-3-gallate (EGCG) has significant neuroprotection against multiple central neural injuries, but the underlying mechanisms still remain poorly elucidated. Here we provide evidence to support the possible involvement of extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphatidylinositol-3 kinase/ protein kinase B (PI3K/AKT) pathways in EGCG-mediated protection against corticosterone-induced neuron injuries. As an essential stress hormone, corticosterone could induce obvious neurotoxicity in primary hippocampal neurons. Pre-treatment with EGCG ameliorated the corticosterone-induced neuronal injuries; however, it was blocked by pharmacological inhibitors for ERK1/2 (U0126) and PI3K/AKT (LY294002). Furthermore, the results confirmed that EGCG restored the corticosterone-induced decrease of ERK1/2 and PI3K/AKT phosphorylation, and attenuated the corticosterone-induced reduction of peroxisome proliferators-activated receptor-γ coactivator-1α (PGC-1α) expression and ATP production. Taken together, these findings indicated that EGCG has significant neuroprotection against corticosterone-induced neuron injuries partly via restoring the ERK1/2 and PI3K/AKT signaling pathways as well as the PGC-1α-mediated ATP production.
[Mh] Termos MeSH primário: Catequina/análogos & derivados
Corticosterona/efeitos adversos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/biossíntese
Animais
Catequina/farmacologia
Células Cultivadas
Hipocampo/citologia
Hipocampo/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Fosforilação
Ratos
Ratos Wistar
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Neuroprotective Agents); 8L70Q75FXE (Adenosine Triphosphate); 8R1V1STN48 (Catechin); BQM438CTEL (epigallocatechin gallate); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180127
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0192083


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[PMID]:29364956
[Au] Autor:Winzi M; Casas Vila N; Paszkowski-Rogacz M; Ding L; Noack S; Theis M; Butter F; Buchholz F
[Ad] Endereço:Medical Systems Biology, Faculty of Medicine Carl Gustav Carus, University Cancer Center, TU Dresden, Dresden, Germany.
[Ti] Título:The long noncoding RNA lncR492 inhibits neural differentiation of murine embryonic stem cells.
[So] Source:PLoS One;13(1):e0191682, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RNA interference (RNAi) screens have been shown to be valuable to study embryonic stem cell (ESC) self-renewal and they have been successfully applied to identify coding as well as noncoding genes required for maintaining pluripotency. Here, we used an RNAi library targeting >640 long noncoding RNAs (lncRNA) to probe for their role in early cell differentiation. Utilizing a Sox1-GFP ESC reporter cell line, we identified the lncRNA lncR492 as lineage-specific inhibitor of neuroectodermal differentiation. Molecular characterization showed that lncR492 interacts with the mRNA binding protein HuR and facilitates its inhibitory function by activation of Wnt signaling. Thus, lncRNAs modulate the fate decision of pluripotent stem cells.
[Mh] Termos MeSH primário: Diferenciação Celular
Células-Tronco Embrionárias/citologia
Neurônios/citologia
RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Animais
Camundongos
Interferência de RNA
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Long Noncoding)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191682


  4 / 236160 MEDLINE  
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[PMID]:29353037
[Au] Autor:Lu Z; Liu Y; Shi Y; Shi X; Wang X; Xu C; Zhao H; Dong Q
[Ad] Endereço:Department of Neurology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200437, PR China.
[Ti] Título:Curcumin protects cortical neurons against oxygen and glucose deprivation/reoxygenation injury through flotillin-1 and extracellular signal-regulated kinase1/2 pathway.
[So] Source:Biochem Biophys Res Commun;496(2):515-522, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, we provided evidence that curcumin could be a promising therapeutic agent for ischemic stroke by activating neuroprotective signaling pathways. Post oxygen and glucose deprivation/reoxygenation (OGD/R), primary mouse cortical neurons treated with curcumin exhibited a significant decrease in cell death, LDH release and enzyme caspase-3 activity under OGD/R circumstances, which were abolished by flotillin-1 downregulation or extracellular signal-regulated kinase (ERK) inhibitor. Moreover, flotillin-1 knockdown led to suppression of curcumin-mediated ERK phosphorylation under OGD/R condition. Based on these findings, we concluded that curcumin could confer neuroprotection against OGD/R injury through a novel flotillin-1 and ERK1/2 pathway.
[Mh] Termos MeSH primário: Isquemia Encefálica/tratamento farmacológico
Curcumina/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Proteínas de Membrana/metabolismo
Neurônios/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
[Mh] Termos MeSH secundário: Animais
Isquemia Encefálica/metabolismo
Células Cultivadas
Córtex Cerebelar/citologia
Córtex Cerebelar/efeitos dos fármacos
Feminino
Glucose/metabolismo
Masculino
Camundongos Endogâmicos BALB C
Neurônios/metabolismo
Oxigênio/metabolismo
Traumatismo por Reperfusão/tratamento farmacológico
Traumatismo por Reperfusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Neuroprotective Agents); 0 (flotillins); IT942ZTH98 (Curcumin); IY9XDZ35W2 (Glucose); S88TT14065 (Oxygen)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180122
[St] Status:MEDLINE


  5 / 236160 MEDLINE  
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[PMID]:29304162
[Au] Autor:Matsushita Y; Manabe M; Kitamura N; Shibuya I
[Ad] Endereço:Laboratory of Veterinary Physiology, Faculty of Agriculture, Tottori University, Tottori, Japan.
[Ti] Título:Adrenergic receptors inhibit TRPV1 activity in the dorsal root ganglion neurons of rats.
[So] Source:PLoS One;13(1):e0191032, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transient receptor potential vanilloid type 1 (TRPV1) is a polymodal receptor channel that responds to multiple types of stimuli, such as heat, acid, mechanical pressure and some vanilloids. Capsaicin is the most commonly used vanilloid to stimulate TRPV1. TRPV1 channels are expressed in dorsal root ganglion neurons that extend to Aδ- and C-fibers and have a role in the transduction of noxious inputs to the skin into the electrical signals of the sensory nerve. Although noradrenergic nervous systems, including the descending antinociceptive system and the sympathetic nervous system, are known to modulate pain sensation, the functional association between TRPV1 and noradrenaline in primary sensory neurons has rarely been examined. In the present study, we examined the effects of noradrenaline on capsaicin-evoked currents in cultured dorsal root ganglion neurons of the rat by the whole-cell voltage clamp method. Noradrenaline at concentrations higher than 0.1 pM significantly reduced the amplitudes of the inward capsaicin currents recorded at -60 mV holding potential. This inhibitory action was reversed by either yohimbine (an α2 antagonist, 10 nM) or propranolol (a ß antagonist, 10 nM). The α2 agonists, clonidine (1 pM) and dexmedetomidine (1 pM) inhibited capsaicin currents, and yohimbine (1 nM) reversed the effects of clonidine. The inhibitory action of noradrenaline was not seen in the neurons pretreated with pertussis toxin (100 µg/ml for 24 h) and the neurons dialyzed intracellularly with guanosine 5'- [ß-thio] diphosphate (GDPßS, 200 µM), the catalytic subunit of protein kinase A (250 U/ml) or okadaic acid (1 µM). These results suggest that noradrenaline directly acts on dorsal root ganglion neurons to inhibit the activity of TRPV1 depending on the activation of α2-adrenoceptors followed by the inhibition of the adenylate cyclase/cAMP/protein kinase A pathway.
[Mh] Termos MeSH primário: Gânglios Espinais/metabolismo
Neurônios/metabolismo
Receptores Adrenérgicos/fisiologia
Canais de Cátion TRPV/metabolismo
[Mh] Termos MeSH secundário: Animais
Capsaicina/farmacologia
Gânglios Espinais/citologia
Gânglios Espinais/efeitos dos fármacos
Masculino
Neurônios/efeitos dos fármacos
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Adrenergic); 0 (TRPV Cation Channels); 0 (Trpv1 protein, rat); S07O44R1ZM (Capsaicin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180106
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191032


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[PMID]:29107146
[Au] Autor:Jang JY; Rhim H; Kang S
[Ad] Endereço:Division of Life Sciences, College of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.
[Ti] Título:NABi, a novel ß-sheet breaker, inhibits Aß aggregation and neuronal toxicity: Therapeutic implications for Alzheimer's disease.
[So] Source:Biochim Biophys Acta;1862(1):71-80, 2018 01.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Amyloid beta (Aß) aggregates are an important therapeutic target for Alzheimer's disease (AD), a fatal neurodegenerative disease. To date, AD still remains a big challenge due to no effective treatments. Based on the property that Aß aggregates have the cross-ß-structure, a common structural feature in amyloids, we systemically designed the Aß-aggregation inhibitor that maintains Aß-interacting ability but removes toxic part from SOD1 (superoxide dismutase 1)-G93A. We identified NABi (Natural Aß Binder and Aß-aggregation inhibitor) composed of ß2-3 strands, a novel breaker of Aß aggregation, which does not self-aggregate and has no cytotoxicity at all. The NABi blocks Aß-fibril formation in vitro and in vivo and prevents neuronal cell death, a hallmark of AD pathogenesis. Such anti-amyloidogenic properties can provide novel strategies for treating AD. Furthermore, our study provides molecular insights into the design of amyloidogenic inhibitors to cure various neurodegenerative and amyloid-associated diseases, as NABi would regulate aggregation of other toxic ß-sheet proteins other than Aß.
[Mh] Termos MeSH primário: Doença de Alzheimer/tratamento farmacológico
Peptídeos beta-Amiloides/antagonistas & inibidores
Neurônios/metabolismo
Agregação Patológica de Proteínas/tratamento farmacológico
[Mh] Termos MeSH secundário: Doença de Alzheimer/metabolismo
Doença de Alzheimer/patologia
Peptídeos beta-Amiloides/metabolismo
Animais
Linhagem Celular Tumoral
Seres Humanos
Camundongos
Neurônios/patologia
Agregação Patológica de Proteínas/metabolismo
Agregação Patológica de Proteínas/patologia
Estrutura Secundária de Proteína
Superóxido Dismutase/antagonistas & inibidores
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); EC 1.15.1.1 (SOD1 G93A protein); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171107
[St] Status:MEDLINE


  7 / 236160 MEDLINE  
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[PMID]:28987401
[Au] Autor:Li B; Guo L; Ku T; Chen M; Li G; Sang N
[Ad] Endereço:College of Environment and Resource, Research Center of Environment and Health, Shanxi University, Taiyuan, Shanxi 030006, PR China.
[Ti] Título:PM exposure stimulates COX-2-mediated excitatory synaptic transmission via ROS-NF-κB pathway.
[So] Source:Chemosphere;190:124-134, 2018 Jan.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Long-term exposure to fine particulate matter (PM ) has been reported to be closely associated with the neuroinflammation and synaptic dysfunction, but the mechanisms underlying the process remain unclear. Cyclooxygenase-2 (COX-2) is a key player in neuroinflammation, and has been also implicated in the glutamatergic excitotoxicity and synaptic plasticity. Thus, we hypothesized that COX-2 was involved in PM -promoted neuroinflammation and synaptic dysfunction. Our results revealed that PM elevated COX-2 expression in primary cultured hippocampal neurons and increased the amplitude of field excitatory postsynaptic potentials (fEPSPs) in hippocampal brain slices. And the administration of NS398 (a COX-2 inhibitor) prevented the increased fEPSPs. PM also induced intracellular reactive oxygen species (ROS) generation accompanied with glutathione (GSH) depletion and the loss of mitochondrial membrane potential (MMP), and the ROS inhibitor, N-acetyl-L-cystein (NAC) suppressed the COX-2 overexpression and the increased fEPSPs. Furthermore, the nuclear factor kappa B (NF-κB) was involved in ROS-induced COX-2 and fEPSP in response to PM exposure. These findings indicated that PM activated COX-2 expression and enhanced the synaptic transmission through ROS-NF-κB pathway, and provided possible biomarkers and specific interventions for PM -induced neurological damage.
[Mh] Termos MeSH primário: Ciclo-Oxigenase 2/fisiologia
NF-kappa B/metabolismo
Material Particulado/toxicidade
Espécies Reativas de Oxigênio/metabolismo
Transmissão Sináptica
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Ciclo-Oxigenase 2/metabolismo
Hipocampo/citologia
Inflamação/etiologia
Camundongos
Neurônios/patologia
Material Particulado/farmacologia
Transmissão Sináptica/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Particulate Matter); 0 (Reactive Oxygen Species); EC 1.14.99.1 (Cyclooxygenase 2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171009
[St] Status:MEDLINE


  8 / 236160 MEDLINE  
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[PMID]:28822947
[Au] Autor:Zong L; Xing J; Liu S; Liu Z; Song F
[Ad] Endereço:National Center of Mass Spectrometry in Changchun, Jilin Province Key Laboratory of Chinese Medicine Chemistry and Mass Spectrometry, Changchun Institute of Applied Chemistry, Chinese Academy of Sciences, Changchun 130022, China; University of Chinese Academy of Sciences, Beijing 100039, China.
[Ti] Título:Cell metabolomics reveals the neurotoxicity mechanism of cadmium in PC12 cells.
[So] Source:Ecotoxicol Environ Saf;147:26-33, 2018 Jan.
[Is] ISSN:1090-2414
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The heavy metals such as cadmium (Cd) can induce neurotoxicity. Extensive studies about the effects of Cd on human health have been reported, however, a systematic investigation on the molecular mechanisms of the effects of Cd on central nervous system is still needed. In this paper, the neuronal PC-12 cells were treated with a series of concentrations of CdCl for 48h. Then the cytotoxicity was evaluated by MTT (3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide) assay. The IC value (15% inhibiting concentration) was selected for further mechanism studies. After PC-12 cells incubated with CdCl at a dose of IC for 48h, the intracellular and extracellular metabolites were profiled using ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS)-based cell metabolomics approach. As found, the effects of the heavy metal Cd produced on the PC-12 cell viability were dose-dependent. The metabolic changes were involved in the glycolysis and gluconeogenesis, biopterin metabolism, tryptophan metabolism, tyrosine metabolism, glycerophospholipid metabolism, and fatty acids beta-oxidation. These could cause the perturbation of cell membrane, redox balance, energy supply, cellular detoxification, further affecting the cellular proliferation and apoptosis and other cellular activities.
[Mh] Termos MeSH primário: Cádmio/toxicidade
Poluentes Ambientais/toxicidade
Metaboloma/efeitos dos fármacos
Metabolômica/métodos
Neurônios/efeitos dos fármacos
Síndromes Neurotóxicas/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Metabolismo Energético/efeitos dos fármacos
Seres Humanos
Neurônios/metabolismo
Neurônios/patologia
Oxirredução
Células PC12
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Environmental Pollutants); 00BH33GNGH (Cadmium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170821
[St] Status:MEDLINE


  9 / 236160 MEDLINE  
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[PMID]:28471062
[Au] Autor:Rao AN; Patil A; Brodnik ZD; Qiang L; España RA; Sullivan KA; Black MM; Baas PW
[Ad] Endereço:Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, Pennsylvania.
[Ti] Título:Pharmacologically increasing microtubule acetylation corrects stress-exacerbated effects of organophosphates on neurons.
[So] Source:Traffic;18(7):433-441, 2017 Jul.
[Is] ISSN:1600-0854
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Many veterans of the 1990-1991 Gulf War contracted Gulf War Illness (GWI), a multisymptom disease that primarily affects the nervous system. Here, we treated cultures of human or rat neurons with diisopropyl fluorophosphate (DFP), an analog of sarin, one of the organophosphate (OP) toxicants to which the military veterans were exposed. All observed cellular defects produced by DFP were exacerbated by pretreatment with corticosterone or cortisol, which, in rat and human neurons, respectively, serves in our experiments to mimic the physical stress endured by soldiers during the war. To best mimic the disease, DFP was used below the level needed to inhibit acetylcholinesterase. We observed a diminution in the ratio of acetylated to total tubulin that was correctable by treatment with tubacin, a drug that inhibits HDAC6, the tubulin deacetylase. The reduction in microtubule acetylation was coupled with deficits in microtubule dynamics, which were correctable by HDAC6 inhibition. Deficits in mitochondrial transport and dopamine release were also improved by tubacin. Thus, various negative effects of the toxicant/stress exposures were at least partially correctable by restoring microtubule acetylation to a more normal status. Such an approach may have therapeutic benefit for individuals suffering from GWI or other neurological disorders linked to OP exposure.
[Mh] Termos MeSH primário: Anilidas/farmacologia
Substâncias para a Guerra Química/toxicidade
Ácidos Hidroxâmicos/farmacologia
Isoflurofato/toxicidade
Microtúbulos/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Estresse Fisiológico
[Mh] Termos MeSH secundário: Acetilação
Animais
Transporte Biológico
Células Cultivadas
Corticosterona/farmacologia
Dopamina/secreção
Relação Dose-Resposta a Droga
Seres Humanos
Hidrocortisona/farmacologia
Microtúbulos/metabolismo
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Síndrome do Golfo Pérsico
Ratos
Tubulina (Proteína)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anilides); 0 (Chemical Warfare Agents); 0 (Hydroxamic Acids); 0 (Tubulin); 02C2G1D30D (tubacin); 12UHW9R67N (Isoflurophate); VTD58H1Z2X (Dopamine); W980KJ009P (Corticosterone); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1111/tra.12489


  10 / 236160 MEDLINE  
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[PMID]:28466069
[Au] Autor:Castillo-Gómez E; Pérez-Rando M; Bellés M; Gilabert-Juan J; Llorens JV; Carceller H; Bueno-Fernández C; García-Mompó C; Ripoll-Martínez B; Curto Y; Sebastiá-Ortega N; Moltó MD; Sanjuan J; Nacher J
[Ad] Endereço:Neurobiology Unit, Cell Biology Department, Interdisciplinary Research Structure for Biotechnology and Biomedicine (BIOTECMED), Universitat De València, Burjassot 46100, Spain.
[Ti] Título:Early Social Isolation Stress and Perinatal NMDA Receptor Antagonist Treatment Induce Changes in the Structure and Neurochemistry of Inhibitory Neurons of the Adult Amygdala and Prefrontal Cortex.
[So] Source:eNeuro;4(2), 2017 Mar-Apr.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The exposure to aversive experiences during early life influences brain development and leads to altered behavior. Moreover, the combination of these experiences with subtle alterations in neurodevelopment may contribute to the emergence of psychiatric disorders, such as schizophrenia. Recent hypotheses suggest that imbalances between excitatory and inhibitory (E/I) neurotransmission, especially in the prefrontal cortex and the amygdala, may underlie their etiopathology. In order to understand better the neurobiological bases of these alterations, we studied the impact of altered neurodevelopment and chronic early-life stress on these two brain regions. Transgenic mice displaying fluorescent excitatory and inhibitory neurons, received a single injection of MK801 (NMDAR antagonist) or vehicle solution at postnatal day 7 and/or were socially isolated from the age of weaning until adulthood (3 months old). We found that anxiety-related behavior, brain volume, neuronal structure, and the expression of molecules related to plasticity and E/I neurotransmission in adult mice were importantly affected by early-life stress. Interestingly, many of these effects were potentiated when the stress paradigm was applied to mice perinatally injected with MK801 ("double-hit" model). These results clearly show the impact of early-life stress on the adult brain, especially on the structure and plasticity of inhibitory networks, and highlight the double-hit model as a valuable tool to study the contribution of early-life stress in the emergence of neurodevelopmental psychiatric disorders, such as schizophrenia.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Córtex Pré-Frontal/efeitos dos fármacos
Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
Isolamento Social/psicologia
[Mh] Termos MeSH secundário: Tonsila do Cerebelo/metabolismo
Animais
Maleato de Dizocilpina/farmacologia
Camundongos Transgênicos
Plasticidade Neuronal/fisiologia
Neurônios/metabolismo
Receptores de N-Metil-D-Aspartato/metabolismo
Transmissão Sináptica/fisiologia
Sinaptofisina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, N-Methyl-D-Aspartate); 0 (Synaptophysin); 6LR8C1B66Q (Dizocilpine Maleate)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE



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