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Pesquisa : D02.092.471.683.152.200 [Categoria DeCS]
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[PMID]:27560450
[Au] Autor:Jiang Y; Lee J; Lee JH; Lee JW; Kim JH; Choi WH; Yoo YD; Cha-Molstad H; Kim BY; Kwon YT; Noh SA; Kim KP; Lee MJ
[Ad] Endereço:a Department of Biochemistry and Molecular Biology , Seoul National University College of Medicine , Seoul , Korea.
[Ti] Título:The arginylation branch of the N-end rule pathway positively regulates cellular autophagic flux and clearance of proteotoxic proteins.
[So] Source:Autophagy;12(11):2197-2212, 2016 Nov.
[Is] ISSN:1554-8635
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The N-terminal amino acid of a protein is an essential determinant of ubiquitination and subsequent proteasomal degradation in the N-end rule pathway. Using para-chloroamphetamine (PCA), a specific inhibitor of the arginylation branch of the pathway (Arg/N-end rule pathway), we identified that blocking the Arg/N-end rule pathway significantly impaired the fusion of autophagosomes with lysosomes. Under ER stress, ATE1-encoded Arg-tRNA-protein transferases carry out the N-terminal arginylation of the ER heat shock protein HSPA5 that initially targets cargo proteins, along with SQSTM1, to the autophagosome. At the late stage of autophagy, however, proteasomal degradation of arginylated HSPA5 might function as a critical checkpoint for the proper progression of autophagic flux in the cells. Consistently, the inhibition of the Arg/N-end rule pathway with PCA significantly elevated levels of MAPT and huntingtin aggregates, accompanied by increased numbers of LC3 and SQSTM1 puncta. Cells treated with the Arg/N-end rule inhibitor became more sensitized to proteotoxic stress-induced cytotoxicity. SILAC-based quantitative proteomics also revealed that PCA significantly alters various biological pathways, including cellular responses to stress, nutrient, and DNA damage, which are also closely involved in modulation of autophagic responses. Thus, our results indicate that the Arg/N-end rule pathway may function to actively protect cells from detrimental effects of cellular stresses, including proteotoxic protein accumulation, by positively regulating autophagic flux.
[Mh] Termos MeSH primário: Arginina/metabolismo
Autofagia
Proteínas/toxicidade
[Mh] Termos MeSH secundário: Animais
Autofagossomos/efeitos dos fármacos
Autofagossomos/metabolismo
Autofagia/efeitos dos fármacos
Biomarcadores/metabolismo
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Células HEK293
Células HeLa
Proteínas de Choque Térmico/metabolismo
Seres Humanos
Proteína Huntingtina/metabolismo
Marcação por Isótopo
Lisossomos/efeitos dos fármacos
Lisossomos/metabolismo
Fusão de Membrana/efeitos dos fármacos
Camundongos
Modelos Biológicos
Complexo de Endopeptidases do Proteassoma/metabolismo
Agregados Proteicos/efeitos dos fármacos
Proteólise/efeitos dos fármacos
Proteômica
Transdução de Sinais/efeitos dos fármacos
Bibliotecas de Moléculas Pequenas/farmacologia
p-Cloroanfetamina/farmacologia
Proteínas tau/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Heat-Shock Proteins); 0 (Huntingtin Protein); 0 (Protein Aggregates); 0 (Proteins); 0 (Small Molecule Libraries); 0 (molecular chaperone GRP78); 0 (tau Proteins); 64-12-0 (p-Chloroamphetamine); 94ZLA3W45F (Arginine); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160826
[St] Status:MEDLINE


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[PMID]:27499251
[Au] Autor:Jin C; Decker AM; Harris DL; Blough BE
[Ad] Endereço:Center for Drug Discovery, Research Triangle Institute , Research Triangle Park, North Carolina 27709, United States.
[Ti] Título:Effect of Substitution on the Aniline Moiety of the GPR88 Agonist 2-PCCA: Synthesis, Structure-Activity Relationships, and Molecular Modeling Studies.
[So] Source:ACS Chem Neurosci;7(10):1418-1432, 2016 Oct 19.
[Is] ISSN:1948-7193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:GPR88, an orphan receptor richly expressed in the striatum, is implicated in a number of basal ganglia-associated disorders. In order to elucidate the functions of GPR88, an in vivo probe appropriate for CNS investigation is required. We previously reported that 2-PCCA was able to modulate GPR88-mediated cAMP production through a Gα -coupled pathway. Early structure-activity relationship (SAR) studies suggested that the aniline moiety of 2-PCCA is a suitable site for diverse modifications. Aimed at elucidating structural requirements in this region, we have designed and synthesized a series of analogues bearing a variety of substituents at the phenyl ring of the aniline moiety. Several compounds (e.g., 5j, 5o) showed improved or comparable potency, but have lower lipophilicity than 2-PCCA (clogP 6.19). These compounds provide the basis for further optimization to probe GPR88 in vivo functions. Computational studies confirmed the SAR trends and supported the notion that 4'-substituents on the biphenyl ring exit through a largely hydrophobic binding site to the extracellular loop.
[Mh] Termos MeSH primário: Cromanos/química
Cromanos/farmacologia
Neurotransmissores/química
Neurotransmissores/farmacologia
Receptores Acoplados a Proteínas-G/agonistas
p-Cloroanfetamina/análogos & derivados
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Compostos de Anilina/química
Animais
Sítios de Ligação
Células CHO
Cromanos/síntese química
Cricetulus
Seres Humanos
Interações Hidrofóbicas e Hidrofílicas
Simulação de Acoplamento Molecular
Estrutura Molecular
Neurotransmissores/síntese química
Receptores Acoplados a Proteínas-G/genética
Receptores Acoplados a Proteínas-G/metabolismo
Relação Estrutura-Atividade
p-Cloroanfetamina/síntese química
p-Cloroanfetamina/química
p-Cloroanfetamina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aniline Compounds); 0 (Chromans); 0 (GPR88 protein, human); 0 (Neurotransmitter Agents); 0 (Receptors, G-Protein-Coupled); 61114-41-8 (2-(4-chlorophenyl)cyclopropylamine); 64-12-0 (p-Chloroamphetamine); SIR7XX2F1K (aniline)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160809
[St] Status:MEDLINE


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[PMID]:27499084
[Au] Autor:Jin Y; Dougherty SE; Wood K; Sun L; Cudmore RH; Abdalla A; Kannan G; Pletnikov M; Hashemi P; Linden DJ
[Ad] Endereço:Solomon H. Snyder Department of Neuroscience, School of Medicine, Johns Hopkins University, 725 North Wolfe Street, Baltimore, MD 21205, USA.
[Ti] Título:Regrowth of Serotonin Axons in the Adult Mouse Brain Following Injury.
[So] Source:Neuron;91(4):748-762, 2016 Aug 17.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It is widely believed that damaged axons in the adult mammalian brain have little capacity to regrow, thereby impeding functional recovery after injury. Studies using fixed tissue have suggested that serotonin neurons might be a notable exception, but remain inconclusive. We have employed in vivo two-photon microscopy to produce time-lapse images of serotonin axons in the neocortex of the adult mouse. Serotonin axons undergo massive retrograde degeneration following amphetamine treatment and subsequent slow recovery of axonal density, which is dominated by new growth with little contribution from local sprouting. A stab injury that transects serotonin axons running in the neocortex is followed by local regression of cut serotonin axons and followed by regrowth from cut ends into and across the stab rift zone. Regrowing serotonin axons do not follow the pathways left by degenerated axons. The regrown axons release serotonin and their regrowth is correlated with recovery in behavioral tests.
[Mh] Termos MeSH primário: Axônios/fisiologia
Lesões Encefálicas/patologia
Neocórtex/citologia
Neocórtex/fisiologia
Regeneração Nervosa/fisiologia
Neurônios Serotoninérgicos/fisiologia
[Mh] Termos MeSH secundário: Animais
Lesões Encefálicas/fisiopatologia
Camundongos
Camundongos Transgênicos
Neocórtex/patologia
Reflexo de Sobressalto/fisiologia
Degeneração Retrógrada/induzido quimicamente
Neurônios Serotoninérgicos/citologia
Neurônios Serotoninérgicos/patologia
Imagem com Lapso de Tempo
p-Cloroanfetamina/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
64-12-0 (p-Chloroamphetamine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170827
[Lr] Data última revisão:
170827
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160809
[St] Status:MEDLINE


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[PMID]:26846719
[Au] Autor:Furlong TM; Leavitt LS; Keefe KA; Son JH
[Ad] Endereço:Department of Pharmacology and Toxicology, University of Utah, 30 S. 2000 E., Rm 201, Salt Lake City, UT, 84112, USA. teri.furlong@utah.edu.
[Ti] Título:Methamphetamine-, d-Amphetamine-, and p-Chloroamphetamine-Induced Neurotoxicity Differentially Effect Impulsive Responding on the Stop-Signal Task in Rats.
[So] Source:Neurotox Res;29(4):569-82, 2016 May.
[Is] ISSN:1476-3524
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Abused amphetamines, such as d-amphetamine (AMPH) and methamphetamine (METH), are highly addictive and destructive to health and productive lifestyles. The abuse of these drugs is associated with impulsive behavior, which is likely to contribute to addiction. The amphetamines also differentially damage dopamine (DA) and serotonin (5-HT) systems, which regulate impulsive behavior; therefore, exposure to these drugs may differentially alter impulsive behavior to effect the progression of addiction. We examined the impact of neurotoxicity induced by three amphetamines on impulsive action using a stop-signal task in rats. Animals were rewarded with a food pellet after lever pressing (i.e., a go trial), unless an auditory cue was presented and withholding lever press gained reward (i.e., a stop trial). Animals were trained on the task and then exposed to a neurotoxic regimen of either AMPH, p-chloroamphetamine (PCA), or METH. These regimens preferentially reduced DA transporter levels in striatum, 5-HT transporter levels in prefrontal cortex, or both, respectively. Assessment of performance on the stop-signal task beginning 1 week after the treatment revealed that AMPH produced a deficit in go-trial performance, whereas PCA did not alter performance on either trial type. In contrast, METH produced a deficit in stop-trial performance (i.e., impulsive action) but not go-trial performance. These findings suggest that the different neurotoxic consequences of substituted amphetamines are associated with different effects on inhibitory control over behavior. Thus, the course of addiction and maladaptive behavior resulting from exposure to these substances is likely to differ.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Estimulantes do Sistema Nervoso Central/toxicidade
Proteínas da Membrana Plasmática de Transporte de Dopamina/metabolismo
Comportamento Impulsivo/efeitos dos fármacos
Síndromes Neurotóxicas/etiologia
Síndromes Neurotóxicas/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Temperatura Corporal/efeitos dos fármacos
Encéfalo/metabolismo
Dextroanfetamina
Modelos Animais de Doenças
Dopamina/metabolismo
Masculino
Metanfetamina
Atividade Motora/efeitos dos fármacos
Testes Neuropsicológicos
Ratos
Ratos Sprague-Dawley
Serotonina/metabolismo
Proteínas da Membrana Plasmática de Transporte de Serotonina
Fatores de Tempo
p-Cloroanfetamina
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Central Nervous System Stimulants); 0 (Dopamine Plasma Membrane Transport Proteins); 0 (Serotonin Plasma Membrane Transport Proteins); 333DO1RDJY (Serotonin); 44RAL3456C (Methamphetamine); 64-12-0 (p-Chloroamphetamine); TZ47U051FI (Dextroamphetamine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170501
[Lr] Data última revisão:
170501
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160206
[St] Status:MEDLINE
[do] DOI:10.1007/s12640-016-9605-9


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[PMID]:26321443
[Au] Autor:Delgermurun D; Ito S; Ohta T; Yamaguchi S; Otsuguro K
[Ad] Endereço:Laboratory of Pharmacology, Department of Biomedical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo 060-0818, Japan.
[Ti] Título:Endogenous 5-HT outflow from chicken aorta by 5-HT uptake inhibitors and amphetamine derivatives.
[So] Source:J Vet Med Sci;78(1):71-6, 2016 Jan.
[Is] ISSN:1347-7439
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Chemoreceptor cells aggregating in clusters in the chicken thoracic aorta contain 5-hydroxytryptamine (5-HT) and have voltage-dependent ion channels and nicotinic acetylcholine receptors, which are characteristics typically associated with neurons. The aim of the present study was to investigate the effects of 5-HT uptake inhibitors, fluvoxamine, fluoxetine and clomipramine (CLM), and amphetamine derivatives, p-chloroamphetamine (PCA) and methamphetamine (MET), on endogenous 5-HT outflow from the isolated chick thoracic aorta in vitro. 5-HT was measured by using a HPLC system with electrochemical detection. The amphetamine derivatives and 5-HT uptake inhibitors caused concentration-dependent increases in endogenous 5-HT outflow. PCA was about ten times more effective in eliciting 5-HT outflow than MET. The 5-HT uptake inhibitors examined had similar potency for 5-HT outflow. PCA and CLM increased 5-HT outflow in a temperature-dependent manner. The outflow of 5-HT induced by PCA or 5-HT uptake inhibitors was independent of extracellular Ca(2+) concentration. The 5-HT outflow induced by CLM, but not that by PCA, was dependent on the extracellular NaCl concentration. These results suggest that the 5-HT uptake system of 5-HT-containing chemoreceptor cells in the chicken thoracic aorta has characteristics similar to those of 5-HT-containing neurons in the mammalian central nervous system (CNS).
[Mh] Termos MeSH primário: Aorta Torácica/efeitos dos fármacos
Metanfetamina/farmacologia
Inibidores da Captação de Serotonina/farmacologia
Serotonina/metabolismo
p-Cloroanfetamina/farmacologia
[Mh] Termos MeSH secundário: Animais
Aorta Torácica/metabolismo
Galinhas
Clomipramina/farmacologia
Fluoxetina/farmacologia
Fluvoxamina/farmacologia
Técnicas In Vitro
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Serotonin Uptake Inhibitors); 01K63SUP8D (Fluoxetine); 333DO1RDJY (Serotonin); 44RAL3456C (Methamphetamine); 64-12-0 (p-Chloroamphetamine); NUV44L116D (Clomipramine); O4L1XPO44W (Fluvoxamine)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150901
[St] Status:MEDLINE
[do] DOI:10.1292/jvms.15-0146


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[PMID]:25486044
[Au] Autor:Méndez Palacios N; Escobar ME; Mendoza MM; Crispín RH; Andrade OG; Melández JH; Martínez AA
[Ad] Endereço:Facultad de Medicina Veterinaria y Zootecnia, Benemérita Universidad Autónoma de Puebla, CP 75470, Tecamachalco, Puebla, México.
[Ti] Título:Prepubertal male rats with high rates of germ-cell apoptosis present exacerbated rates of germ-cell apoptosis after serotonin depletion.
[So] Source:Reprod Fertil Dev;28(6):806-14, 2016 Apr.
[Is] ISSN:1031-3613
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Male germ-cell apoptosis occurs naturally and can be increased by exposure to drugs and toxic chemicals. Individuals may have different rates of apoptosis and are likely to also exhibit differential sensitivity to outside influences. Previously, we reported that p-chloroamphetamine (pCA), a substance that inhibits serotonin synthesis, induced germ-cell apoptosis in prepubertal male rats. Here, we identified prepubertal rats with naturally high or low rates of germ-cell apoptosis and evaluated gene expression in both groups. Bax and Shbg mRNA levels were higher in rats with high rates of germ-cell apoptosis. Rats were then treated with pCA and the neuro-hormonal response and gene expression were evaluated. Treatment with pCA induced a reduction in serotonin concentrations but levels of sex hormones and gonadotrophins were not changed. Rats with initially high rates of germ-cell apoptosis had even higher rates of germ-cell apoptosis after treatment with pCA. In rats with high rates of germ-cell apoptosis Bax mRNA expression remained high after treatment with pCA. On the basis of category, an inverse relationship between mRNA expression of Bax and Bcl2, Bax and AR and Bax and Hsd3b2 was found. Here we provide evidence that innate levels of germ-cell apoptosis could be explained by the level of mRNA expression of genes involved with apoptosis and spermatogenesis.
[Mh] Termos MeSH primário: Apoptose
Regulação da Expressão Gênica no Desenvolvimento
Serotonina/metabolismo
Maturidade Sexual
Espermatogênese
Espermatogônias/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Ácido Hidroxi-Indolacético/metabolismo
Cinética
Masculino
Progesterona Redutase/genética
Progesterona Redutase/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
RNA Mensageiro/metabolismo
Distribuição Aleatória
Ratos
Receptores Androgênicos/genética
Receptores Androgênicos/metabolismo
Receptores de Superfície Celular/genética
Receptores de Superfície Celular/metabolismo
Serotoninérgicos/farmacologia
Maturidade Sexual/efeitos dos fármacos
Espermatogênese/efeitos dos fármacos
Espermatogônias/citologia
Espermatogônias/efeitos dos fármacos
Proteína X Associada a bcl-2/genética
Proteína X Associada a bcl-2/metabolismo
p-Cloroanfetamina/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bax protein, rat); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (RNA, Messenger); 0 (Receptors, Androgen); 0 (Receptors, Cell Surface); 0 (Serotonin Agents); 0 (bcl-2-Associated X Protein); 0 (sex hormone-binding globulin receptor); 333DO1RDJY (Serotonin); 54-16-0 (Hydroxyindoleacetic Acid); 64-12-0 (p-Chloroamphetamine); EC 1.1.1.145 (3 beta-hydroxysteroid dehydrogenase type II); EC 1.1.1.145 (Progesterone Reductase)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170405
[Lr] Data última revisão:
170405
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141209
[St] Status:MEDLINE
[do] DOI:10.1071/RD13382


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[PMID]:25560581
[Au] Autor:Cegielska-Perun K; Tatarkiewicz J; Siwek A; Dybala M; Bujalska-Zadrozny M
[Ad] Endereço:Department of Pharmacodynamics, Centre for Preclinical Research and Technology (CePT) Laboratory, Medical University of Warsaw, Warszawa, Poland. Electronic address: kcegielska@wum.edu.pl.
[Ti] Título:Mechanisms of morphine-venlafaxine interactions in diabetic neuropathic pain model.
[So] Source:Pharmacol Rep;67(1):90-6, 2015 Feb.
[Is] ISSN:1734-1140
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: we investigated the possible mechanisms involved in the interactions of venlafaxine (VFX), a selective serotonin and noradrenaline reuptake inhibitor, and morphine (MRF), an opioid receptor agonist, after acute and chronic VFX treatment in diabetic neuropathic pain model (DNPM). METHODS: The studies were performed on male rats. The changes in nociceptive thresholds were determined by using mechanical stimuli (the Randall-Selitto and the von Frey tests). Diabetes was induced by intramuscular administration of streptozotocin. In order to investigate the mechanism of interaction, animals were also pretreated with naloxone (NLX), a nonselective opioid antagonist, yohimbine (YOH), a nonselective α2-adrenergic antagonist, and p-chloroamphetamine (PCA), a neurotoxin that destroys serotonergic neurons. The µ-opioid receptors' density was determined with the use of radioligand binding assay. RESULTS: VFX potentiated antinociceptive action of MRF after acute administration of VFX and this effect was decreased by pretreatment of NLX, YOH and PCA. On the contrary, VFX administered for 21 days prior to MRF significantly decreased the analgesic action of MRF; this effect was augmented only after YOH pretreatment. Also, 21-days administration of VFX caused decreasing tendency in the number of µ-opioid receptors in the brain stem. CONCLUSIONS: The results of our study show that single administration of VFX potentiates antinociceptive action of morphine in DNPM. This effect is probably mediated by both, noradrenergic and serotonergic systems. On the other hand, 21-days administration of VFX significantly decreases analgesic action of MRF. Moreover, there is a possibility that VFX acts as an antagonist of N-methyl-d-aspartate receptors.
[Mh] Termos MeSH primário: Analgésicos Opioides/uso terapêutico
Analgésicos/uso terapêutico
Nefropatias Diabéticas/tratamento farmacológico
Morfina/uso terapêutico
Neuralgia/tratamento farmacológico
Cloridrato de Venlafaxina/uso terapêutico
[Mh] Termos MeSH secundário: Antagonistas de Receptores Adrenérgicos alfa 2/uso terapêutico
Analgésicos Opioides/antagonistas & inibidores
Animais
Tronco Encefálico/efeitos dos fármacos
Diabetes Mellitus Experimental/complicações
Sinergismo Farmacológico
Masculino
Morfina/antagonistas & inibidores
Limiar da Dor
Estimulação Física
Ratos
Receptores Opioides mu/efeitos dos fármacos
Serotoninérgicos/farmacologia
Cloridrato de Venlafaxina/antagonistas & inibidores
Ioimbina/uso terapêutico
p-Cloroanfetamina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenergic alpha-2 Receptor Antagonists); 0 (Analgesics); 0 (Analgesics, Opioid); 0 (Receptors, Opioid, mu); 0 (Serotonin Agents); 2Y49VWD90Q (Yohimbine); 64-12-0 (p-Chloroamphetamine); 76I7G6D29C (Morphine); 7D7RX5A8MO (Venlafaxine Hydrochloride)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:150106
[Lr] Data última revisão:
150106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150107
[St] Status:MEDLINE


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[PMID]:25267548
[Au] Autor:García-García L; Delgado M; Al-Sayed AA; Bascuñana P; Fernández de la Rosa R; Bermejo-Bescós P; Martín-Aragón S; Pozo MA
[Ad] Endereço:Departamento de Farmacología, Facultad de Farmacia, Universidad Complutense de Madrid, Plaza Ramón y Cajal s/n, 28040, Madrid, Spain, lgarciag@ucm.es.
[Ti] Título:In vivo [¹8F] FDG PET imaging reveals that p-chloroamphetamine neurotoxicity is associated with long-term cortical and hippocampal hypometabolism.
[So] Source:Mol Imaging Biol;17(2):239-47, 2015 Apr.
[Is] ISSN:1860-2002
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: p-Chloroamphetamine (PCA) is a neurotoxin that selectively degenerates the serotonin (5-HT) axon terminals. In order to study the brain metabolic consequences induced by serotonergic denervation, a single dose of PCA (2.5 or 10 mg/kg i.p.) was administered to male adult rats. PROCEDURES: In vivo regional brain metabolism was evaluated 3 and 21 days after PCA (2.5 or 10 mg/kg; i.p.) injection by 2-deoxy-2-[(18)F] fluoro-D-glucose ([(18)F] FDG) positron emission tomography (PET). At day 22, the following markers of neurotoxicity were determined: (a) 5-HT axon terminal lesion by 5-HT transporter (SERT) autoradiography, (b) reactive gliosis by glial fibrillary acidic protein immunohistochemistry, and (c) eventual neurodegeneration by DAPI/Fluoro-Jade C labeling. RESULTS: An average of 20 % reduction of [(18)F] FDG uptake in most brain areas was observed at day 21 under 10 mg/kg PCA treatment. Instead, 2.5 mg/kg PCA only reduced metabolic activity in neocortex. Likewise, the high dose of PCA exerted a strong decrease (>30 %) in SERT density in several 5-HT innervated regions, but no effect was found in midbrain raphe nuclei, the main source of serotonergic neurons. Although PCA induced astroglial activation both in hippocampus and cortex in response to axotomy, no signs of neuronal death in these areas were detected. CONCLUSIONS: Overall, [(18)F] FDG PET revealed that the reduction of the brain metabolic activity induced by PCA is related to 5-HT axon terminal lesion, with no apparent affectation of neuronal viability.
[Mh] Termos MeSH primário: Fluordesoxiglucose F18
Hipocampo/diagnóstico por imagem
Hipocampo/metabolismo
Neurotoxinas/toxicidade
Tomografia por Emissão de Pósitrons
p-Cloroanfetamina/toxicidade
[Mh] Termos MeSH secundário: Animais
Autorradiografia
Fluoresceínas/metabolismo
Proteína Glial Fibrilar Ácida/metabolismo
Glucose/metabolismo
Hipocampo/efeitos dos fármacos
Imuno-Histoquímica
Indóis/metabolismo
Masculino
Degeneração Neural/diagnóstico por imagem
Degeneração Neural/patologia
Ratos Sprague-Dawley
Proteínas da Membrana Plasmática de Transporte de Serotonina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fluoresceins); 0 (Glial Fibrillary Acidic Protein); 0 (Indoles); 0 (Neurotoxins); 0 (Serotonin Plasma Membrane Transport Proteins); 0 (fluoro-jade C); 0Z5B2CJX4D (Fluorodeoxyglucose F18); 47165-04-8 (DAPI); 64-12-0 (p-Chloroamphetamine); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141001
[St] Status:MEDLINE
[do] DOI:10.1007/s11307-014-0794-4


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[PMID]:24824549
[Au] Autor:De Felice LJ; Cameron KN
[Ad] Endereço:Department Physiology and Biophysics, Virginia Commonwealth University, Richmond, VA, USA.
[Ti] Título:Comments on 'A quantitative model of amphetamine action on the serotonin transporter', by Sandtner et al., Br J Pharmacol 171: 1007-1018.
[So] Source:Br J Pharmacol;172(19):4772-4, 2015 Oct.
[Is] ISSN:1476-5381
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Modelos Biológicos
N-Metil-3,4-Metilenodioxianfetamina/farmacologia
Serotoninérgicos/farmacologia
Proteínas da Membrana Plasmática de Transporte de Serotonina/fisiologia
Serotonina/farmacologia
p-Cloroanfetamina/farmacologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:COMMENT; LETTER
[Nm] Nome de substância:
0 (Serotonin Agents); 0 (Serotonin Plasma Membrane Transport Proteins); 333DO1RDJY (Serotonin); 64-12-0 (p-Chloroamphetamine); KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140515
[St] Status:MEDLINE
[do] DOI:10.1111/bph.12767


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[PMID]:24824446
[Au] Autor:Schmid D; Koenig X; Bulusu S; Schicker K; Freissmuth M; Sitte HH; Sandtner W
[Ad] Endereço:Center of Physiology and Pharmacology, Medical University Vienna, Vienna, Austria.
[Ti] Título:The conservative view: is it necessary to implant a stent into the dopamine transporter?
[So] Source:Br J Pharmacol;172(19):4775-8, 2015 Oct.
[Is] ISSN:1476-5381
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Modelos Biológicos
N-Metil-3,4-Metilenodioxianfetamina/farmacologia
Serotoninérgicos/farmacologia
Proteínas da Membrana Plasmática de Transporte de Serotonina/fisiologia
Serotonina/farmacologia
p-Cloroanfetamina/farmacologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:COMMENT; LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Serotonin Agents); 0 (Serotonin Plasma Membrane Transport Proteins); 333DO1RDJY (Serotonin); 64-12-0 (p-Chloroamphetamine); KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140515
[St] Status:MEDLINE
[do] DOI:10.1111/bph.12766



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