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[PMID]:29216332
[Au] Autor:Kanatani S; Fuks JM; Olafsson EB; Westermark L; Chambers B; Varas-Godoy M; Uhlén P; Barragan A
[Ad] Endereço:Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
[Ti] Título:Voltage-dependent calcium channel signaling mediates GABAA receptor-induced migratory activation of dendritic cells infected by Toxoplasma gondii.
[So] Source:PLoS Pathog;13(12):e1006739, 2017 Dec.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The obligate intracellular parasite Toxoplasma gondii exploits cells of the immune system to disseminate. Upon T. gondii-infection, γ-aminobutyric acid (GABA)/GABAA receptor signaling triggers a hypermigratory phenotype in dendritic cells (DCs) by unknown signal transduction pathways. Here, we demonstrate that calcium (Ca2+) signaling in DCs is indispensable for T. gondii-induced DC hypermotility and transmigration in vitro. We report that activation of GABAA receptors by GABA induces transient Ca2+ entry in DCs. Murine bone marrow-derived DCs preferentially expressed the L-type voltage-dependent Ca2+ channel (VDCC) subtype Cav1.3. Silencing of Cav1.3 by short hairpin RNA or selective pharmacological antagonism of VDCCs abolished the Toxoplasma-induced hypermigratory phenotype. In a mouse model of toxoplasmosis, VDCC inhibition of adoptively transferred Toxoplasma-infected DCs delayed the appearance of cell-associated parasites in the blood circulation and reduced parasite dissemination to target organs. The present data establish that T. gondii-induced hypermigration of DCs requires signaling via VDCCs and that Ca2+ acts as a second messenger to GABAergic signaling via the VDCC Cav1.3. The findings define a novel motility-related signaling axis in DCs and unveil that interneurons and DCs share common GABAergic motogenic pathways. T. gondii employs GABAergic non-canonical pathways to induce host cell migration and facilitate dissemination.
[Mh] Termos MeSH primário: Canais de Cálcio Tipo L/imunologia
Sinalização do Cálcio
Células Dendríticas/imunologia
Receptores de GABA-A/imunologia
Toxoplasma/imunologia
Toxoplasmose/imunologia
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Movimento Celular
Células Cultivadas
Células Dendríticas/parasitologia
GABAérgicos/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Toxoplasma/fisiologia
Toxoplasmose/parasitologia
Ácido gama-Aminobutírico/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cacna1d protein, mouse); 0 (Calcium Channels, L-Type); 0 (GABA Agents); 0 (Receptors, GABA-A); 56-12-2 (gamma-Aminobutyric Acid)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171220
[Lr] Data última revisão:
171220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006739


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[PMID]:28834857
[Au] Autor:Yeo QM; Wiley TL; Smith MN; Hammond DA
[Ad] Endereço:Department of Pharmacy, Changi General Hospital, Singapore (Dr Yeo); Department of Pharmacy, The University of Mississippi Medical Center, Jackson (Dr Wiley); Department of Pharmacy, Medical University of South Carolina, Charleston (Dr Smith); and Department of Pharmacy, Rush University Medical Center, Chicago, Illinois (Dr Hammond).
[Ti] Título:Oral Agents for the Management of Agitation and Agitated Delirium in Critically Ill Patients.
[So] Source:Crit Care Nurs Q;40(4):344-362, 2017 Oct/Dec.
[Is] ISSN:1550-5111
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Agitation is one of the most common issues that critically ill patients experience. Medications used to manage agitation are often administered intravenously or intramuscularly in the acutely agitated, critically ill patient. However, a multimodal approach that utilizes multiple routes of administration may be appropriate. This review summarizes the available literature on oral antipsychotics, clonidine, and valproic acid to manage agitation in critically ill patients while also focusing on their pharmacology and appropriate monitoring. Despite inconclusive findings from different studies, antipsychotics, clonidine, and valproic acid may provide benefit for specific patient populations. As more evidence emerges, these agents may start playing a greater role in the management of agitation, which is not amenable to first-line agents. As health care professionals, it is prudent to be familiar with their dosing regimens, common adverse effects, and the monitoring required to maximize patient benefits and minimize harms.
[Mh] Termos MeSH primário: Administração Oral
Agonistas de Receptores Adrenérgicos alfa 2/uso terapêutico
Antipsicóticos/uso terapêutico
Clonidina/uso terapêutico
Estado Terminal
Delírio/tratamento farmacológico
GABAérgicos/uso terapêutico
Agitação Psicomotora/tratamento farmacológico
Ácido Valproico/uso terapêutico
[Mh] Termos MeSH secundário: Protocolos Clínicos
Cuidados Críticos
Enfermagem de Cuidados Críticos
Delírio/etiologia
Seres Humanos
Agitação Psicomotora/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenergic alpha-2 Receptor Agonists); 0 (Antipsychotic Agents); 0 (GABA Agents); 614OI1Z5WI (Valproic Acid); MN3L5RMN02 (Clonidine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:N
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1097/CNQ.0000000000000172


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[PMID]:28575529
[Au] Autor:Uchida T; Lossin C; Ihara Y; Deshimaru M; Yanagawa Y; Koyama S; Hirose S
[Ad] Endereço:Central Research Institute for the Pathomechanisms of Epilepsy, Fukuoka University, Fukuoka, Japan.
[Ti] Título:Abnormal γ-aminobutyric acid neurotransmission in a Kcnq2 model of early onset epilepsy.
[So] Source:Epilepsia;58(8):1430-1439, 2017 Aug.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Mutations of the KCNQ2 gene, which encodes the K 7.2 subunit of voltage-gated M-type potassium channels, have been associated with epilepsy in the neonatal period. This developmental stage is unique in that the neurotransmitter gamma aminobutyric acid (GABA), which is inhibitory in adults, triggers excitatory action due to a reversed chloride gradient. METHODS: To examine whether KCNQ2-related neuronal hyperexcitability involves neonatally excitatory GABA, we examined 1-week-old knockin mice expressing the K 7.2 variant p.Tyr284Cys (Y284C). RESULTS: Brain slice electrophysiology revealed elevated CA1 hippocampal GABAergic interneuron activity with respect to presynaptic firing and postsynaptic current frequency. Blockade with the GABA receptor antagonist bicuculline decreased ictal-like bursting in brain slices with lowered divalent ion concentration, which is consistent with GABA mediating an excitatory function that contributes to the hyperexcitability observed in mutant animals. SIGNIFICANCE: We conclude that excitatory GABA contributes to the phenotype in these animals, which raises the question of whether this special type of neurotransmission has broader importance in neonatal epilepsy than is currently recognized.
[Mh] Termos MeSH primário: Epilepsia/genética
Epilepsia/metabolismo
Canal de Potássio KCNQ2/genética
Mutação/genética
Proteínas do Tecido Nervoso/genética
Transmissão Sináptica/genética
Ácido gama-Aminobutírico/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Biofísica
Região CA1 Hipocampal/citologia
Região CA1 Hipocampal/metabolismo
Modelos Animais de Doenças
Estimulação Elétrica
GABAérgicos/farmacologia
Técnicas In Vitro
Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos
Potenciais Pós-Sinápticos Inibidores/genética
Interneurônios/efeitos dos fármacos
Interneurônios/fisiologia
Magnésio/farmacologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Técnicas de Patch-Clamp
Transmissão Sináptica/efeitos dos fármacos
Ácido gama-Aminobutírico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA Agents); 0 (KCNQ2 Potassium Channel); 0 (Kcnq2 protein, mouse); 0 (Nerve Tissue Proteins); 56-12-2 (gamma-Aminobutyric Acid); I38ZP9992A (Magnesium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170603
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13807


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[PMID]:28407680
[Au] Autor:Gobshtis N; Tfilin M; Wolfson M; Fraifeld VE; Turgeman G
[Ad] Endereço:Departments of Pre-Medical Studies & Molecular Biology, Ariel University, Ariel, Israel.
[Ti] Título:Transplantation of mesenchymal stem cells reverses behavioural deficits and impaired neurogenesis caused by prenatal exposure to valproic acid.
[So] Source:Oncotarget;8(11):17443-17452, 2017 Mar 14.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neurodevelopmental impairment can affect lifelong brain functions such as cognitive and social behaviour, and may contribute to aging-related changes of these functions. In the present study, we hypothesized that bone marrow-derived mesenchymal stem cells (MSC) administration may repair neurodevelopmental behavioural deficits by modulating adult hippocampal neurogenesis. Indeed, postnatal intracerebral transplantation of MSC has restored cognitive and social behaviour in mice prenatally exposed to valproic acid (VPA). MSC transplantation also restored post-developmental hippocampal neurogenesis, which was impaired in VPA-exposed mice displaying delayed differentiation and maturation of newly formed neurons in the granular cell layer of the dentate gyrus. Importantly, a statistically significant correlation was found between neuronal differentiation scores and behavioural scores, suggesting a mechanistic relation between the two. We thus conclude that post-developmental MSC administration can overcome prenatal neurodevelopmental deficits and restore cognitive and social behaviours via modulation of hippocampal adult neurogenesis.
[Mh] Termos MeSH primário: Hipocampo
Transplante de Células-Tronco Mesenquimais/métodos
Transtornos do Neurodesenvolvimento/complicações
Neurogênese
Efeitos Tardios da Exposição Pré-Natal/terapia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/fisiologia
Modelos Animais de Doenças
Feminino
GABAérgicos/toxicidade
Imuno-Histoquímica
Aprendizagem em Labirinto
Camundongos
Transtornos do Neurodesenvolvimento/induzido quimicamente
Neurogênese/fisiologia
Neurônios/citologia
Gravidez
Efeitos Tardios da Exposição Pré-Natal/etiologia
Comportamento Social
Ácido Valproico/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA Agents); 614OI1Z5WI (Valproic Acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170415
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15245


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[PMID]:28326934
[Au] Autor:Koga K; Matsuzaki Y; Honda K; Eto F; Furukawa T; Migita K; Irie K; Mishima K; Ueno S
[Ad] Endereço:1 Department of Neurophysiology, Hirosaki University Graduate School of Medicine, Japan.
[Ti] Título:Activations of muscarinic M receptors in the anterior cingulate cortex contribute to the antinociceptive effect via GABAergic transmission.
[So] Source:Mol Pain;13:1744806917692330, 2017 Jan.
[Is] ISSN:1744-8069
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background Cholinergic systems regulate the synaptic transmission resulting in the contribution of the nociceptive behaviors. Anterior cingulate cortex is a key cortical area to play roles in nociception and chronic pain. However, the effect of the activation of cholinergic system for nociception is still unknown in the cortical area. Here, we tested whether the activation of cholinergic receptors can regulate nociceptive behaviors in adult rat anterior cingulate cortex by integrative methods including behavior, immunohistochemical, and electrophysiological methods. Results We found that muscarinic M receptors were clearly expressed in the anterior cingulate cortex. Using behavioral tests, we identified that microinjection of a selective muscarinic M receptors agonist McN-A-343 into the anterior cingulate cortex dose dependently increased the mechanical threshold. In contrast, the local injection of McN-A-343 into the anterior cingulate cortex showed normal motor function. The microinjection of a selective M receptors antagonist pirenzepine blocked the McN-A-343-induced antinociceptive effect. Pirenzepine alone into the anterior cingulate cortex decreased the mechanical thresholds. The local injection of the GABA receptors antagonist bicuculline into the anterior cingulate cortex also inhibited the McN-A-343-induced antinociceptive effect and decreased the mechanical threshold. Finally, we further tested whether the activation of M receptors could regulate GABAergic transmission using whole-cell patch-clamp recordings. The activation of M receptors enhanced the frequency of spontaneous and miniature inhibitory postsynaptic currents as well as the amplitude of spontaneous inhibitory postsynaptic currents in the anterior cingulate cortex. Conclusions These results suggest that the activation of muscarinic M receptors in part increased the mechanical threshold by increasing GABAergic transmitter release and facilitating GABAergic transmission in the anterior cingulate cortex.
[Mh] Termos MeSH primário: Analgésicos/uso terapêutico
Giro do Cíngulo/metabolismo
Hiperalgesia/tratamento farmacológico
Receptor Muscarínico M1/metabolismo
Transmissão Sináptica/fisiologia
Ácido gama-Aminobutírico/metabolismo
[Mh] Termos MeSH secundário: Cloreto de (4-(m-Clorofenilcarbamoiloxi)-2-butinil)trimetilamônio/farmacologia
Cloreto de (4-(m-Clorofenilcarbamoiloxi)-2-butinil)trimetilamônio/uso terapêutico
Analgésicos/farmacologia
Animais
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Fármacos atuantes sobre Aminoácidos Excitatórios/farmacologia
GABAérgicos/farmacologia
Giro do Cíngulo/efeitos dos fármacos
Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos
Potenciais Pós-Sinápticos Inibidores/fisiologia
Masculino
Atividade Motora/efeitos dos fármacos
Atividade Motora/fisiologia
Agonistas Muscarínicos/farmacologia
Agonistas Muscarínicos/uso terapêutico
Antagonistas Muscarínicos/farmacologia
Pirenzepina/farmacologia
Ratos
Ratos Wistar
Transmissão Sináptica/efeitos dos fármacos
Ácido gama-Aminobutírico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (Excitatory Amino Acid Agents); 0 (GABA Agents); 0 (Muscarinic Agonists); 0 (Muscarinic Antagonists); 0 (Receptor, Muscarinic M1); 3G0285N20N (Pirenzepine); 55-45-8 ((4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethylammonium Chloride); 56-12-2 (gamma-Aminobutyric Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE
[do] DOI:10.1177/1744806917692330


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[PMID]:28300552
[Au] Autor:Hirono M; Nagao S; Yanagawa Y; Konishi S
[Ad] Endereço:Organization for Research Initiatives and Development, Doshisha University, Kyoto 610-0394, Japan; Laboratory for Motor Learning Control, RIKEN BSI, Wako 351-0198, Japan. Electronic address: mhirono@mail.doshisha.ac.jp.
[Ti] Título:Monoaminergic modulation of GABAergic transmission onto cerebellar globular cells.
[So] Source:Neuropharmacology;118:79-89, 2017 May 15.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cerebellar Purkinje cells (PCs) project their axon collaterals to underneath of the PC layer and make GABAergic synaptic contacts with globular cells, a subgroup of Lugaro cells. GABAergic transmission derived from the PC axon collaterals is so powerful that it could inhibit globular cells and regulate their firing patterns. However, the physiological properties and implications of the GABAergic synapses on globular cells remain unknown. Using whole-cell patch-clamp recordings from globular cells in the mouse cerebellum, we examined the monoaminergic modulation of GABAergic inputs to these cells. Application of either serotonin (5-HT) or noradrenaline (NA) excited globular cells, thereby leading to their firing. The 5-HT- and NA-induced firing was temporally confined and attenuated by GABAergic transmission, although 5-HT and NA exerted an inhibitory effect on the release of GABA from presynaptic terminals of PC axon collaterals. Agonists for 5-HT receptors and α -adrenoceptors mimicked the 5-HT- and NA-induced suppression of GABAergic activity. Through their differential modulatory actions on the cerebellar inhibitory neural circuits, 5-HT facilitated PC firing, whereas NA suppressed it. These results indicate that 5-HT and NA regulate the membrane excitability of globular cells and PCs through their differential modulation of not only the membrane potential but also GABAergic synaptic circuits. Monoaminergic modulation of the neural connections between globular cells and PCs could play a role in cerebellar motor coordination.
[Mh] Termos MeSH primário: Monoaminas Biogênicas/farmacologia
Cerebelo/citologia
Neurônios GABAérgicos/fisiologia
Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos
Transmissão Sináptica/efeitos dos fármacos
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Animais Recém-Nascidos
Proteínas de Bactérias/genética
Proteínas de Bactérias/metabolismo
Fármacos atuantes sobre Aminoácidos Excitatórios/farmacologia
GABAérgicos/farmacologia
Glutamato Descarboxilase/genética
Glutamato Descarboxilase/metabolismo
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Modelos Biológicos
Norepinefrina/farmacologia
Serotonina/farmacologia
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/genética
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Biogenic Monoamines); 0 (Excitatory Amino Acid Agents); 0 (GABA Agents); 0 (Luminescent Proteins); 0 (Sodium Channel Blockers); 0 (Vesicular Inhibitory Amino Acid Transport Proteins); 0 (Viaat protein, mouse); 0 (yellow fluorescent protein, Bacteria); 333DO1RDJY (Serotonin); 4368-28-9 (Tetrodotoxin); EC 4.1.1.15 (Glutamate Decarboxylase); EC 4.1.1.15 (glutamate decarboxylase 1); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170317
[St] Status:MEDLINE


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[PMID]:28232472
[Au] Autor:Camilleri M; Boeckxstaens G
[Ad] Endereço:Clinical Enteric Neuroscience Translational and Epidemiological Research (CENTER), Mayo Clinic, Rochester, Minnesota, USA.
[Ti] Título:Dietary and pharmacological treatment of abdominal pain in IBS.
[So] Source:Gut;66(5):966-974, 2017 May.
[Is] ISSN:1468-3288
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:This review introduces the principles of visceral sensation and appraises the current approaches to management of visceral pain in functional GI diseases, principally IBS. These approaches include dietary measures including fibre supplementation, low fermentable oligosaccharides, disaccharides, monosaccharides and polyols diet, and pharmacological approaches such as antispasmodics, peppermint oil, antidepressants (tricyclic agents, selective serotonin reuptake inhibitors), 5-HT receptor antagonists (alosetron, ondansetron, ramosetron), non-absorbed antibiotic (rifaximin), secretagogues (lubiprostone, linaclotide), µ-opioid receptor (OR) and κ-OR agonist, δ-OR antagonist (eluxadoline), histamine H1 receptor antagonist (ebastine), neurokinin-2 receptor antagonist (ibodutant) and GABAergic agents (gabapentin and pregabalin). Efficacy and safety are discussed based on pivotal trials or published systematic reviews and meta-analysis, expressing ORs or relative risks and their 95% CIs. Potential new approaches may be based on recent insights on mucosal expression of genes, and microRNA and epigenetic markers in human biopsies and in animal models of visceral hypersensitivity.The objectives of this review are to appraise the physiology and anatomy of gut sensation and the efficacy in the relief of visceral pain (typically in IBS) of several classes of therapies. These include fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) and different classes of medications (box 1). Box 1Classes of pharmacological agents for visceral painAntidepressants (tricyclic agents, selective serotonin reuptake inhibitors)Peppermint oil5-HT receptor antagonists (alosetron, ondansetron, ramosetron)Non-absorbed antibiotic (rifaximin)Secretagogues (lubiprostone, linaclotide)µ-Opioid receptor (OR) and κ-OR agonist and δ-OR antagonist (eluxadoline)Histamine H1 receptor antagonist (ebastine)Neurokinin-2 receptor antagonist (ibodutant)GABAergic agents (gabapentin and pregabalin).
[Mh] Termos MeSH primário: Dor Abdominal/dietoterapia
Dor Abdominal/tratamento farmacológico
Síndrome do Intestino Irritável/complicações
Dor Visceral/dietoterapia
Dor Visceral/tratamento farmacológico
[Mh] Termos MeSH secundário: Dor Abdominal/etiologia
Anti-Infecciosos/uso terapêutico
Antidepressivos/uso terapêutico
Butirofenonas/uso terapêutico
Dipeptídeos/uso terapêutico
GABAérgicos/uso terapêutico
Fármacos Gastrointestinais/uso terapêutico
Antagonistas dos Receptores Histamínicos H1/uso terapêutico
Seres Humanos
Imidazóis/uso terapêutico
Parassimpatolíticos/uso terapêutico
Fenilalanina/análogos & derivados
Fenilalanina/uso terapêutico
Piperidinas/uso terapêutico
Óleos Vegetais/uso terapêutico
Probióticos/uso terapêutico
Compostos de Amônio Quaternário/uso terapêutico
Rifamicinas/uso terapêutico
Antagonistas do Receptor 5-HT3 de Serotonina/uso terapêutico
Tiofenos/uso terapêutico
Dor Visceral/etiologia
Dor Visceral/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Infective Agents); 0 (Antidepressive Agents); 0 (Butyrophenones); 0 (Dipeptides); 0 (GABA Agents); 0 (Gastrointestinal Agents); 0 (Histamine H1 Antagonists); 0 (Imidazoles); 0 (Parasympatholytics); 0 (Piperidines); 0 (Plant Oils); 0 (Quaternary Ammonium Compounds); 0 (Rifamycins); 0 (Serotonin 5-HT3 Receptor Antagonists); 0 (Thiophenes); 1H7RSQ28BJ (ibodutant); 26095-59-0 (octylonium); 45TPJ4MBQ1 (eluxadoline); 47E5O17Y3R (Phenylalanine); AV092KU4JH (peppermint oil); L36O5T016N (rifaximin); TQD7Q784P1 (ebastine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE
[do] DOI:10.1136/gutjnl-2016-313425


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[PMID]:28108734
[Au] Autor:Tseng JH; Chen CY; Chen PC; Hsiao SH; Fan CC; Liang YC; Chen CP
[Ad] Endereço:Department of Neurosurgery, Taipei City Hospital, Renai Branch, Taipei 106, Taiwan.
[Ti] Título:Valproic acid inhibits glioblastoma multiforme cell growth via paraoxonase 2 expression.
[So] Source:Oncotarget;8(9):14666-14679, 2017 Feb 28.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We studied the potential mechanisms of valproic acid (VPA) in the treatment of glioblastoma multiforme (GBM). Using the human U87, GBM8401, and DBTRG-05MG GBM-derived cell lines, VPA at concentrations of 5 to 20 mM induced G2/M cell cycle arrest and increased the production of reactive oxygen species (ROS). Stress-related molecules such as paraoxonase 2 (PON2), cyclin B1, cdc2, and Bcl-xL were downregulated, but p27, p21 and Bim were upregulated by VPA treatment. VPA response element on the PON2 promoter was localized at position -400/-1. PON2 protein expression was increased in GBM cells compared with normal brain tissue and there was a negative correlation between the expression of PON2 and Bim. These findings were confirmed by the public Bredel GBM microarray (Gene Expression Omnibus accession: GSE2223) and the Cancer Genome Atlas GBM microarray datasets. Overexpression of PON2 in GBM cells significantly decreased intracellular ROS levels, and PON2 expression was decreased after VPA stimulation compared with controls. Bim expression was significantly induced by VPA in GBM cells with PON2 silencing. These observations were further shown in the subcutaneous GBM8401 cell xenograft of BALB/c nude mice. Our results suggest that VPA reduces PON2 expression in GBM cells, which in turn increases ROS production and induces Bim production that inhibits cancer progression via the PON2-Bim cascade.
[Mh] Termos MeSH primário: Arildialquilfosfatase/metabolismo
Neoplasias Encefálicas/tratamento farmacológico
Proliferação Celular/efeitos dos fármacos
Glioblastoma/tratamento farmacológico
Ácido Valproico/farmacologia
[Mh] Termos MeSH secundário: Animais
Arildialquilfosfatase/genética
Proteína 11 Semelhante a Bcl-2/genética
Proteína 11 Semelhante a Bcl-2/metabolismo
Western Blotting
Neoplasias Encefálicas/genética
Neoplasias Encefálicas/metabolismo
Linhagem Celular Tumoral
Proliferação Celular/genética
GABAérgicos/farmacologia
Perfilação da Expressão Gênica/métodos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Glioblastoma/genética
Glioblastoma/metabolismo
Seres Humanos
Camundongos Endogâmicos BALB C
Camundongos Nus
Regiões Promotoras Genéticas/genética
Interferência de RNA
Espécies Reativas de Oxigênio/metabolismo
Elementos de Resposta/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bcl-2-Like Protein 11); 0 (GABA Agents); 0 (Reactive Oxygen Species); 614OI1Z5WI (Valproic Acid); EC 3.1.8.1 (Aryldialkylphosphatase); EC 3.1.8.1 (PON2 protein, human)
[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:170122
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.14716


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[PMID]:28071892
[Au] Autor:Nguyen MD; Wang Y; Ganesana M; Venton BJ
[Ad] Endereço:Department of Chemistry and Neuroscience Graduate Program, University of Virginia , Charlottesville, Virginia 22904, United States.
[Ti] Título:Transient Adenosine Release Is Modulated by NMDA and GABA Receptors.
[So] Source:ACS Chem Neurosci;8(2):376-385, 2017 Feb 15.
[Is] ISSN:1948-7193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adenosine is a neuroprotective agent that modulates neurotransmission and is modulated by other neurotransmitters. Spontaneous, transient adenosine is a recently discovered mode of signaling where adenosine is released and cleared from the extracellular space quickly, in less than three seconds. Spontaneous adenosine release is regulated by adenosine A and A receptors, but regulation by other neurotransmitter receptors has not been studied. Here, we examined the effect of glutamate and GABA receptors on the concentration and frequency of spontaneous, transient adenosine release by measuring adenosine with fast-scan cyclic voltammetry in the rat caudate-putamen. The glutamate NMDA antagonist, 3-(R-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP, 6.25 mg/kg i.p.), increased the frequency of adenosine transients and the concentration of individual transients, but NMDA (agonist, 50 mg/kg, i.p.) did not change the frequency. In contrast, antagonists of other glutamate receptors had no effect on the frequency or concentration of transient adenosine release, including the AMPA antagonist NBQX (15 mg/kg i.p.) and the mGlu2/3 glutamate receptor antagonist LY 341495 (5 mg/kg i.p.). The GABA antagonist CGP 52432 (30 mg/kg i.p.) significantly decreased the number of adenosine release events while the GABA agonist baclofen (4 mg/kg i.p.) increased the frequency of adenosine release. The GABA antagonist bicuculline (5 mg/kg i.p.) had no significant effects on adenosine. NMDA and GABA likely act presynaptically, affecting the overall cell excitability for vesicular release. The ability to regulate adenosine with NMDA and GABA receptors will help control the modulatory effects of transient adenosine release.
[Mh] Termos MeSH primário: Adenosina/metabolismo
Técnicas Eletroquímicas
N-Metilaspartato/farmacologia
Receptores de GABA-A/metabolismo
Receptores de N-Metil-D-Aspartato/metabolismo
[Mh] Termos MeSH secundário: Animais
Núcleo Caudado/efeitos dos fármacos
Núcleo Caudado/metabolismo
Relação Dose-Resposta a Droga
Fármacos atuantes sobre Aminoácidos Excitatórios/farmacologia
GABAérgicos/farmacologia
Masculino
Putamen/efeitos dos fármacos
Putamen/metabolismo
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Excitatory Amino Acid Agents); 0 (GABA Agents); 0 (Receptors, GABA-A); 0 (Receptors, N-Methyl-D-Aspartate); 6384-92-5 (N-Methylaspartate); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170111
[St] Status:MEDLINE
[do] DOI:10.1021/acschemneuro.6b00318


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[PMID]:28067943
[Au] Autor:Diana A; Pillai R; Bongioanni P; O'Keeffe AG; Miller RG; Moore DH
[Ad] Endereço:Department of Biomedical Sciences, University of Cagliari, Citta Universitaria di Monserrato (Cagliari), Monserrato (Cagliari), Italy, 09042.
[Ti] Título:Gamma aminobutyric acid (GABA) modulators for amyotrophic lateral sclerosis/motor neuron disease.
[So] Source:Cochrane Database Syst Rev;1:CD006049, 2017 01 09.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Imbalance of gamma aminobutyric acid (GABA) and related modulators has been implicated as an important factor in the pathogenesis of amyotrophic lateral sclerosis (ALS), which is also known as motor neuron disease (MND). In this context, the role and mechanism of action of gabapentin and baclofen have been extensively investigated, although with conflicting results. This is the first systematic review to assess clinical trials of GABA modulators for the treatment of ALS. OBJECTIVES: To examine the efficacy of gabapentin, baclofen, or other GABA modulators in delaying the progression of ALS, and to evaluate adverse effects of these interventions SEARCH METHODS: On 16 August 2016, we searched the Cochrane Neuromuscular Specialised Register, Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, Embase, CINAHL Plus, AMED, and LILACS. In addition, we checked the bibliographies of the trials found in order to identify any other trials, and contacted trial authors to identify relevant unpublished results or additional clinical trials. On 30 August 2016, we searched two clinical trials registries. SELECTION CRITERIA: Types of studies: double-blind randomized controlled trials (RCTs) or quasi-RCTsTypes of participants: adults with a diagnosis of probable or definite ALSTypes of interventions: gabapentin, baclofen, or other GABA modulators compared with placebo, no treatment, or each otherPrimary outcome: survival at one year from study enrollmentSecondary outcomes: individual rate of decline of maximum voluntary isometric contraction (MVIC), expressed as arm megascore; rate of decline of per cent predicted forced vital capacity (FVC); rate of decline of ALS Functional Rating Scale (ALSFRS); health-related quality of life; survival evaluated by pooling hazards; and adverse events DATA COLLECTION AND ANALYSIS: At least two review authors independently checked titles and abstracts identified by the searches. The review authors obtained and independently analyzed original individual participant data from each included study; additional review authors and the Cochrane Neuromuscular Managing Editor checked the outcome data. Two authors independently assessed the risk of bias in included studies. Data collection and analysis: At least two review authors independently checked titles and abstracts identified by the searches. The review authors obtained and independently analyzed original individual participant data from each included study; additional review authors and the Cochrane Neuromuscular Managing Editor checked the outcome data. Two authors independently assessed the risk of bias in included studies. MAIN RESULTS: We identified two double-blind RCTs of gabapentin treatment in ALS for inclusion in this review. We found no eligible RCTs of baclofen or other GABA modulators. The selected studies were phase II and phase III trials, which lasted six and nine months, respectively. They were highly comparable because both were comparisons of oral gabapentin and placebo, performed by the same investigators. The trials enrolled 355 participants with ALS: 80 in the gabapentin group and 72 in the placebo group in the first (phase II) trial and 101 in the gabapentin group and 102 in the placebo group in the second (phase III) trial. Neither trial was long enough to report survival at one year, which was our primary outcome. We found little or no difference in estimated one-year survival between the treated group and the placebo group (78% versus 77%, P = 0.63 by log-rank test; high-quality evidence). We also found little or no difference in the rate of decline of MVIC expressed as arm megascore, or rate of FVC decline (high-quality evidence). One trial investigated monthly decline in the ALSFRS and quality of life measured using the 12-Item Short Form Survey (SF-12) and found little or no difference between groups (moderate-quality evidence). The trials reported similar adverse events. Complaints that were clearly elevated in those taking gabapentin, based on analyses of the combined data, were light-headedness, drowsiness, and limb swelling (high-quality evidence). Fatigue and falls occurred more frequently with gabapentin than with placebo in one trial, but when we combined the data for fatigue from both trials, there was no clear difference between the groups. We assessed the overall risk of bias in the included trials as low. AUTHORS' CONCLUSIONS: According to high-quality evidence, gabapentin is not effective in treating ALS. It does not extend survival, slow the rate of decline of muscle strength, respiratory function and, based on moderate-quality evidence, probably does not improve quality of life or slow monthly decline in the ALSFRS. Other GABA modulators have not been studied in randomized trials.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/tratamento farmacológico
GABAérgicos/uso terapêutico
Ácido gama-Aminobutírico/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Esclerose Amiotrófica Lateral/mortalidade
Baclofeno/uso terapêutico
Ensaios Clínicos Fase II como Assunto
Ensaios Clínicos Fase III como Assunto
GABAérgicos/efeitos adversos
Seres Humanos
Ensaios Clínicos Controlados Aleatórios como Assunto
Fatores de Tempo
Ácido gama-Aminobutírico/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (GABA Agents); 56-12-2 (gamma-Aminobutyric Acid); H789N3FKE8 (Baclofen)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170426
[Lr] Data última revisão:
170426
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170110
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD006049.pub2



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