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Pesquisa : G11.561.484 [Categoria DeCS]
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[PMID]:28850671
[Au] Autor:Dupuis N; Enderlin J; Thomas J; Desnous B; Dournaud P; Allorge D; Auvin S
[Ad] Endereço:National Institute of Health and Medical Research, U1141, Paris, France.
[Ti] Título:Anti-ictogenic and antiepileptogenic properties of perampanel in mature and immature rats.
[So] Source:Epilepsia;58(11):1985-1992, 2017 Nov.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Perampanel (PER) is a selective noncompetitive antagonist at α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, the first of its class approved for the adjunctive treatment of partial onset seizures and generalized seizures. This study explored anti-ictogenic and antiepileptogenic effects of PER in rats at different stages of development. METHODS: Using a rapid kindling model in postnatal day 14 (P14), P21, P28, and P60 rats, we studied two doses of PER: 1 and 2 mg/kg injected intraperitoneally 30 min before afterdischarge assessment. We also assessed blood and brain concentrations of PER 30 min after the injection. RESULTS: PER 2 mg/kg significantly increased the afterdischarge threshold (ADT) at all ages, whereas PER at 1 mg/kg increased ADT only in P21 rats. PER 2 mg/kg also shortened the afterdischarge duration in P14 and P28 rats. PER increased the number of stimulations required to achieve a stage 4-5 seizure in a dose-dependent manner in P14 and P21 rats, with almost complete elimination of stage 4-5 seizures. At P28, only PER 2 mg/kg increased the number of stimulations required to develop a stage 4-5 seizure. In contrast, PER had no effect on the number of stage 4-5 seizures at P60. We did not observed any age-dependent significant difference in the serum and brain levels of PER 30 min after the injection. SIGNIFICANCE: PER exerted anti-ictogenic effects from P14 to P60 independent of brain maturation. PER also exhibited antiepileptogenic effects with a stronger effect in the younger animals.
[Mh] Termos MeSH primário: Anticonvulsivantes/farmacologia
Excitação Neurológica/efeitos dos fármacos
Piridonas/farmacologia
Receptores de AMPA/antagonistas & inibidores
[Mh] Termos MeSH secundário: Fatores Etários
Animais
Animais Recém-Nascidos
Relação Dose-Resposta a Droga
Excitação Neurológica/fisiologia
Masculino
Ratos
Ratos Wistar
Receptores de AMPA/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticonvulsants); 0 (Pyridones); 0 (Receptors, AMPA); H821664NPK (perampanel)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13894


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[PMID]:28710841
[Au] Autor:Liu S; Shen Y; Shultz SR; Nguyen A; Hovens C; Adlard PA; Bush AI; Chan J; Kwan P; O'Brien TJ; Jones NC
[Ad] Endereço:Department of Medicine, Royal Melbourne Hospital, The University of Melbourne, Parkville, Victoria, Australia.
[Ti] Título:Accelerated kindling epileptogenesis in Tg4510 tau transgenic mice, but not in tau knockout mice.
[So] Source:Epilepsia;58(9):e136-e141, 2017 Sep.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The biologic processes underlying epileptogenesis following a brain insult are not fully understood, but several lines of evidence suggest that hyperphosphorylation of tau may be an important factor in these processes. To provide further insight into the causal relationship between tau and epileptogenesis, this study applied amygdala kindling to rTg4510 mice that, concurrent with other pathologies, overexpress phosphorylated tau, tau knockout mice, or their respective wild-type controls. Mice were electrically stimulated twice daily, 5 days per week for 3 weeks. Electroencephalography was recorded to measure the primary afterdischarge duration, and the behavioral progression of kindling-induced seizures was assessed. rTg4510 mice (n = 10) had increased primary afterdischarge durations (p < 0.001), and significantly more rapid progression of kindling (p < 0.001), compared with wild-type mice (n = 10). Tau knockout mice (n = 7), however, did not differ from their wild-type counterparts (n = 8) on any of the seizure outcomes. These results suggest that Tg4510 mice are more vulnerable to epileptogenesis, but that the presence of tau itself is not necessary for kindling epileptogenesis to occur.
[Mh] Termos MeSH primário: Excitação Neurológica/metabolismo
Proteínas tau/fisiologia
[Mh] Termos MeSH secundário: Tonsila do Cerebelo/metabolismo
Animais
Feminino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Fosforilação
Proteínas tau/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (tau Proteins)
[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:170716
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13847


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[PMID]:28632301
[Au] Autor:Medel-Matus JS; Reynolds A; Shin D; Sankar R; Mazarati A
[Ad] Endereço:Department of Pediatrics, David Geffen School of Medicine at UCLA, Los Angeles, California, U.S.A.
[Ti] Título:Regulation of kindling epileptogenesis by hippocampal Toll-like receptors 2.
[So] Source:Epilepsia;58(8):e122-e126, 2017 Aug.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study examined whether Toll-like receptors 2 (TLR2) contribute to rapid kindling epileptogenesis. A TLR2 agonist, lipoteichoic acid (LTA), LTA antibody (LTA-A), or normal saline (control) was administered daily over 3 consecutive days, unilaterally into ventral hippocampus of adult male Wistar rats. Thirty minutes after the last injection, the animals were subjected to a rapid kindling procedure. The ictogenesis was gauged by comparing afterdischarge threshold (ADT) and afterdischarge duration (ADD) before the treatments, after the treatments prior to kindling, and 24 h after kindling. Kindling progression and retention were analyzed using video recording. The results showed that before kindling, LTA produced an ADT reduction. Neither LTA nor LTA-A affected baseline ADD. On kindling progression, LTA accelerated occurrence of generalized seizures, whereas LTA-A delayed this effect. Treatment with LTA-A reduced the number of secondary generalized complex partial seizures. Twenty-four hours after kindling, the rats of both the saline and LTA groups showed increased hippocampal excitability as compared with prekindling parameters. Administration of LTA-A prevented kindling-induced increase of hippocampal excitability. Immunostaining revealed that LTA-A attenuated the inflammatory response produced by seizures. These findings suggest that the activation of TLR2 in the hippocampus may facilitate limbic epileptogenesis.
[Mh] Termos MeSH primário: Hipocampo/metabolismo
Excitação Neurológica/patologia
Receptor 2 Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Animais
Anticorpos/farmacologia
Eletroencefalografia
Lateralidade Funcional
Hipocampo/efeitos dos fármacos
Excitação Neurológica/efeitos dos fármacos
Lipopolissacarídeos/imunologia
Lipopolissacarídeos/farmacologia
Masculino
Ratos
Ratos Wistar
Ácidos Teicoicos/imunologia
Ácidos Teicoicos/farmacologia
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Lipopolysaccharides); 0 (Teichoic Acids); 0 (Tlr2 protein, rat); 0 (Toll-Like Receptor 2); 0 (Tumor Necrosis Factor-alpha); 56411-57-5 (lipoteichoic acid)
[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:170621
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13826


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[PMID]:28591482
[Au] Autor:Scholly J; Staack AM; Kahane P; Scavarda D; Régis J; Hirsch E; Bartolomei F
[Ad] Endereço:Medical and Surgical Epilepsy Unit, Hautepierre Hospital, University of Strasbourg, Strasbourg, France.
[Ti] Título:Hypothalamic hamartoma: Epileptogenesis beyond the lesion?
[So] Source:Epilepsia;58 Suppl 2:32-40, 2017 Jun.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The discovery of intrinsic epileptogenicity of the hypothalamic hamartoma (HH) marked a new area in understanding the associated clinical syndrome, often manifesting as progressive epileptic encephalopathy. However, therapeutic procedures targeting the HH proved to be inefficient to cure seizures in up to 50% of cases, whereas in cases with partial improvement, the electroclinical patterns of persisting seizures suggest an involvement of distant cortical regions. The concept of kindling-like secondary epileptogenesis has been suggested as a possible underlying mechanism. Yet the role of the hypothalamic lesion in the pathophysiology of the syndrome remains debatable. In the Strasbourg-Kork series, the best outcomes were obtained when the duration of epilepsy before endoscopic HH surgery did not exceed 10 years. In two patients with HH ablation followed at a later time by a temporal lobectomy, only this second surgical step allowed complete seizure freedom. These findings suggest the existence of an independent, third stage of secondary epileptogenesis in human. In the Grenoble series, stereotactic intracerebral recordings (stereo electroencephalography [SEEG]) of five HH cases demonstrated that gelastic/dacrystic seizures were correlated with discharges within the HH, whereas other seizure types were related to discharges affecting cortical regions, which sometimes seemed to be triggered by HH. In the Marseille series, two cases explored by SEEG provided evidence of extended epileptogenicity outside the limits of the HH, forming complex epileptogenic networks, with HH still triggering clusters of neocortical seizures in the first, but not obligatory involved in spontaneous seizures in the second case. Taken together, our data argue for the existence of dynamic ictal network organization, with possible "kindling-like" relationships between the HH and the neocortex or widespread epileptogenesis. Despite the existence of secondary epileptogenesis, the epileptogenic zone could still be limited to the hamartoma, for which early surgical treatment should be pragmatically considered as a first surgical step.
[Mh] Termos MeSH primário: Epilepsias Parciais/fisiopatologia
Hamartoma/fisiopatologia
Doenças Hipotalâmicas/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Lobectomia Temporal Anterior
Criança
Pré-Escolar
Modelos Animais de Doenças
Progressão da Doença
Dominância Cerebral/fisiologia
Eletrodos Implantados
Eletroencefalografia
Epilepsias Parciais/diagnóstico
Epilepsias Parciais/cirurgia
Feminino
Hamartoma/diagnóstico
Hamartoma/cirurgia
Hipocampo/fisiopatologia
Seres Humanos
Doenças Hipotalâmicas/diagnóstico
Doenças Hipotalâmicas/cirurgia
Excitação Neurológica/fisiologia
Masculino
Neocórtex/fisiopatologia
Neocórtex/cirurgia
Rede Nervosa/fisiopatologia
Rede Nervosa/cirurgia
Neurônios/fisiologia
Processamento de Sinais Assistido por Computador
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170705
[Lr] Data última revisão:
170705
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13755


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[PMID]:28591476
[Au] Autor:Striano S; Striano P
[Ad] Endereço:Department of Neurosciences, Reproductive and Odontostomatological Sciences, Epilepsy Center, School of Medicine, Federico II University, Napoli, Italy.
[Ti] Título:Clinical features and evolution of the gelastic seizures-hypothalamic hamartoma syndrome.
[So] Source:Epilepsia;58 Suppl 2:12-15, 2017 Jun.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gelastic seizures, usually with onset in early infancy, are the hallmark manifestation of hypothalamic hamartoma. This seizure type is directly generated by hamartoma itself, intrinsically epileptogenic because of its anatomofunctional organization. Other types of seizures, focal or generalized, may appear during the evolution, probably resulting from mechanisms of secondary epileptogenesis. Nevertheless, the clinical expression and the severity of the syndrome, ranging from a focal drug-resistant epilepsy to a catastrophic generalized encephalopathy with severe cognitive and behavioral impairments, depends on the size and the site of attachment of the hamartoma. Early suspicion, timely diagnosis, and appropriate treatment are mandatory to reverse a potential catastrophic evolution of this condition.
[Mh] Termos MeSH primário: Epilepsias Parciais/diagnóstico
Hamartoma/diagnóstico
Doenças Hipotalâmicas/diagnóstico
[Mh] Termos MeSH secundário: Criança
Transtornos do Comportamento Infantil/diagnóstico
Transtornos do Comportamento Infantil/fisiopatologia
Transtornos do Comportamento Infantil/cirurgia
Pré-Escolar
Transtornos Cognitivos/diagnóstico
Transtornos Cognitivos/fisiopatologia
Transtornos Cognitivos/cirurgia
Progressão da Doença
Epilepsia Resistente a Medicamentos/diagnóstico
Epilepsia Resistente a Medicamentos/fisiopatologia
Epilepsia Resistente a Medicamentos/cirurgia
Diagnóstico Precoce
Intervenção Médica Precoce
Eletroencefalografia
Epilepsias Parciais/fisiopatologia
Epilepsias Parciais/cirurgia
Epilepsia Generalizada/diagnóstico
Epilepsia Generalizada/fisiopatologia
Epilepsia Generalizada/cirurgia
Hamartoma/fisiopatologia
Hamartoma/cirurgia
Seres Humanos
Doenças Hipotalâmicas/fisiopatologia
Doenças Hipotalâmicas/cirurgia
Hipotálamo/fisiopatologia
Hipotálamo/cirurgia
Lactente
Excitação Neurológica/fisiologia
Tomografia por Emissão de Pósitrons
Prognóstico
Radiocirurgia
Processamento de Sinais Assistido por Computador
Síndrome
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170705
[Lr] Data última revisão:
170705
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170608
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13753


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[PMID]:28436625
[Au] Autor:Wang X; Tang O; Ye Y; Zheng M; Hu J; Chen Z; Zhong K
[Ad] Endereço:Department of Basic Medical Science, Hangzhou Medicine College, Hangzhou 310053, China.
[Ti] Título:[Effects of crocin on hippocampus rapid kindling epilepsy in mice].
[So] Source:Zhejiang Da Xue Xue Bao Yi Xue Ban;46(1):7-14, 2017 Jan 25.
[Is] ISSN:1008-9292
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the effect of crocin on the progression and generalized seizure of temporal lobe epilepsy in mice. Hippocampus rapid kindling model was established in C57BL/6J mice. The effects of crocin on seizure stage, afterdischarge duration (ADD), number of stimulation in each stage and final state, the incidence of generalized seizure (GS), average seizure stage and ADD were observed. Crocin (20 mg/kg) significantly retarded behavioral seizure stages ( <0.05) and shortened cumulative ADD ( <0.01) during hippocampus rapid kindling acquisition in mice compared with vehicle group. Meanwhile, number of stimulations in stage 1-2 was significantly increased ( <0.05) and the incidence of fully kindled animals was significantly decreased ( <0.01). However, 10 or 50 mg/kg crocin showed no significant effect on the above indexes (all >0.05). Crocin (100 or 200 mg/kg) significantly decreased the incidence of GS (all <0.01) and reduced average seizure stages (all <0.01) in fully-kindled mice compared with vehicle group; Fifty mg/kg crocin only reduced average seizure stages ( <0.05). Low-dose crocin can retard the progression in hippocampus rapid kindling acquisition in mice, while high-dose crocin relieves the GS in fully-kindled mice, which suggests that crocin may be a potential anti-epileptic compound.
[Mh] Termos MeSH primário: Carotenoides/farmacologia
Carotenoides/uso terapêutico
Epilepsia do Lobo Temporal/tratamento farmacológico
Excitação Neurológica/efeitos dos fármacos
Convulsões/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Anticonvulsivantes/farmacologia
Relação Dose-Resposta a Droga
Estimulação Elétrica
Epilepsia do Lobo Temporal/induzido quimicamente
Hipocampo/efeitos dos fármacos
Hipocampo/fisiopatologia
Excitação Neurológica/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Convulsões/classificação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticonvulsants); 36-88-4 (Carotenoids); 877GWI46C2 (crocin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE


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[PMID]:28436624
[Au] Autor:Zhang L; Chen G; Chen J; He X; Hu X
[Ad] Endereço:Department of Neurology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou 310016, China.
[Ti] Título:[Mechanisms of histamine ameliorating memory impairment induced by pentylenetetrazole-kindling epilepsy in rats].
[So] Source:Zhejiang Da Xue Xue Bao Yi Xue Ban;46(1):1-6, 2017 Jan 25.
[Is] ISSN:1008-9292
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the effects of neuronal histamine on spatial memory acquisition impairment in rats with pentylenetetrazole-kindling epilepsy, and to explore its mechanisms. A subconvulsive dose of pentylenetetrazole (35 mg/kg) was intraperitoneally injected in rats every 48 h to induce chemical kindling until fully kindled. Morris water maze was used to measure the spatial memory acquisition of the rats one week after fully pentylenetetrazole-kindled, and the histamine contents in different brain areas were measured spectrofluorometrically. Different dosages of hitidine (the precursor of histamine), pyrilamine (H1 receptor antagonist), and zolantidine (H2 receptor antagonist) were intraperitoneally injected, and their effects on spatial memory acquisition of the rats were observed. Compared with control group, escape latencies were significantly prolonged on Morris water maze training day 2 and day 3 in pentylenetetrazole-kindling epilepsy rats (all <0.05); and the histamine contents in hippocampus, thalamus and hypothalamus were decreased significantly (all <0.05). Escape latencies were markedly shortened on day 3 by intraperitoneally injected with histidine 500 mg/kg, and on day 2 and day 3 by intraperitoneally injected with histidine 1000 mg/kg in pentylenetetrazole-kindling epilepsy rats (all <0.05). The protection of histidine was reversed by zolantidine (10 and 20 mg/kg), but not by pyrilamine. Neuronal histamine can improve the spatial memory acquisition impairment in rats with pentylenetetrazole-kindling epilepsy, and the activation of H2 receptors is possibly involved in the protective effects of histamine.
[Mh] Termos MeSH primário: Transtornos da Memória/tratamento farmacológico
Receptores Histamínicos H2/efeitos dos fármacos
Receptores Histamínicos H2/fisiologia
Memória Espacial/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Benzotiazóis/farmacologia
Química Encefálica/efeitos dos fármacos
Epilepsia/induzido quimicamente
Epilepsia/complicações
Hipocampo/química
Antagonistas dos Receptores Histamínicos H1/farmacologia
Antagonistas dos Receptores Histamínicos H2/farmacologia
Histidina/farmacologia
Hipotálamo/química
Excitação Neurológica/fisiologia
Transtornos da Memória/etiologia
Pentilenotetrazol
Fenoxipropanolaminas/farmacologia
Piperidinas/farmacologia
Pirilamina/farmacologia
Ratos
Ratos Sprague-Dawley
Espectrometria de Fluorescência
Tálamo/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzothiazoles); 0 (Histamine H1 Antagonists); 0 (Histamine H2 Antagonists); 0 (Phenoxypropanolamines); 0 (Piperidines); 0 (Receptors, Histamine H2); 4QD397987E (Histidine); HPE317O9TL (Pyrilamine); M1108XAY01 (zolantidine); WM5Z385K7T (Pentylenetetrazole)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE


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[PMID]:28373988
[Au] Autor:Jalilifar M; Yadollahpour A; Moazedi AA; Ghotbeddin Z
[Ad] Endereço:Department of Medical Physics, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz 6135715794, Iran.
[Ti] Título:Low Frequency Electrical Stimulation Either Prior to Or after Rapid Kindling Stimulation Inhibits the Kindling-Induced Epileptogenesis.
[So] Source:Biomed Res Int;2017:8623743, 2017.
[Is] ISSN:2314-6141
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:. Studies are ongoing to find appropriate low frequency stimulation (LFS) protocol for treatment of epilepsy. The present study aimed at assessing the antiepileptogenesis effects of LFS with the same protocol applied either just before or immediately after kindling stimulations. . This experimental animal study was conducted on adult Wistar rats (200 ± 20 g) randomly divided into kindle ( = 7), LFS + Kindle ( = 6), and Kindle + LFS groups ( = 6). All animals underwent rapid kindling procedure and four packages of LFS (1 Hz) with 5 min interval were applied either immediately before (LFS-K) or after kindling stimulation (K-LFS). The after discharge duration (ADD), daily stages of kindling, and kindling seizure stage and number of stimulations required to reach each stage were compared between the three groups using two-way analysis of variance (ANOVA) followed by Tukey post hoc and one-way ANOVA, and Kruskal-Wallis test, respectively. . LFS in both protocols significantly decreased the ADD ( < 0.05) and daily seizure stages ( < 0.05) and increased the number of stimulations required to achieve stage 3 and stages 4 and 5 of kindling compared with the kindle group (stage 2: > 0.05, stages 3 to 5: < 0.05). . Although LFS-K showed more inhibiting effect than K-LFS, the difference was not statistically significant.
[Mh] Termos MeSH primário: Terapia por Estimulação Elétrica/métodos
Epilepsia/terapia
Convulsões/terapia
[Mh] Termos MeSH secundário: Animais
Epilepsia/fisiopatologia
Seres Humanos
Excitação Neurológica
Ratos
Ratos Wistar
Convulsões/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[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:170405
[St] Status:MEDLINE
[do] DOI:10.1155/2017/8623743


  9 / 3780 MEDLINE  
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[PMID]:28320185
[Au] Autor:Namvar S; Fathollahi Y; Javan M; Zeraati M; Mohammad-Zadeh M; Shojaei A; Mirnajafi-Zadeh J
[Ad] Endereço:Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.
[Ti] Título:The antiepileptogenic effect of low-frequency stimulation on perforant path kindling involves changes in regulators of G-protein signaling in rat.
[So] Source:J Neurol Sci;375:450-459, 2017 Apr 15.
[Is] ISSN:1878-5883
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:G-protein coupled receptors may have a role in mediating the antiepileptogenic effect of low-frequency stimulation (LFS) on kindling acquisition. This effect is accompanied by changes at the intracellular level of cAMP. In the present study, the effect of rolipram as a phosphodiesterase inhibitor on the antiepileptogenic effect of LFS was investigated. Meanwhile, the expression of α - and α -subunit of G proteins and regulators of G-protein signaling (RGS) proteins following LFS application was measured. Male Wistar rats were kindled by perforant path stimulation in a semi-rapid kindling manner (12 stimulations per day) during a period of 6days. Application of LFS (0.1ms pulse duration at 1Hz, 200 pulses, 50-150µA, 5min after termination of daily kindling stimulations) to the perforant path retarded the kindling development and prevented the kindling-induced potentiation and kindling-induced changes in paired pulse indices in the dentate gyrus. Intra-cerebroventricular microinjection of rolipram (0.25µM) partially prevented these LFS effects. Twenty-four hours after the last kindling stimulation, the dentate gyrus was removed and changes in protein expression were measured by Western blotting. There was no significant difference in the expression of α-subunit of G and G proteins in different experimental groups. However, application of LFS during the kindling procedure decreased the expression RGS4 and RGS10 proteins (that reduce the activity of G ) and prevented the kindling-induced decrease of RGS2 protein (which reduces the G activity). Therefore, it can be postulated that the G protein signaling pathways may be involved in antiepileptogenetic effect of LFS, and this is why decreasing the cAMP metabolism by rolipram attenuates this effect of LFS.
[Mh] Termos MeSH primário: Estimulação Elétrica/métodos
Epilepsia/terapia
Via Perfurante/fisiologia
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Antidepressivos/uso terapêutico
Biofísica
Modelos Animais de Doenças
Proteínas de Ligação ao GTP/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/fisiologia
Excitação Neurológica
Masculino
Ratos
Ratos Wistar
Rolipram/uso terapêutico
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidepressive Agents); EC 3.6.1.- (GTP-Binding Proteins); K676NL63N7 (Rolipram)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170705
[Lr] Data última revisão:
170705
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE


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[PMID]:28131095
[Au] Autor:Abdel-Zaher AO; Farghaly HSM; Farrag MMY; Abdel-Rahman MS; Abdel-Wahab BA
[Ad] Endereço:Department of Pharmacology, Faculty of Medicine, Assiut University, Assiut, Egypt. Electronic address: ahmedosmanaz@hotmail.com.
[Ti] Título:A potential mechanism for the ameliorative effect of thymoquinone on pentylenetetrazole-induced kindling and cognitive impairments in mice.
[So] Source:Biomed Pharmacother;88:553-561, 2017 Apr.
[Is] ISSN:1950-6007
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Cognitive dysfunction is commonly observed in epileptic patients. Pentylenetetrazole (PTZ) kindling is a well established animal model which simulates clinical epilepsy. This study evaluated the potential role of glutamate, oxidative stress and nitric oxide (NO) overproduction in pentylenetetrazole (PTZ)-induced kindling and associated cognitive impairments in mice and effect of thymoquinone on these parameters. Repeated treatment of mice with a subconvulsive dose of PTZ (35mg/kg i.p.) once every alternate-day for 12 injections induced kindling. PTZ-kindled mice showed learning and memory impairments as assessed by acquisition and probe trials of Morris water maze and step-through latency of passive avoidance tests. Concurrently, the brain glutamate, malondialdehyde and nitrite levels were increased while the brain intracellular reduced glutathione level and glutathione peroxidase activity were decreased in PTZ-kindled mice. Also, the brain inducible but not neuronal NO synthase mRNA and protein expressions were increased in PTZ-kindled mice. Treatment of mice with thymoquinonne (5, 10 and 20mg/kg i.p.) along with alternate-day subconvulsive dose of PTZ produced dose-dependent protection against PTZ-induced kindling and learning and memory impairments. Moreover, treatment of mice with thymoquinonne (20mg/kg) inhibited the biochemical alterations induced by PTZ in the brain except the elevation of brain glutamate level. The associated increase in brain inducible NO synthase mRNA and protein expressions were also inhibited. These results suggest that glutamate, and subsequent oxidative stress and NO overproduction, via inducible NO synthase, play an important role in the pathophysiology of PTZ-induced kindling and cognitive impairments in mice. Thymoquinone dose-dependently protects against PTZ-induced kindling and cognitive impairments. Inhibition of PTZ-induced brain oxidative stress and NO overproduction, via increase the expression and activity of inducible NO synthase, may play an important role in thymoquinone action.
[Mh] Termos MeSH primário: Benzoquinonas/uso terapêutico
Disfunção Cognitiva/tratamento farmacológico
Excitação Neurológica/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Aprendizagem da Esquiva/efeitos dos fármacos
Comportamento Animal/efeitos dos fármacos
Benzoquinonas/farmacologia
Encéfalo/efeitos dos fármacos
Encéfalo/enzimologia
Encéfalo/patologia
Disfunção Cognitiva/enzimologia
Disfunção Cognitiva/patologia
Glutationa/metabolismo
Glutationa Peroxidase/metabolismo
Imuno-Histoquímica
Isoenzimas/metabolismo
Masculino
Malondialdeído/metabolismo
Aprendizagem em Labirinto/efeitos dos fármacos
Camundongos
Óxido Nítrico Sintase Tipo I/metabolismo
Nitritos/metabolismo
Pentilenotetrazol
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzoquinones); 0 (Isoenzymes); 0 (Nitrites); 0 (RNA, Messenger); 490-91-5 (thymoquinone); 4Y8F71G49Q (Malondialdehyde); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.14.13.39 (Nitric Oxide Synthase Type I); GAN16C9B8O (Glutathione); WM5Z385K7T (Pentylenetetrazole)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170627
[Lr] Data última revisão:
170627
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170129
[St] Status:MEDLINE



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