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  1 / 3063 MEDLINE  
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[PMID]:29215244
[Au] Autor:Khnychenko LK; Okunevich IV; Losev NA; Sapronov NS
[Ti] Título:[Hypolipidemic activity of N-cholinergic antagonist Benzohexonium in the experiments ].
[So] Source:Patol Fiziol Eksp Ter;60(1):36-43, 2016 Jan-Mar.
[Is] ISSN:0031-2991
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Methods: Experiments were carried out on outbred albino male rats (n = 150, 230-250 g). For modeling dislipoproteinemia (DLP) we used 3 models: single intraperitoneal injection of the detergent triton WR-1339; administration of ethanol; maintenance on a special hypercholesterolaemic diet (HD) during 21 days. Animals were divided into four groups: normal control, model group, gemfibrozil (Gfb) group, benzohexonium (Benz) group. Rats received per os benzohexonium (20mg/kg), reference drug gemfibrozil (50 mg/kg). We determined content of total cholesterol (TCh), triglycerides (TG) in samples of blood serum and liver, TCh in aorta. TCh, TG and Ch-HDL were analyzed spectrophotometrically using of standardized methods. Results: Compared with model group the contents of TCh, TG in serum and liver were significantly decreased in model + Benz group, whereas Ch-HDL was raised in rats fed special HD (P<0.05). Calculated index of atherogenity (TCh - Ch-HDL) / (Ch-HDL) showed the positive effect. Conclusion: The results obtained were shown the hypolipidemic activity of N-cholinergic antagonist Benzohexonium (20 mg/kg) lowered the content of lipids in blood, liver, and aorta.
[Mh] Termos MeSH primário: Agonistas Colinérgicos
Dislipidemias
Compostos de Hexametônio
Hipolipemiantes
[Mh] Termos MeSH secundário: Animais
Agonistas Colinérgicos/farmacocinética
Agonistas Colinérgicos/farmacologia
Dislipidemias/sangue
Dislipidemias/tratamento farmacológico
Compostos de Hexametônio/farmacocinética
Compostos de Hexametônio/farmacologia
Hipolipemiantes/farmacocinética
Hipolipemiantes/farmacologia
Masculino
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholinergic Agonists); 0 (Hexamethonium Compounds); 0 (Hypolipidemic Agents); V26UVZ0360 (benzohexonium)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171221
[Lr] Data última revisão:
171221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE


  2 / 3063 MEDLINE  
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[PMID]:27417712
[Au] Autor:Piotrovskiy LB; Litasova EV; Dumpis MA; Nikolaev DN; Yakovleva EE; Dravolina OA; Bespalov AY
[Ad] Endereço:Institute of Experimental Medicine, St. Petersburg, Russia. levon-piotrovsky@yandex.ru.
[Ti] Título:Enhanced brain penetration of hexamethonium in complexes with derivatives of fullerene C60.
[So] Source:Dokl Biochem Biophys;468(1):173-5, 2016 May.
[Is] ISSN:1608-3091
[Cp] País de publicação:Russia (Federation)
[La] Idioma:eng
[Ab] Resumo:The present report describes development of hexamethonium complexes based on fullerene C60. Hexamethonium has a limited penetration into CNS and therefore can antagonize central effects of nicotine only when given at high doses. In the present studies conducted in laboratory rodents, intraperitoneal administration of hexamethonium-fullerene complexes blocked effects of nicotine (convulsions and locomotor stimulation). When compared to equimolar doses of hexamethonium, complexes of hexamethonium with derivatives of fullerene C60 were 40 times more potent indicating an enhanced ability to interact with central nicotine receptors. Thus, fullerene C60 derivatives should be explored further as potential carrier systems for polar drug delivery into CNS.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Fulerenos/farmacocinética
Compostos de Hexametônio/farmacocinética
Antagonistas Nicotínicos/farmacocinética
[Mh] Termos MeSH secundário: Aminocaproatos/química
Animais
Anticonvulsivantes/química
Anticonvulsivantes/farmacocinética
Encéfalo/metabolismo
Relação Dose-Resposta a Droga
Fulerenos/administração & dosagem
Fulerenos/química
Compostos de Hexametônio/administração & dosagem
Compostos de Hexametônio/química
Locomoção/efeitos dos fármacos
Masculino
Camundongos
Nicotina
Antagonistas Nicotínicos/administração & dosagem
Antagonistas Nicotínicos/química
Ratos Wistar
Convulsões/tratamento farmacológico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminocaproates); 0 (Anticonvulsants); 0 (Fullerenes); 0 (Hexamethonium Compounds); 0 (Nicotinic Antagonists); 6M3C89ZY6R (Nicotine); NP9U26B839 (fullerene C60)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160716
[St] Status:MEDLINE
[do] DOI:10.1134/S1607672916030030


  3 / 3063 MEDLINE  
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[PMID]:24288752
[Au] Autor:Berezina TP; Ovsyannikov VI
[Ad] Endereço:Department for Physiology of Visceral Systems, Research Institute of Experimental Medicine, Northwestern Division of the Russian Academy of Medical Sciences, Saint Petersburg, Russia. vladovs@mail.ru.
[Ti] Título:Changes in contractile activity of the large intestine in rabbits during the poststress period before and after blockade of muscarinic and nicotinic receptors.
[So] Source:Bull Exp Biol Med;155(6):729-33, 2013 Oct.
[Is] ISSN:1573-8221
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The rabbits were exposed twice to stress, fixation to a frame in the supine position, for 60 min. Contractile activity of all portions of the large intestine was shown to increase significantly during the poststress period. These changes were not observed under conditions of blockade of muscarinic and nicotinic receptors. This state can be considered as dyskinesia impairing large intestinal transit of chyme.
[Mh] Termos MeSH primário: Compostos de Hexametônio/farmacologia
Intestino Grosso/fisiopatologia
Antagonistas Muscarínicos/farmacologia
Contração Muscular/efeitos dos fármacos
Antagonistas Nicotínicos/farmacologia
Oxifenônio/farmacologia
Estresse Psicológico/fisiopatologia
[Mh] Termos MeSH secundário: Potenciais de Ação
Antagonistas Adrenérgicos beta/farmacologia
Animais
Feminino
Motilidade Gastrointestinal/efeitos dos fármacos
Intestino Grosso/efeitos dos fármacos
Masculino
Propranolol/farmacologia
Coelhos
Restrição Física
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); 0 (Hexamethonium Compounds); 0 (Muscarinic Antagonists); 0 (Nicotinic Antagonists); 9Y8NXQ24VQ (Propranolol); D2G5508Y7I (Oxyphenonium); V26UVZ0360 (benzohexonium)
[Em] Mês de entrada:1407
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131130
[St] Status:MEDLINE


  4 / 3063 MEDLINE  
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[PMID]:22977852
[Au] Autor:Khnychenko LK; Okunevich IV; Losev NA; Sapronov NS; Yakovleva EE
[Ad] Endereço:Institute of Experimental Medicine, North-Western Division of the Russian Academy of Medical Sciences, St. Petersburg, Russia. Ludmila.Konst83@ mail.ru
[Ti] Título:A new activity of N-cholinolytic drug benzohexonium.
[So] Source:Bull Exp Biol Med;153(4):487-9, 2012 Aug.
[Is] ISSN:1573-8221
[Cp] País de publicação:United States
[La] Idioma:eng; rus
[Ab] Resumo:We have found that N-cholinolytic drug benzohexonium produces a hypolipidemic effect: it reduces dyslipoproteinemia, fatty infiltration of the liver, and risk of atherosclerotic lesions.
[Mh] Termos MeSH primário: Antagonistas Colinérgicos/farmacologia
Modelos Animais de Doenças
Dislipidemias/tratamento farmacológico
Fígado Gorduroso/tratamento farmacológico
Compostos de Hexametônio/farmacologia
Hipolipemiantes/farmacologia
Placa Aterosclerótica/prevenção & controle
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Antagonistas Colinérgicos/uso terapêutico
Cobaias
Compostos de Hexametônio/uso terapêutico
Hipolipemiantes/uso terapêutico
Metabolismo dos Lipídeos/efeitos dos fármacos
Masculino
Ratos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholinergic Antagonists); 0 (Hexamethonium Compounds); 0 (Hypolipidemic Agents); V26UVZ0360 (benzohexonium)
[Em] Mês de entrada:1301
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120915
[St] Status:MEDLINE


  5 / 3063 MEDLINE  
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[PMID]:22405726
[Au] Autor:Gomes da Silva AQ; Xavier CH; Campagnole-Santos MJ; Caligiorne SM; Baltatu OC; Bader M; Santos RA; Fontes MA
[Ad] Endereço:Departamento de Biorregulação, Instituto de Ciências da Saúde, Universidade Federal da Bahia, BA, Brazil.
[Ti] Título:Cardiovascular responses evoked by activation or blockade of GABA(A) receptors in the hypothalamic PVN are attenuated in transgenic rats with low brain angiotensinogen.
[So] Source:Brain Res;1448:101-10, 2012 Apr 11.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Previous evidence indicates that a balance between inhibitory gabaergic and excitatory angiotensinergic factors in the PVN is important for cardiovascular control. We investigated the cardiovascular response evoked from activation or blockade of GABA(A) receptors in the paraventricular nucleus (PVN), in transgenic rats with low brain angiotensinogen [TGR(ASrAOGEN)]. Brain Ang II and Ang-(1-7) levels were also determined. In functional experiments, TGR(ASrAOGEN) and Sprague-Dawley rats (SD, control) were anesthetized with urethane and blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were recorded. Brain Ang II and Ang-(1-7) levels were largely reduced in TGR(ASrAOGEN) compared with SD rats. Inhibition of PVN neurons with the GABA(A) agonist, muscimol (1 nmol/100 nL), resulted in an attenuated fall in all cardiovascular variables in TGR(ASrAOGEN) compared with SD rats. This difference was particularly pronounced in HR (TGR Mus -23±6 bpm vs. -77±9 bpm SD Mus; P<0.05) and RSNA (TGR -3±10% vs.-29±8% SD; P<0.05). Furthermore, the sympathetic response evoked by blockade of GABA(A) receptors in the PVN of TGR(ASrAOGEN) was also largely suppressed. The present data indicate that the sympathetic outflow mediated by PVN neurons under basal conditions is suppressed in TGR(ASrAOGEN) rats corroborating the functional significance of brain angiotensin production in the central regulation of sympathetic output to the cardiovascular system.
[Mh] Termos MeSH primário: Angiotensinogênio/deficiência
Química Encefálica/efeitos dos fármacos
Agonistas GABAérgicos/farmacologia
Antagonistas GABAérgicos/farmacologia
Hemodinâmica/efeitos dos fármacos
Hemodinâmica/fisiologia
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
Receptores de GABA-A/fisiologia
[Mh] Termos MeSH secundário: Animais
Anti-Hipertensivos/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Química Encefálica/genética
Expressão Gênica/efeitos dos fármacos
Frequência Cardíaca/efeitos dos fármacos
Compostos de Hexametônio/farmacologia
Rim/inervação
Rim/fisiologia
Radioimunoensaio
Ratos
Ratos Sprague-Dawley
Ratos Transgênicos
Sistema Nervoso Simpático/fisiologia
Transgenes/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (GABA Agonists); 0 (GABA Antagonists); 0 (Hexamethonium Compounds); 0 (Receptors, GABA-A); 11002-13-4 (Angiotensinogen)
[Em] Mês de entrada:1208
[Cu] Atualização por classe:120320
[Lr] Data última revisão:
120320
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120313
[St] Status:MEDLINE
[do] DOI:10.1016/j.brainres.2012.02.021


  6 / 3063 MEDLINE  
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[PMID]:19529847
[Au] Autor:Berezina TP; Ovsyannikov VI
[Ad] Endereço:Laboratory for Physiology of Digestion, Department for Physiology of Visceral Systems, Institute of Experimental Medicine, Russian Academy of Medical Sciences, St. Petersburg, Russia.
[Ti] Título:Mechanism for the inhibition of contractile activity of the gastric antrum and pylorus in rabbits during psychogenic stress.
[So] Source:Bull Exp Biol Med;147(3):296-300, 2009 Mar.
[Is] ISSN:1573-8221
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Psychogenic stress in rabbits (fixation to a frame) was accompanied by the inhibition of contractile activity of the gastric antrum and pylorus. These changes persisted during blockade of muscarinic receptors, nicotinic receptors, alpha(2)-adrenoceptors, and beta(1)/beta(2) adrenoceptors. A stress-induced decrease in gastric motor activity was mediated by the nonadrenergic noncholinergic mechanism. It resulted from the influence of a hormonal stress factor on the stomach, which was probably realized through nonadrenergic inhibitory neurons of the enteric nervous system.
[Mh] Termos MeSH primário: Antro Pilórico/fisiopatologia
Piloro/fisiopatologia
Estresse Psicológico/fisiopatologia
[Mh] Termos MeSH secundário: Antagonistas de Receptores Adrenérgicos alfa 2
Antagonistas Adrenérgicos alfa/farmacologia
Antagonistas Adrenérgicos beta/farmacologia
Animais
Di-Hidroergotoxina/farmacologia
Bloqueadores Ganglionares/farmacologia
Motilidade Gastrointestinal/efeitos dos fármacos
Motilidade Gastrointestinal/fisiologia
Compostos de Hexametônio/farmacologia
Masculino
Antagonistas Muscarínicos/farmacologia
Contração Muscular/efeitos dos fármacos
Contração Muscular/fisiologia
Músculo Liso/fisiopatologia
Oxifenônio/farmacologia
Propranolol/farmacologia
Antro Pilórico/efeitos dos fármacos
Piloro/efeitos dos fármacos
Coelhos
Receptores Adrenérgicos beta/metabolismo
Receptores Muscarínicos/metabolismo
Receptores Nicotínicos/metabolismo
Ioimbina/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 (Adrenergic alpha-Antagonists); 0 (Adrenergic beta-Antagonists); 0 (Ganglionic Blockers); 0 (Hexamethonium Compounds); 0 (Muscarinic Antagonists); 0 (Receptors, Adrenergic, beta); 0 (Receptors, Muscarinic); 0 (Receptors, Nicotinic); 11032-41-0 (Dihydroergotoxine); 2Y49VWD90Q (Yohimbine); 9Y8NXQ24VQ (Propranolol); D2G5508Y7I (Oxyphenonium); V26UVZ0360 (benzohexonium)
[Em] Mês de entrada:0910
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090617
[St] Status:MEDLINE


  7 / 3063 MEDLINE  
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[PMID]:19150858
[Au] Autor:Cassaglia PA; Griffiths RI; Walker AM
[Ad] Endereço:Ritchie Centre for Baby Health Research, Monash Institute of Medical Research, Monash University, Melbourne, Australia.
[Ti] Título:Cerebral sympathetic nerve activity has a major regulatory role in the cerebral circulation in REM sleep.
[So] Source:J Appl Physiol (1985);106(4):1050-6, 2009 Apr.
[Is] ISSN:8750-7587
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sympathetic nerve activity (SNA) in neurons projecting to skeletal muscle blood vessels increases during rapid-eye-movement (REM) sleep, substantially exceeding SNA of non-REM (NREM) sleep and quiet wakefulness (QW). Similar SNA increases to cerebral blood vessels may regulate the cerebral circulation in REM sleep, but this is unknown. We hypothesized that cerebral SNA increases during phasic REM sleep, constricting cerebral vessels as a protective mechanism against cerebral hyperperfusion during the large arterial pressure surges that characterize this sleep state. We tested this hypothesis using a newly developed model to continuously record SNA in the superior cervical ganglion (SCG) before, during, and after arterial pressure surges occurring during REM in spontaneously sleeping lambs. Arterial pressure (AP), intracranial pressure (ICP), cerebral blood flow (CBF), cerebral vascular resistance [CVR = (AP - ICP)/CBF], and SNA from the SCG were recorded in lambs (n = 5) undergoing spontaneous sleep-wake cycles. In REM sleep, CBF was greatest (REM > QW = NREM, P < 0.05) and CVR was least (REM < QW = NREM, P < 0.05). SNA in the SCG did not change from QW to NREM sleep but increased during tonic REM sleep, with a further increase during phasic REM sleep (phasic REM > tonic REM > QW = NREM, P < 0.05). Coherent averaging revealed that SNA increases preceded AP surges in phasic REM sleep by 12 s (P < 0.05). We report the first recordings of cerebral SNA during natural sleep-wake cycles. SNA increases markedly during tonic REM sleep, and further in phasic REM sleep. As SNA increases precede AP surges, they may serve to protect the brain against potentially damaging intravascular pressure changes or hyperperfusion in REM sleep.
[Mh] Termos MeSH primário: Encéfalo/fisiologia
Circulação Cerebrovascular/fisiologia
Sono REM/fisiologia
Sistema Nervoso Simpático/fisiologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Bloqueadores Ganglionares/farmacologia
Hemodinâmica/fisiologia
Compostos de Hexametônio/farmacologia
Lobo Parietal/fisiologia
Polissonografia
Ovinos
Fases do Sono
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ganglionic Blockers); 0 (Hexamethonium Compounds)
[Em] Mês de entrada:0905
[Cu] Atualização por classe:130926
[Lr] Data última revisão:
130926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090120
[St] Status:MEDLINE
[do] DOI:10.1152/japplphysiol.91349.2008


  8 / 3063 MEDLINE  
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[PMID]:18834075
[Au] Autor:Jahan-Parwar B; Chhetri DK; Ye M; Hart S; Berke GS
[Ad] Endereço:Division of Head and Neck Surgery, University of California-Los Angeles Medical Center, Los Angeles, California 90095, USA.
[Ti] Título:Hylan B gel restores structure and function to laser-ablated canine vocal folds.
[So] Source:Ann Otol Rhinol Laryngol;117(9):703-7, 2008 Sep.
[Is] ISSN:0003-4894
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: We evaluated cross-linked hyaluronic acid (hylan B gel) as a scaffold for tissue regeneration and mucosal wave restoration in carbon dioxide laser-ablated canine vocal folds. METHODS: Five beagles underwent stroboscopy before ablation of the left vocal fold with a carbon dioxide laser. Four weeks later, stroboscopy was repeated before and after submucosal injection of hylan B gel into the left vocal fold of 4 animals and of saline solution in 1 animal. Stroboscopy was repeated 12 weeks later, and histologic analysis was performed. RESULTS: Four weeks after laser ablation, all animals had soft tissue defects and absence of mucosal waves. Hylan B injection restored mucosal waves, and saline injection did not. Twelve weeks after injection, hylan B-injected larynges had tissue regeneration and mucosal waves, and the saline-injected larynx had neither. Histology showed regenerated lamina propria with residual foci of hylan B in the hylan B-injected larynges and dense submucosal scar in the saline-injected animal. CONCLUSIONS: Submucosal hylan B gel injection in laser-ablated canine vocal folds restored tissue volume and mucosal waves and facilitated functional tissue regeneration over 12 weeks. Hylan B gel may have utility as a soft tissue scaffold for rehabilitation of phonatory function in vocal folds with lamina propria defects.
[Mh] Termos MeSH primário: Celulose/farmacologia
Compostos de Hexametônio/farmacologia
Ácido Hialurônico/análogos & derivados
Terapia a Laser
Tantálio/farmacologia
Trombina/farmacologia
Tecidos Suporte
Prega Vocal/lesões
[Mh] Termos MeSH secundário: Animais
Cães
Combinação de Medicamentos
Regeneração Tecidual Guiada/métodos
Ácido Hialurônico/farmacologia
Membrana Mucosa/fisiologia
Estroboscopia
Prega Vocal/cirurgia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Drug Combinations); 0 (Hexamethonium Compounds); 0 (hylan gel); 6424HBN274 (Tantalum); 9004-34-6 (Cellulose); 9004-61-9 (Hyaluronic Acid); EC 3.4.21.5 (Thrombin)
[Em] Mês de entrada:0810
[Cu] Atualização por classe:170214
[Lr] Data última revisão:
170214
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:081007
[St] Status:MEDLINE


  9 / 3063 MEDLINE  
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[PMID]:18565636
[Au] Autor:Pickering C; Bergenheim V; Schiöth HB; Ericson M
[Ad] Endereço:University of Gothenburg, Institute of Neuroscience and Physiology, Section of Psychiatry and Neurochemistry, PO Box 410, SE-40530 Göteborg, Sweden.
[Ti] Título:Sensitization to nicotine significantly decreases expression of GABA transporter GAT-1 in the medial prefrontal cortex.
[So] Source:Prog Neuropsychopharmacol Biol Psychiatry;32(6):1521-6, 2008 Aug 01.
[Is] ISSN:0278-5846
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:This study investigated GABA signaling following induction of behavioural sensitization to nicotine. Rats were repeatedly injected with saline, nicotine or hexamethonium for 18 days and gene expression was measured with qPCR. Nicotine upregulated GABAA alpha1 subunit expression in the nucleus accumbens (p<0.05) while no changes were observed for GABAA alpha3, alpha4 or alpha5. In the medial prefrontal cortex, no change in expression of the GABAA subunits was observed. We found that nicotine significantly decreased expression of the transporter GAT-1/SLC6A1 (p<0.05) in the medial prefrontal cortex while the expression of the GAT-3/SLC6A11 (p<0.05) transporter was increased in the nucleus accumbens. This provides the first evidence of neuroadaptive changes in the GABA system after nicotine sensitization and the first demonstration of an effect on GAT-1 or GAT-3 transporters in the addiction field. The GAT-1 findings also provide evidence for an alternative theory of why most schizophrenic individuals also use tobacco products.
[Mh] Termos MeSH primário: Proteínas da Membrana Plasmática de Transporte de GABA/biossíntese
Nicotina/farmacologia
Agonistas Nicotínicos/farmacologia
Córtex Pré-Frontal/metabolismo
[Mh] Termos MeSH secundário: Animais
Primers do DNA
DNA Complementar/biossíntese
DNA Complementar/genética
Interpretação Estatística de Dados
Proteínas da Membrana Plasmática de Transporte de GABA/efeitos dos fármacos
Compostos de Hexametônio/farmacologia
Masculino
Atividade Motora/efeitos dos fármacos
Neurotransmissores/metabolismo
Córtex Pré-Frontal/efeitos dos fármacos
RNA/biossíntese
RNA/genética
Ratos
Ratos Wistar
Receptores de GABA-A/biossíntese
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA Primers); 0 (DNA, Complementary); 0 (GABA Plasma Membrane Transport Proteins); 0 (Hexamethonium Compounds); 0 (Neurotransmitter Agents); 0 (Nicotinic Agonists); 0 (Receptors, GABA-A); 63231-63-0 (RNA); 6M3C89ZY6R (Nicotine)
[Em] Mês de entrada:0810
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080621
[St] Status:MEDLINE
[do] DOI:10.1016/j.pnpbp.2008.05.011


  10 / 3063 MEDLINE  
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[PMID]:18423439
[Au] Autor:Okada S; Yamaguchi-Shima N; Shimizu T; Arai J; Lianyi L; Wakiguchi H; Yokotani K
[Ad] Endereço:Department of Pharmacology, Graduate School of Medicine, Kochi University, Nankoku, Kochi 783-8505, Japan. okadas@kochi-u.ac.jp
[Ti] Título:Role of brain nicotinic acetylcholine receptor in centrally administered corticotropin-releasing factor-induced elevation of plasma corticosterone in rats.
[So] Source:Eur J Pharmacol;587(1-3):322-9, 2008 Jun 10.
[Is] ISSN:0014-2999
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The present study was undertaken to clarify the central mechanisms involved in the intracerebroventricularly administered corticotropin-releasing factor-induced elevation of plasma corticosterone in urethane- and alpha-chloralose-anesthetized rats using microdialysis and immunohistochemical techniques. When corticotropin-releasing factor was given at 0.5, 1.5, and 3.0 nmol/animal intracerebroventricularly, it dose-dependently increased noradrenaline release but not adrenaline release in the hypothalamic paraventricular nucleus. The 1.5 nmol/animal dose of corticotropin-releasing factor-induced noradrenaline release was attenuated by CP-154,526 (butyl-ethyl-{2,5-dimethyl-7-(2,4,6 trimethylphenyl)-7H-pyrrolo[2,3-d]pyrimidin-4-yl}amine), a selective corticotropin-releasing factor receptor 1 antagonist, at 1.3 micromol/animal, intracerebroventricularly, and was also abolished by phentolamine at 0.66 micromol/animal, intracerebroventricularly. In addition, the corticotropin-releasing factor-induced elevation of noradrenaline release in the hypothalamic paraventricular nucleus and plasma corticosterone were abolished by hexamethonium, a non-selective nicotinic acetylcholine receptor antagonist, at 1.8 micromol/animal, intracerebroventricularly, and alpha-conotoxin MII, a potent alpha(3)beta(2) nicotinic acetylcholine receptor antagonist, at 30 nmol/animal, i.c.v. Corticotropin-releasing factor at 1.5 nmol/animal, i.c.v. evoked a significant expression of Fos, an immediate-early transcription factor in neurons, on the dopamine-beta-hydroxylase-containing neurons and alpha(3) nicotinic acetylcholine receptor subunit-expressing neurons in the locus coeruleus, but not in the medullary A(1) and A(2) regions containing noradrenergic neurons. These results suggest that centrally administered corticotrophin-releasing factor elevates plasma corticosterone by the corticotropin-releasing factor 1 receptor and alpha(3) subunit-containing nicotinic acetylcholine receptor (probably alpha(3)beta(2) nicotinic acetylcholine receptor) mediated activation of the locus coeruleus noradrenergic neurons projecting to the paraventricular nucleus in rats.
[Mh] Termos MeSH primário: Química Encefálica/fisiologia
Corticosterona/sangue
Hormônio Liberador da Corticotropina/farmacologia
Receptores Nicotínicos/fisiologia
[Mh] Termos MeSH secundário: Córtex Suprarrenal/efeitos dos fármacos
Antagonistas Adrenérgicos alfa/administração & dosagem
Antagonistas Adrenérgicos alfa/farmacologia
Animais
Conotoxinas/farmacologia
Hormônio Liberador da Corticotropina/administração & dosagem
Dopamina beta-Hidroxilase/metabolismo
Bloqueadores Ganglionares/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Genes fos/efeitos dos fármacos
Compostos de Hexametônio/farmacologia
Sistema Hipotálamo-Hipofisário/efeitos dos fármacos
Imuno-Histoquímica
Injeções Intraventriculares
Locus Cerúleo/efeitos dos fármacos
Masculino
Microdiálise
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
Fentolamina/administração & dosagem
Fentolamina/farmacologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenergic alpha-Antagonists); 0 (Conotoxins); 0 (Ganglionic Blockers); 0 (Hexamethonium Compounds); 0 (Receptors, Nicotinic); 0 (alpha-conotoxin MII); 9015-71-8 (Corticotropin-Releasing Hormone); EC 1.14.17.1 (Dopamine beta-Hydroxylase); W980KJ009P (Corticosterone); Z468598HBV (Phentolamine)
[Em] Mês de entrada:0808
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080422
[St] Status:MEDLINE
[do] DOI:10.1016/j.ejphar.2008.03.005



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