Base de dados : MEDLINE
Pesquisa : D03.383.773.050 [Categoria DeCS]
Referências encontradas : 1192 [refinar]
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[PMID]:28958943
[Au] Autor:Reddy GS; Mukhopadhyay AG; Dey CS
[Ad] Endereço:Kusuma School of Biological Sciences, Indian Institute of Technology Delhi, Hauz Khas, New Delhi 110016, India.
[Ti] Título:The p38 MAP kinase inhibitor, PD 169316, inhibits flagellar motility in Leishmania donovani.
[So] Source:Biochem Biophys Res Commun;493(4):1425-1429, 2017 Dec 02.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitogen-activated protein kinases (MAPKs) have been demonstrated to regulate flagellar/ciliary motility of spermatozoa and miracidia of Schistosoma mansoni. However, the role of MAPKs in mediating flagella-driven motility of Leishmania donovani is unexplored. We investigated the function of MAPKs in motility regulation of L. donovani using pharmacological inhibitors and activators of various MAPKs and fast-capture videomicroscopy. Our studies have revealed that the inhibitor of p38 MAPK, PD 169316, significantly affected various motility parameters such as flagellar beat frequency, parasite swimming speed, waveform of the flagellum and resulted in reduced parasite motility. Together, our results suggest that a MAPK, similar to human p38 MAPK, is implicated in flagellar motility regulation of L. donovani.
[Mh] Termos MeSH primário: Flagelos/efeitos dos fármacos
Imidazóis/farmacologia
Leishmania donovani/efeitos dos fármacos
Leishmania donovani/fisiologia
Inibidores de Proteínas Quinases/farmacologia
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Anisomicina/farmacologia
Antracenos/farmacologia
Flagelos/fisiologia
Flavonoides/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Sistema de Sinalização das MAP Quinases/fisiologia
Microscopia de Vídeo
Movimento/efeitos dos fármacos
Movimento/fisiologia
Proteínas de Protozoários/antagonistas & inibidores
Proteínas de Protozoários/fisiologia
Proteínas Quinases p38 Ativadas por Mitógeno/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one); 0 (Anthracenes); 0 (Flavonoids); 0 (Imidazoles); 0 (Protein Kinase Inhibitors); 0 (Protozoan Proteins); 1TW30Y2766 (pyrazolanthrone); 6C74YM2NGI (Anisomycin); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); GX3Y2V80CV (2-(4-nitrophenyl)-4-(4-fluorophenyl)-5-(4-pyridinyl)-1H-imidazole)
[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:170930
[St] Status:MEDLINE


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[PMID]:28781168
[Au] Autor:Wong HH; Lin JQ; Ströhl F; Roque CG; Cioni JM; Cagnetta R; Turner-Bridger B; Laine RF; Harris WA; Kaminski CF; Holt CE
[Ad] Endereço:Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge CB2 3DY, UK.
[Ti] Título:RNA Docking and Local Translation Regulate Site-Specific Axon Remodeling In Vivo.
[So] Source:Neuron;95(4):852-868.e8, 2017 Aug 16.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nascent proteins can be positioned rapidly at precise subcellular locations by local protein synthesis (LPS) to facilitate localized growth responses. Axon arbor architecture, a major determinant of synaptic connectivity, is shaped by localized growth responses, but it is unknown whether LPS influences these responses in vivo. Using high-resolution live imaging, we examined the spatiotemporal dynamics of RNA and LPS in retinal axons during arborization in vivo. Endogenous RNA tracking reveals that RNA granules dock at sites of branch emergence and invade stabilized branches. Live translation reporter analysis reveals that de novo ß-actin hotspots colocalize with docked RNA granules at the bases and tips of new branches. Inhibition of axonal ß-actin mRNA translation disrupts arbor dynamics primarily by reducing new branch emergence and leads to impoverished terminal arbors. The results demonstrate a requirement for LPS in building arbor complexity and suggest a key role for pre-synaptic LPS in assembling neural circuits.
[Mh] Termos MeSH primário: Axônios/fisiologia
Regulação da Expressão Gênica no Desenvolvimento/genética
RNA/metabolismo
[Mh] Termos MeSH secundário: Actinas/genética
Actinas/metabolismo
Animais
Anisomicina/farmacologia
Biotina/metabolismo
Blastômeros
Carbocianinas/metabolismo
Cicloeximida/farmacologia
Nucleotídeos de Desoxiuracil/metabolismo
Embrião não Mamífero
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Técnicas In Vitro
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Mitocôndrias/metabolismo
Morfolinos/farmacologia
Oligonucleotídeos Antissenso/farmacologia
Técnicas de Cultura de Órgãos
Inibidores da Síntese de Proteínas/farmacologia
RNA/genética
Retina/citologia
Xenopus laevis
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3'-deoxy-5-(cyanine dye 5)uridine 5'-trisphosphate); 0 (Actins); 0 (Carbocyanines); 0 (Deoxyuracil Nucleotides); 0 (Luminescent Proteins); 0 (Morpholinos); 0 (Oligonucleotides, Antisense); 0 (Protein Synthesis Inhibitors); 63231-63-0 (RNA); 6C74YM2NGI (Anisomycin); 6SO6U10H04 (Biotin); 98600C0908 (Cycloheximide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE


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[PMID]:28349059
[Au] Autor:Chen S; Wang Y; Yang Y; Xiang T; Liu J; Zhou H; Wu X
[Ad] Endereço:Department of Traditional Chinese Medicine, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China.
[Ti] Título:Psoralen Inhibited Apoptosis of Osteoporotic Osteoblasts by Modulating IRE1-ASK1-JNK Pathway.
[So] Source:Biomed Res Int;2017:3524307, 2017.
[Is] ISSN:2314-6141
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Osteoporosis is a common disease causing fracture in older populations. Abnormal apoptosis of osteoblasts contributes to the genesis of osteoporosis. Inhibiting apoptosis of osteoblasts provides a promising strategy to prevent osteoporosis. The proliferation of osteoblasts isolated from osteoporotic patients or healthy subjects was determined by MTT assay. Apoptosis was determined by Annexin V/PI assay. Protein expression was measured by western blot. The proliferation of osteoblasts isolated from osteoporotic patients was inhibited and the apoptosis level of these cells was higher than the osteoblasts from healthy subjects. Incubation with psoralen or estradiol significantly enhanced the proliferation and decreased the apoptosis level of osteoporotic osteoblasts. Western blot demonstrated that psoralen or estradiol treatment downregulated the expression of IRE1, p-ASK, p-JNK, and Bax. Meanwhile, expression of Bcl-2 was upregulated. Pretreatment by IRE1 agonist tunicamycin or JNK agonist anisomycin attenuated the effect of psoralen on osteoporotic osteoblasts. Psoralen inhibited apoptosis of osteoporotic osteoblasts by regulating IRE1-ASK1-JNK pathway.
[Mh] Termos MeSH primário: Endorribonucleases/genética
Ficusina/administração & dosagem
MAP Quinase Quinase 4/genética
MAP Quinase Quinase Quinase 5/genética
Osteoporose/tratamento farmacológico
Proteínas Serina-Treonina Quinases/genética
[Mh] Termos MeSH secundário: Anisomicina/administração & dosagem
Apoptose/efeitos dos fármacos
Diferenciação Celular/genética
Proliferação Celular/efeitos dos fármacos
Endorribonucleases/biossíntese
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
MAP Quinase Quinase 4/biossíntese
MAP Quinase Quinase Quinase 5/biossíntese
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Meia-Idade
Osteoblastos/efeitos dos fármacos
Osteoporose/genética
Osteoporose/patologia
Cultura Primária de Células
Proteínas Serina-Treonina Quinases/biossíntese
Proteínas Proto-Oncogênicas c-bcl-2/biossíntese
Tunicamicina/administração & dosagem
Proteína X Associada a bcl-2/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-bcl-2); 0 (bcl-2-Associated X Protein); 11089-65-9 (Tunicamycin); 6C74YM2NGI (Anisomycin); EC 2.7.11.1 (ERN1 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.25 (MAP Kinase Kinase Kinase 5); EC 2.7.11.25 (MAP3K5 protein, human); EC 2.7.12.2 (MAP Kinase Kinase 4); EC 3.1.- (Endoribonucleases); KTZ7ZCN2EX (Ficusin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.1155/2017/3524307


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[PMID]:27879498
[Au] Autor:Li Y; Wu X; Jin X; Wang J; Togo Y; Suzuki T; Hashimoto T; Yamada Y; Nakanishi Y; Kanematsu A; Nojima M; Kakehi Y; Yamamoto S
[Ad] Endereço:aDepartment of Urology, Hyogo College of Medicine, Hyogo bDepartment of Urology, Kagawa University Faculty of Medicine, Kagawa, Japan cKey Laboratory of Cancer Prevention and Treatment of Heilongjiang dDepartment of Dermatology, Mudanjiang Medical University, Heilongjiang, China.
[Ti] Título:Enhancement of death receptor 4-mediated apoptosis and cytotoxicity in renal cell carcinoma cells by anisomycin.
[So] Source:Anticancer Drugs;28(2):180-186, 2017 Feb.
[Is] ISSN:1473-5741
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Renal cell carcinoma (RCC) is one of the most drug-resistant malignancies, and an effective therapy is lacking for metastatic RCC. Anisomycin is known to inhibit protein synthesis and induce ribotoxic stress. The aim of this study was to explore whether anisomycin enhances the cytotoxic effects of mapatumumab, a human agonistic monoclonal antibody specific for death receptor 4 (DR4), in human RCC cells. We examined the cytotoxicity of anisomycin alone and in combination with mapatumumab in human RCC cell lines and primary RCC cell cultures. RCC cells treated with anisomycin showed cytotoxicity in a dose-dependent manner. Anisomyin in combination with mapatumumab showed a synergistic effect not only in two human RCC cell lines but also in five primary RCC cell cultures. The synergy between anisomycin and mapatumumab for cytotoxicity was also observed for apoptosis. Interestingly, anisomycin significantly increased DR4 expression at both the mRNA and the protein level. Furthermore, the combination-induced cytotoxicity was significantly suppressed by a human recombinant DR4:Fc chimeric protein. The combination of anisomycin and mapatumumab also enhanced the activity of caspases 8 and 3, the downstream molecules of death receptors. These findings indicate that anisomycin sensitizes RCC cells to DR4-mediated apoptosis through the induction of DR4, suggesting that combinational treatment with anisomycin and mapatumumab might represent a novel therapeutic strategy for the treatment of RCC.
[Mh] Termos MeSH primário: Anisomicina/farmacologia
Carcinoma de Células Renais/tratamento farmacológico
Neoplasias Renais/tratamento farmacológico
Receptores do Ligante Indutor de Apoptose Relacionado a TNF/metabolismo
[Mh] Termos MeSH secundário: Anisomicina/administração & dosagem
Anticorpos Monoclonais/administração & dosagem
Anticorpos Monoclonais/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Apoptose/efeitos dos fármacos
Carcinoma de Células Renais/metabolismo
Carcinoma de Células Renais/patologia
Caspase 3/metabolismo
Caspase 8/metabolismo
Linhagem Celular Tumoral
Sinergismo Farmacológico
Ativação Enzimática/efeitos dos fármacos
Seres Humanos
Neoplasias Renais/metabolismo
Neoplasias Renais/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand); 0 (TNFRSF10A protein, human); 6C74YM2NGI (Anisomycin); EC 3.4.22.- (CASP8 protein, human); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 8); WZ1025JPGR (mapatumumab)
[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:161124
[St] Status:MEDLINE
[do] DOI:10.1097/CAD.0000000000000450


  5 / 1192 MEDLINE  
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[PMID]:27864653
[Au] Autor:Zhang YC; Jin L; Zhu HY; Guo Q; Li XC; Zhang GL; Xing XX; Xuan MF; Luo QR; Luo ZB; Wang JX; Cui CD; Li WX; Cui ZY; Yin XJ; Kang JD
[Ad] Endereço:Jilin Provincial Key Laboratory of Transgenic Animal and Embryo Engineering, Yanbian University, Yanji, 133002, Jilin, China.
[Ti] Título:The developmental competence of oocytes parthenogenetically activated by an electric pulse and anisomycin treatment.
[So] Source:Biotechnol Lett;39(2):189-196, 2017 Feb.
[Is] ISSN:1573-6776
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The aim of this study was to investigate the developmental competence of oocytes parthenogenetically activated by an electric pulse (EP) and treated with anisomycin and to determine whether this method is applicable to somatic cell nuclear transfer (SCNT). RESULTS: Embryos derived from porcine oocytes parthenogenetically activated by an EP and treatment with 0.01 µg/mL anisomycin had a significantly improved in vitro developmental capacity. Furthermore, 66.6% of blastocysts derived from these embryos had a diploid karyotype. The blastocyst formation rate of cloned embryos was similar between oocytes activated by an EP and treated with 2 mM 6-dimethylaminopurine for 4 h and those activated by an EP and treated with 0.01 µg/mL anisomycin for 4 h. The level of maturation-promoting factor was significantly decreased in oocytes activated by an EP and treated with anisomycin. Finally, the mRNA expression levels of apoptosis-related genes (Bax and Bcl-2) and pluripotency-related genes (Oct4, Nanog, and Sox2) were checked by RT-PCR. CONCLUSION: Our results demonstrate that porcine oocyte activation via an EP in combination with anisomycin treatment can lead to a high blastocyst formation rate in parthenogenetic activation and SCNT experiments.
[Mh] Termos MeSH primário: Anisomicina/farmacologia
Oócitos/efeitos dos fármacos
Oócitos/metabolismo
Partenogênese/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Estimulação Elétrica
Desenvolvimento Embrionário
Feminino
Técnicas de Transferência Nuclear
Oócitos/fisiologia
Gravidez
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
6C74YM2NGI (Anisomycin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170308
[Lr] Data última revisão:
170308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161120
[St] Status:MEDLINE
[do] DOI:10.1007/s10529-016-2249-2


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[PMID]:27766028
[Au] Autor:Yang ZH; Wu BL; Ye C; Jia S; Yang XJ; Hou R; Lei DL; Wang L
[Ad] Endereço:State Key Laboratory of Military Stomatology, Department of Oral and Maxillofacial Surgery, School of Stomatology, the Fourth Military Medical University, China.
[Ti] Título:Targeting P38 Pathway Regulates Bony Formation MSC Recruitment during Mandibular Distraction Osteogenesis in Rats.
[So] Source:Int J Med Sci;13(10):783-789, 2016.
[Is] ISSN:1449-1907
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Distraction osteogenesis (DO) is a widely used self-tissue engineering. However, complications and discomfort due to the long treatment period are still the bottleneck of DO. Novel strategies to accelerate bone formation in DO are still needed. P38 is capable of regulating the osteogenic differentiation of both mesenchymal stem cells (MSCs) and osteoblasts, which are crucial to bone regeneration. However, it is not clear whether targeting p38 could regulate bony formation in DO. The purpose of the current work was to investigate the effects of local application of either p38 agonist anisomycin or p38 inhibitor SB203580 in a rat model of DO. 30 adult rats were randomly divided into 3 groups: (A) rats injected with DMSO served as the control group; (B) rats injected with p38 agonist anisomycin; (C) rats injected with p38 inhibitor SB203580. All the rats were subjected to mandibular distraction and the injection was performed daily during this period. The distracted mandibles were harvested on days 15 and 30 after surgery and subjected to the following analysis. Micro-computed tomography and histological evaluation results showed that local application of p38 agonist anisomycin increased new bone formation in DO, whereas p38 inhibitor SB203580 decreased it. Immunohistochemical analysis suggested that anisomycin promoted MSC recruitment in the distraction gap. In conclusion, this study demonstrated that local application of p38 agonist anisomycin can increase new bone formation during DO. This study may lead to a novel cell-based strategy for the improvement of bone regeneration.
[Mh] Termos MeSH primário: Anisomicina/farmacologia
Regeneração Óssea/efeitos dos fármacos
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Células Mesenquimais Estromais/efeitos dos fármacos
Osteogênese por Distração/métodos
Osteogênese/efeitos dos fármacos
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Mh] Termos MeSH secundário: Animais
Inibidores Enzimáticos/farmacologia
Imidazóis/farmacologia
Masculino
Mandíbula/fisiologia
Mandíbula/cirurgia
Células Mesenquimais Estromais/enzimologia
Células Mesenquimais Estromais/fisiologia
Piridinas/farmacologia
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
Microtomografia por Raio-X
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Imidazoles); 0 (Pyridines); 6C74YM2NGI (Anisomycin); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); OU13V1EYWQ (SB 203580)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170330
[Lr] Data última revisão:
170330
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161022
[St] Status:MEDLINE


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[PMID]:27764671
[Au] Autor:Schanzenbächer CT; Sambandan S; Langer JD; Schuman EM
[Ad] Endereço:Max Planck Institute for Brain Research, Max von Laue Strasse 4, 60438 Frankfurt am Main, Germany; Max Planck Institute for Biophysics, Max von Laue Strasse 3, 60438 Frankfurt am Main, Germany.
[Ti] Título:Nascent Proteome Remodeling following Homeostatic Scaling at Hippocampal Synapses.
[So] Source:Neuron;92(2):358-371, 2016 Oct 19.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Homeostatic scaling adjusts the strength of synaptic connections up or down in response to large changes in input. To identify the landscape of proteomic changes that contribute to opposing forms of homeostatic plasticity, we examined the plasticity-induced changes in the newly synthesized proteome. Cultured rat hippocampal neurons underwent homeostatic up-scaling or down-scaling. We used BONCAT (bio-orthogonal non-canonical amino acid tagging) to metabolically label, capture, and identify newly synthesized proteins, detecting and analyzing 5,940 newly synthesized proteins using mass spectrometry and label-free quantitation. Neither up- nor down-scaling produced changes in the number of different proteins translated. Rather, up- and down-scaling elicited opposing translational regulation of several molecular pathways, producing targeted adjustments in the proteome. We discovered ∼300 differentially regulated proteins involved in neurite outgrowth, axon guidance, filopodia assembly, excitatory synapses, and glutamate receptor complexes. We also identified differentially regulated proteins that are associated with multiple diseases, including schizophrenia, epilepsy, and Parkinson's disease.
[Mh] Termos MeSH primário: Hipocampo/metabolismo
Homeostase
Neurônios/metabolismo
Proteoma/metabolismo
Sinapses/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Anisomicina/farmacologia
Orientação de Axônios/efeitos dos fármacos
Bicuculina/farmacologia
Células Cultivadas
Cromatografia Líquida
Antagonistas de Receptores de GABA-A/farmacologia
Hipocampo/citologia
Hipocampo/efeitos dos fármacos
Crescimento Neuronal/efeitos dos fármacos
Plasticidade Neuronal
Neurônios/efeitos dos fármacos
Técnicas de Patch-Clamp
Inibidores da Síntese de Proteínas/farmacologia
Proteoma/efeitos dos fármacos
Pseudópodes/efeitos dos fármacos
Pseudópodes/metabolismo
Ratos
Ratos Sprague-Dawley
Receptores de Glutamato/efeitos dos fármacos
Receptores de Glutamato/metabolismo
Sinapses/efeitos dos fármacos
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA-A Receptor Antagonists); 0 (Protein Synthesis Inhibitors); 0 (Proteome); 0 (Receptors, Glutamate); 6C74YM2NGI (Anisomycin); Y37615DVKC (Bicuculline)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE


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[PMID]:27733615
[Au] Autor:Levitan D; Fortis-Santiago Y; Figueroa JA; Reid EE; Yoshida T; Barry NC; Russo A; Katz DB
[Ad] Endereço:Program of Neuroscience, dbkatz@brandeis.edu levitand@brandeis.edu.
[Ti] Título:Memory Retrieval Has a Dynamic Influence on the Maintenance Mechanisms That Are Sensitive to ζ-Inhibitory Peptide (ZIP).
[So] Source:J Neurosci;36(41):10654-10662, 2016 Oct 12.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In neuroscientists' attempts to understand the long-term storage of memory, topics of particular importance and interest are the cellular and system mechanisms of maintenance (e.g., those sensitive to ζ-inhibitory peptide, ZIP) and those induced by memory retrieval (i.e., reconsolidation). Much is known about each of these processes in isolation, but less is known concerning how they interact. It is known that ZIP sensitivity and memory retrieval share at least some molecular targets (e.g., recycling α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, AMPA, receptors to the plasma membrane); conversely, the fact that sensitivity to ZIP emerges only after consolidation ends suggests that consolidation (and by extension reconsolidation) and maintenance might be mutually exclusive processes, the onset of one canceling the other. Here, we use conditioned taste aversion (CTA) in rats, a cortically dependent learning paradigm, to test this hypothesis. First, we demonstrate that ZIP infusions into gustatory cortex begin interfering with CTA memory 43-45 h after memory acquisition-after consolidation ends. Next, we show that a retrieval trial administered after this time point interrupts the ability of ZIP to induce amnesia and that ZIP's ability to induce amnesia is reengaged only 45 h after retrieval. This pattern of results suggests that memory retrieval and ZIP-sensitive maintenance mechanisms are mutually exclusive and that the progression from one to the other are similar after acquisition and retrieval. They also reveal concrete differences between ZIP-sensitive mechanisms induced by acquisition and retrieval: the latency with which ZIP-sensitive mechanisms are expressed differ for the two processes. SIGNIFICANCE STATEMENT: Memory retrieval and the molecular mechanisms that are sensitive to ζ-inhibitory peptide (ZIP) are the few manipulations that have been shown to effect memory maintenance. Although much is known about their effect on maintenance separately, it is unknown how they interact. Here, we describe a model for the interaction between memory retrieval and ZIP-sensitive mechanisms, showing that retrieval trials briefly (i.e., for 45 h) interrupt these mechanisms. ZIP sensitivity emerges across a similar time window after memory acquisition and retrieval; the maintenance mechanisms that follow acquisition and retrieval differ, however, in the latency with which the impact of ZIP is expressed.
[Mh] Termos MeSH primário: Aprendizagem da Esquiva/efeitos dos fármacos
Lipopeptídeos/farmacologia
Memória/efeitos dos fármacos
Rememoração Mental/efeitos dos fármacos
Paladar/efeitos dos fármacos
[Mh] Termos MeSH secundário: Amnésia/induzido quimicamente
Amnésia/psicologia
Animais
Anisomicina/farmacologia
Condicionamento Clássico/efeitos dos fármacos
Feminino
Lipopeptídeos/administração & dosagem
Microinjeções
Inibidores da Síntese de Proteínas/farmacologia
Ratos
Ratos Long-Evans
Córtex Somatossensorial/anatomia & histologia
Córtex Somatossensorial/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipopeptides); 0 (Protein Synthesis Inhibitors); 0 (myristoylated zeta-pseudosubstrate inhibitory peptide); 6C74YM2NGI (Anisomycin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161014
[St] Status:MEDLINE


  9 / 1192 MEDLINE  
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[PMID]:27605622
[Au] Autor:Holehonnur R; Phensy AJ; Kim LJ; Milivojevic M; Vuong D; Daison DK; Alex S; Tiner M; Jones LE; Kroener S; Ploski JE
[Ad] Endereço:School of Behavioral and Brain Sciences and Department of Molecular and Cell Biology, The University of Texas at Dallas, Dallas, Texas 75080.
[Ti] Título:Increasing the GluN2A/GluN2B Ratio in Neurons of the Mouse Basal and Lateral Amygdala Inhibits the Modification of an Existing Fear Memory Trace.
[So] Source:J Neurosci;36(36):9490-504, 2016 Sep 07.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Reconsolidation updating is a form of memory modification in which an existing memory can become destabilized upon retrieval and subsequently be modified via protein-synthesis-dependent reconsolidation. However, not all memories appear to destabilize upon retrieval and thus are not modifiable via reconsolidation updating approaches and the neurobiological basis for this remains poorly understood. Here, we report that auditory fear memories created with 10 tone-shock pairings are resistant to retrieval-dependent memory destabilization and are associated with an increase in the synaptic GluN2A/GluN2B ratio in neurons of the basal and lateral amygdala (BLA) compared with weaker fear memories created via one or three tone-shock pairings. To increase the GluN2A/GluN2B ratio after learning, we generated a line of mice that expresses an inducible and doxycycline-dependent GFP-GluN2A transgene specifically in α-CaMKII-positive neurons. Our findings indicate that increasing the GluN2A/GluN2B ratio in BLA α-CaMKII-positive neurons after a weak fear memory has consolidated inhibits retrieval-dependent memory destabilization and modification of the fear memory trace. This was associated with a reduction in retrieval-dependent AMPA receptor trafficking, as evidenced by a reduction in retrieval-dependent phosphorylation of GluR1 at serine-845. In addition, we determined that increasing the GluN2A/GluN2B ratio before fear learning significantly impaired long term memory consolidation, whereas short-term memory remained unaltered. An increase in the GluN2A/GluN2B ratio after fear learning had no influence on fear extinction or expression. Our results underscore the importance of NMDAR subunit composition for memory destabilization and suggest a mechanism for why some memories are resistant to modification. SIGNIFICANCE STATEMENT: Memory modification using reconsolidation updating is being examined as one of the potential treatment approaches for attenuating maladaptive memories associated with emotional disorders. However, studies have shown that, whereas weak memories can be modified using reconsolidation updating, strong memories can be resistant to this approach. Therefore, treatments targeting the reconsolidation process are unlikely to be clinically effective unless methods are devised to enhance retrieval-dependent memory destabilization. Currently, little is known about the cellular and molecular events that influence the induction of reconsolidation updating. Here, we determined that an increase in the GluN2A/GluN2B ratio interferes with retrieval-dependent memory destabilization and inhibits the initiation of reconsolidation updating.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/metabolismo
Medo/psicologia
Memória/fisiologia
Receptores de N-Metil-D-Aspartato/metabolismo
[Mh] Termos MeSH secundário: Estimulação Acústica
Análise de Variância
Animais
Anisomicina/farmacologia
Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/genética
Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/metabolismo
Proteína 4 Homóloga a Disks-Large
Fármacos atuantes sobre Aminoácidos Excitatórios/farmacologia
Extinção Psicológica/efeitos dos fármacos
Feminino
Guanilato Quinases/metabolismo
Masculino
Proteínas de Membrana/metabolismo
Rememoração Mental/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Inibidores da Síntese de Proteínas/farmacologia
Receptores de N-Metil-D-Aspartato/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Disks Large Homolog 4 Protein); 0 (Dlg4 protein, mouse); 0 (Excitatory Amino Acid Agents); 0 (Membrane Proteins); 0 (N-methyl D-aspartate receptor subtype 2A); 0 (NR2B NMDA receptor); 0 (Protein Synthesis Inhibitors); 0 (Receptors, N-Methyl-D-Aspartate); 6C74YM2NGI (Anisomycin); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2); EC 2.7.4.8 (Guanylate Kinases)
[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:160909
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1743-16.2016


  10 / 1192 MEDLINE  
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[PMID]:27517693
[Au] Autor:Abbas AK
[Ad] Endereço:Institute of Neuroscience and Physiology, University of Gothenburg, Box 432, SE-40530, Gothenburg, Sweden.
[Ti] Título:Protein Synthesis Inhibitors Did Not Interfere with Long-Term Depression Induced either Electrically in Juvenile Rats or Chemically in Middle-Aged Rats.
[So] Source:PLoS One;11(8):e0161270, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In testing the hypothesis that long-term potentiation (LTP) maintenance depends on triggered protein synthesis, we found no effect of protein synthesis inhibitors (PSIs) on LTP stabilization. Similarly, some studies reported a lack of effect of PSIs on long-term depression (LTD); the lack of effect on LTD has been suggested to be resulting from the short time recordings. If this proposal were true, LTD might exhibit sensitivity to PSIs when the recording intervals were enough long. We firstly induced LTD by a standard protocol involving low frequency stimulation, which is suitable for eliciting NMDAR-LTD in CA1 area of hippocampal slices obtained from juvenile Sprague-Dawley rats. This LTD was persistent for intervals in range of 8-10 h. Treating slices with anisomycin, however, did not interfere with the magnitude and persistence of this form of LTD. The failure of anisomycin to block synaptic-LTD might be relied on the age of animal, the type of protein synthesis inhibitors and/or the inducing protocol. To verify whether those variables altogether were determinant, NMDA or DHPG was used to chemically elicit LTD recorded up to 10 h on hippocampal slices obtained from middle-aged rats. In either form of LTD, cycloheximide did not interfere with LTD stabilization. Furthermore, DHPG application did show an increase in the global protein synthesis as assayed by radiolabeled methodology indicating that though triggered protein synthesis can occur but not necessarily required for LTD expression. The findings confirm that stabilized LTD in either juvenile, or middle-aged rats can be independent of triggered protein synthesis. Although the processes responsible for the independence of LTD stabilization on the triggered protein synthesis are not yet defined, these findings raise the possibility that de novo protein synthesis is not universally necessary.
[Mh] Termos MeSH primário: Estimulação Elétrica
Hipocampo/efeitos dos fármacos
Potenciação de Longa Duração/efeitos dos fármacos
Depressão Sináptica de Longo Prazo/efeitos dos fármacos
Biossíntese de Proteínas/efeitos dos fármacos
Inibidores da Síntese de Proteínas/farmacologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Anisomicina/farmacologia
Cicloeximida/farmacologia
Eletrofisiologia
Hipocampo/metabolismo
Masculino
Plasticidade Neuronal/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Synthesis Inhibitors); 6C74YM2NGI (Anisomycin); 98600C0908 (Cycloheximide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160813
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0161270



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