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[PMID]:23486957
[Au] Autor:Lingappa JR; Zigmond RE
[Ad] Endereço:Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA. jais@u.washington.edu
[Ti] Título:Limited recovery of pineal function after regeneration of preganglionic sympathetic axons: evidence for loss of ganglionic synaptic specificity.
[So] Source:J Neurosci;33(11):4867-74, 2013 Mar 13.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cervical sympathetic trunks (CSTs) contain axons of preganglionic neurons that innervate the superior cervical ganglia (SCGs). Because regeneration of CST fibers can be extensive and can reestablish certain specific patterns of SCG connections, restoration of end organ function would be expected. This expectation was examined with respect to the pineal gland, an organ innervated by the two SCGs. The activity of pineal serotonin N-acetyltransferase (NAT) exhibits a large circadian rhythm that is dependent on the sympathetic input of the gland, with high activity at night. Thirty-six hours after the CSTs were crushed bilaterally, nocturnal NAT was decreased by 99%. Three months later, enzyme activity had recovered only to 15% of control values, a recovery dependent on regeneration of CST fibers. Nevertheless, a small day/night rhythm was present in lesioned animals. Neither the density of the adrenergic innervation of the gland nor the ability of an adrenergic agonist to stimulate NAT activity was reduced in rats with regenerated CSTs. In addition, stimulation of the regenerated CST at a variety of frequencies was at least as effective in increasing NAT activity as seen with control nerves. These data suggest that the failure of pineal function to recover is not attributable to a quantitative deficit in the extent of reinnervation or synaptic efficacy. Rather, we suggest that there is some loss of specificity in the synaptic connections made in the SCG during reinnervation, resulting in a loss of the central neuronal information necessary for directing a normal NAT rhythm and thus normal pineal function.
[Mh] Termos MeSH primário: Doenças do Sistema Nervoso Autônomo/patologia
Doenças do Sistema Nervoso Autônomo/fisiopatologia
Axônios/patologia
Regeneração Nervosa/fisiologia
Glândula Pineal/fisiopatologia
Gânglio Cervical Superior/patologia
[Mh] Termos MeSH secundário: Animais
Arilalquilamina N-Acetiltransferase/metabolismo
Axônios/efeitos dos fármacos
Biofísica
Brocresina/farmacologia
Ritmo Circadiano/fisiologia
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Estimulação Elétrica
Inibidores Enzimáticos/farmacologia
Regulação Enzimológica da Expressão Gênica/fisiologia
Isoproterenol/farmacologia
Masculino
Nordefrin/farmacologia
Glândula Pineal/metabolismo
Ratos
Ratos Sprague-Dawley
Gânglio Cervical Superior/efeitos dos fármacos
Simpatomiméticos/farmacologia
Fatores de Tempo
Tirosina 3-Mono-Oxigenase
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Sympathomimetics); 11F6O06WN0 (Brocresine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 2.3.1.87 (Arylalkylamine N-Acetyltransferase); L628TT009W (Isoproterenol); R81X549E70 (Nordefrin)
[Em] Mês de entrada:1305
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130315
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.3829-12.2013


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[PMID]:15105275
[Au] Autor:Youdim MB; Stephenson G; Ben Shachar D
[Ad] Endereço:Eve Topf and US National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases Research, and Department of Pharmacology, Technion-Rappaport Faculty of Medicine, Haifa, Israel. youdim@tx.technion.ac.il
[Ti] Título:Ironing iron out in Parkinson's disease and other neurodegenerative diseases with iron chelators: a lesson from 6-hydroxydopamine and iron chelators, desferal and VK-28.
[So] Source:Ann N Y Acad Sci;1012:306-25, 2004 Mar.
[Is] ISSN:0077-8923
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In Parkinson's disease (PD) and its neurotoxin-induced models, 6-hydroxydopamine (6-OHDA) and N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), significant accumulation of iron occurs in the substantia nigra pars compacta. The iron is thought to be in a labile pool, unbound to ferritin, and is thought to have a pivotal role to induce oxidative stress-dependent neurodegeneration of dopamine neurons via Fenton chemistry. The consequence of this is its interaction with H(2)O(2) to generate the most reactive radical oxygen species, the hydroxyl radical. This scenario is supported by studies in both human and neurotoxin-induced parkinsonism showing that disposition of H(2)O(2) is compromised via depletion of glutathione (GSH), the rate-limiting cofactor of glutathione peroxide, the major enzyme source to dispose H(2)O(2) as water in the brain. Further, radical scavengers have been shown to prevent the neurotoxic action of the above neurotoxins and depletion of GSH. However, our group was the first to demonstrate that the prototype iron chelator, desferal, is a potent neuroprotective agent in the 6-OHDA model. We have extended these studies and examined the neuroprotective effect of intracerebraventricular (ICV) pretreatment with the prototype iron chelator, desferal (1.3, 13, 134 mg), on ICV induced 6-OHDA (250 micro g) lesion of striatal dopamine neurons. Desferal alone at the doses studied did not affect striatal tyrosine hydroxylase (TH) activity or dopamine (DA) metabolism. All three pretreatment (30 min) doses of desferal prevented the fall in striatal and frontal cortex DA, dihydroxyphenylacetic acid, and homovalinic acid, as well as the left and right striatum TH activity and DA turnover resulting from 6-OHDA lesion of dopaminergic neurons. A concentration bell-shaped neuroprotective effect of desferal was observed in the striatum, with 13 micro g being the most effective. Neither desferal nor 6-OHDA affected striatal serotonin, 5-hydroxyindole acetic acid, or noradrenaline. Desferal also protected against 6-OHDA-induced deficit in locomotor activity, rearing, and exploratory behavior (sniffing) in a novel environment. Since the lowest neuroprotective dose (1.3 micro g) of desferal was 200 times less than 6-OHDA, its neuroprotective activity may not be attributed to interference with the neurotoxin activity, but rather iron chelation. These studies led us to develop novel brain-permeable iron chelators, the VK-28 series, with iron chelating and neuroprotective activity similar to desferal for ironing iron out from PD and other neurodegenerative diseases, such as Alzheimer's disease, Friedreich's ataxia, and Huntington's disease.
[Mh] Termos MeSH primário: Desferroxamina/uso terapêutico
Quelantes de Ferro/uso terapêutico
Ferro/metabolismo
Doenças Neurodegenerativas
Oxidopamina
Doença de Parkinson
[Mh] Termos MeSH secundário: Ácido 3,4-Di-Hidroxifenilacético/análise
Análise de Variância
Animais
Comportamento Animal/efeitos dos fármacos
Encéfalo/anatomia & histologia
Encéfalo/metabolismo
Brocresina/farmacologia
Cromatografia Líquida de Alta Pressão/métodos
Modelos Animais de Doenças
Dopamina
Dopaminérgicos/farmacologia
Relação Dose-Resposta a Droga
Interações Medicamentosas
Inibidores Enzimáticos/farmacologia
Comportamento Exploratório/efeitos dos fármacos
Lateralidade Funcional
Ácido Homovanílico/análise
Levodopa/farmacologia
Masculino
Atividade Motora/efeitos dos fármacos
Doenças Neurodegenerativas/induzido quimicamente
Doenças Neurodegenerativas/tratamento farmacológico
Doenças Neurodegenerativas/metabolismo
Neurotransmissores/análise
Doença de Parkinson/tratamento farmacológico
Doença de Parkinson/metabolismo
Piperazinas/farmacocinética
Piperazinas/uso terapêutico
Quinolinas/farmacocinética
Quinolinas/uso terapêutico
Ratos
Ratos Sprague-Dawley
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dopamine Agents); 0 (Enzyme Inhibitors); 0 (Iron Chelating Agents); 0 (Neurotransmitter Agents); 0 (Piperazines); 0 (Quinolines); 102-32-9 (3,4-Dihydroxyphenylacetic Acid); 11F6O06WN0 (Brocresine); 46627O600J (Levodopa); 8HW4YBZ748 (Oxidopamine); E1UOL152H7 (Iron); J06Y7MXW4D (Deferoxamine); VTD58H1Z2X (Dopamine); X77S6GMS36 (Homovanillic Acid)
[Em] Mês de entrada:0405
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:040424
[St] Status:MEDLINE


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[PMID]:12536039
[Au] Autor:Arrue A; Ruiz-Ortega JA; Ugedo L; Giralt MT
[Ad] Endereço:Department of Pharmacology, Faculty of Medicine and Odontology, University of the Basque Country, 48940-Leioa, Vizcaya, Spain.
[Ti] Título:Short-term effects of 3,4-methylenedioximethamphetamine on noradrenergic activity in locus coeruleus and hippocampus of the rat.
[So] Source:Neurosci Lett;337(3):123-6, 2003 Feb 13.
[Is] ISSN:0304-3940
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:This study was undertaken to investigate the effects of the administration of 3,4-methylenedioxymethamphetamine (MDMA) on the locus coeruleus firing rate, on the sensitivity of the alpha(2)-adrenoceptors which regulate neuronal activity and on the in vivo tyrosine hydroxylase activity in hippocampus. The basal firing rate was not modified by either a single dose or repeated doses of MDMA, although the latter produced a shift to the right in the dose-response curve for clonidine-induced inhibition of the firing rate (ED(50) increased by 59%) and a reduction in tyrosine hydroxylase activity (20%) in the hippocampus. However, 8 days after the final dose alpha(2)-adrenoceptor sensitivity and tyrosine hydroxylase activity had returned to control values. Our results show a desensitization of alpha(2)-adrenoceptors in locus coeruleus and the existence of short-term changes in the noradrenergic system.
[Mh] Termos MeSH primário: Inibidores da Captação Adrenérgica/farmacologia
Hipocampo/efeitos dos fármacos
Locus Cerúleo/efeitos dos fármacos
N-Metil-3,4-Metilenodioxianfetamina/farmacologia
[Mh] Termos MeSH secundário: Agonistas alfa-Adrenérgicos/farmacologia
Análise de Variância
Animais
Brocresina/farmacologia
Clonidina/farmacologia
Di-Hidroxifenilalanina/metabolismo
Relação Dose-Resposta a Droga
Eletrofisiologia
Inibidores Enzimáticos/farmacologia
Fenclonina/farmacologia
Hipocampo/metabolismo
Locus Cerúleo/metabolismo
Masculino
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Norepinefrina/metabolismo
Ratos
Ratos Sprague-Dawley
Receptores Adrenérgicos alfa 2/efeitos dos fármacos
Tirosina 3-Mono-Oxigenase/efeitos dos fármacos
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenergic Uptake Inhibitors); 0 (Adrenergic alpha-Agonists); 0 (Enzyme Inhibitors); 0 (Receptors, Adrenergic, alpha-2); 11F6O06WN0 (Brocresine); 63-84-3 (Dihydroxyphenylalanine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine); MN3L5RMN02 (Clonidine); R5J7E3L9SP (Fenclonine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:0303
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:030122
[St] Status:MEDLINE


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[PMID]:8100518
[Au] Autor:Arbogast LA; Soares MJ; Robertson MC; Voogt JL
[Ad] Endereço:Department of Physiology, University of Kansas Medical Center, Kansas City 66160-7401.
[Ti] Título:A factor(s) from a trophoblast cell line increases tyrosine hydroxylase activity in fetal hypothalamic cell cultures.
[So] Source:Endocrinology;133(1):111-20, 1993 Jul.
[Is] ISSN:0013-7227
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously reported that a factor(s) from rat choriocarcinoma (Rcho-1) cells suppresses circulating PRL levels and increases tyrosine hydroxylase activity in tuberoinfundibular dopaminergic neurons in vivo. The purposes of this study were to determine whether this factor(s) increases tyrosine hydroxylase activity in fetal hypothalamic cells in vitro and to evaluate its chemical nature. The Rcho-1 cells are of placental origin and have the capacity to differentiate into giant cells and produce members of the placental PRL family. MMQ cells, a pituitary cell line that secretes PRL, and HRP-1, a placental cell line that does not produce any known members of the PRL family, were used as control cells. Tyrosine hydroxylase activity was assessed by incubation of hypothalamic cells for 1 h with 100 microM brocresine, an inhibitor of aromatic L-amino acid decarboxylase. Tyrosine hydroxylase activity was increased in a density-dependent manner when Rcho-1, but not HRP-1 or MMQ, cells were cocultured with hypothalamic cells for 24 h. Control and Rcho-1-stimulated tyrosine hydroxylase activities were markedly reduced with 1 mM alpha-methyl-p-tyrosine, a specific inhibitor of tyrosine hydroxylase. Tyrosine hydroxylase activity was not altered when hypothalamic cells were incubated for 24 h with rat PRL or recombinant rat placental lactogen-I, whereas a 24-h stimulation with 100,000 Rcho-1 cells and a 1-h stimulation with 5 mM (Bu)2cAMP increased tyrosine hydroxylase activity 3.7- and 3-fold, respectively. The magnitudes of the increase in tyrosine hydroxylase activity were similar when hypothalamic cells were cocultured with Rcho-1 cells for 1 and 24 h. Acetic acid extracts of Rcho-1, but not HRP-1 or MMQ, cells increased tyrosine hydroxylase activity within 1 h in a concentration-dependent manner. The 3-fold increase in tyrosine hydroxylase activity observed with 500,000 Rcho-1 cell equivalents was markedly reduced with 1 mM alpha-methyl-p-tyrosine. The mol wt range of the tyrosine hydroxylase-activating factor(s) (THAF) was estimated using ultrafiltration membranes. The majority of activity was found in the eluate from a 1,000 mol wt cut-off membrane. THAF activity in Rcho-1 cell extracts was decreased by preincubation with pronase, a nonspecific proteolytic enzyme, suggesting that the factor(s) is a peptide. THAF was resistant to inactivation by trypsin or chymotrypsin pretreatment. However, both enzymes destroyed the ability of pituitary adenylate cyclase-activating peptide, either alone or with Rcho-1 cell extracts, to increase tyrosine hydroxylase activity. Oxidation of Rcho-1 cell extracts with performic acid abolished THAF activity.(ABSTRACT TRUNCATED AT 400 WORDS)
[Mh] Termos MeSH primário: Hipotálamo/embriologia
Hipotálamo/enzimologia
Peptídeos/farmacologia
Trofoblastos/metabolismo
Tirosina 3-Mono-Oxigenase/metabolismo
[Mh] Termos MeSH secundário: Animais
Inibidores das Descarboxilases de Aminoácidos Aromáticos
Brocresina/farmacologia
Linhagem Celular
Dopamina/metabolismo
Endopeptidases/farmacologia
Ativação Enzimática/efeitos dos fármacos
Feminino
Masculino
Metiltirosinas/farmacologia
Peso Molecular
Neurônios/metabolismo
Peptídeos/química
Peptídeos/isolamento & purificação
Hipófise/metabolismo
Ratos
Ratos Sprague-Dawley
Tirosina 3-Mono-Oxigenase/antagonistas & inibidores
alfa-Metiltirosina
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Aromatic Amino Acid Decarboxylase Inhibitors); 0 (Methyltyrosines); 0 (Peptides); 11F6O06WN0 (Brocresine); 658-48-0 (alpha-Methyltyrosine); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 3.4.- (Endopeptidases); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:9308
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:930701
[St] Status:MEDLINE


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[PMID]:1680164
[Au] Autor:Dahmer MK; Hart PM; Perlman RL
[Ad] Endereço:Department of Pediatrics, University of Chicago, IL 60637.
[Ti] Título:Insulin-like growth factor-I enhances tyrosine hydroxylase activation in bovine chromaffin cells.
[So] Source:J Neurochem;57(4):1347-53, 1991 Oct.
[Is] ISSN:0022-3042
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Previous studies have shown that insulin-like growth factor-I (IGF-I) enhances secretagogue-stimulated Ca2+ uptake and catecholamine release in bovine chromaffin cells. This report describes the effect of IGF-I on the activity of tyrosine hydroxylase (tyrosine 3-monooxygenase, EC 1.14.16.2), the major regulatory enzyme in the pathway of catecholamine biosynthesis. Tyrosine hydroxylase activity was assayed by measuring 3,4-dihydroxyphenylalanine (Dopa) accumulation in the presence of brocresine, an inhibitor of Dopa decarboxylase. Chromaffin cells cultured in serum-free medium produced approximately 40% less Dopa when stimulated by 55 mM K+ than did cells that had been cultured in the presence of serum. Incubation of cells for 3 days in serum-free medium containing 10 nM IGF-I restored high K(+)-stimulated Dopa accumulation to a level comparable to that seen in cells cultured continuously in serum-containing medium. In eight experiments, IGF-I increased high K(+)-stimulated Dopa accumulation (expressed as picomoles per minute per milligram of protein) by 96 +/- 13%. IGF-I increased the protein content of chromaffin cells by approximately 30%; consequently, its effect on tyrosine hydroxylase activity was even greater when Dopa synthesis was expressed as picomoles per minute per 10(7) cells. IGF-I also enhanced the rate of Dopa accumulation in cells stimulated by dimethylphenylpiperazinium, 8-bromo-cyclic AMP, phorbol 12,13-dibutyrate, or Ba2+. The effect of IGF-I on high K(+)-stimulated tyrosine hydroxylase activity was measurable when enzyme activity was assayed in vitro, suggesting that this effect was due to a stable modification of the enzyme.(ABSTRACT TRUNCATED AT 250 WORDS)
[Mh] Termos MeSH primário: Sistema Cromafim/enzimologia
Fator de Crescimento Insulin-Like I/farmacologia
Tirosina 3-Mono-Oxigenase/metabolismo
[Mh] Termos MeSH secundário: Animais
Brocresina/farmacologia
Bovinos
Células Cultivadas
Sistema Cromafim/citologia
Sistema Cromafim/metabolismo
Di-Hidroxifenilalanina/metabolismo
Ativação Enzimática
Immunoblotting
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
11F6O06WN0 (Brocresine); 63-84-3 (Dihydroxyphenylalanine); 67763-96-6 (Insulin-Like Growth Factor I); EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
[Em] Mês de entrada:9110
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:911001
[St] Status:MEDLINE


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[PMID]:1675837
[Au] Autor:Scherkl R; Hashem A; Frey HH
[Ad] Endereço:Department of Pharmacology and Toxicology, School of Veterinary Medicine, Free University of Berlin.
[Ti] Título:Importance of histamine for seizure susceptibility.
[So] Source:Agents Actions Suppl;33:85-9, 1991.
[Is] ISSN:0379-0363
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The influence of drugs affecting the turnover of histamine in brain and histamine antagonists on pentetrazole seizure threshold in mice was studied. A rise in histamine brain concentration as well as treatment with central acting H1-, but not H2- and H3-antagonists led to an increase of the convulsive threshold. It is therefore concluded that histamine has a certain anticonvulsant effect which is mediated through H1-receptors.
[Mh] Termos MeSH primário: Histamina/fisiologia
Convulsões/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Brocresina/farmacologia
Dimetideno/farmacologia
Antagonistas dos Receptores Histamínicos/farmacologia
Antagonistas dos Receptores Histamínicos H1/farmacologia
Histidina Descarboxilase/antagonistas & inibidores
Masculino
Camundongos
Pentilenotetrazol
Prometazina/farmacologia
Pirimetamina/análogos & derivados
Pirimetamina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histamine Antagonists); 0 (Histamine H1 Antagonists); 11F6O06WN0 (Brocresine); 2L9RKX796Q (metoprine); 661FH77Z3P (Dimethindene); 820484N8I3 (Histamine); EC 4.1.1.22 (Histidine Decarboxylase); FF28EJQ494 (Promethazine); WM5Z385K7T (Pentylenetetrazole); Z3614QOX8W (Pyrimethamine)
[Em] Mês de entrada:9107
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:910101
[St] Status:MEDLINE


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[PMID]:3183949
[Au] Autor:Spina MB; Cohen G
[Ad] Endereço:Department of Neurology, Mount Sinai School of Medicine, City University of New York, New York.
[Ti] Título:Exposure of striatal [corrected] synaptosomes to L-dopa increases levels of oxidized glutathione.
[So] Source:J Pharmacol Exp Ther;247(2):502-7, 1988 Nov.
[Is] ISSN:0022-3565
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Incubation of striatal synaptosomes with L-dopa and glucose in either the presence or absence of 10 microM reserpine resulted in a rise in the level of oxidized glutathione (GSSG) within the isolated tissue pellet. The rise in GSSG was concentration dependent in the range of 0.04-1.0 mM L-dopa. With 1.0 mM L-dopa in the presence of reserpine, the GSSG level was elevated by 7.0 +/- 0.7 pmol/mg original striatal tissue, which corresponds to an increase of 38.0 +/- 4.5% compared with control. The rise in GSSG reflects an oxidative stress. The oxidation of dopamine by monoamine oxidase generates H2O2, which is normally detoxified by glutathione peroxidase to yield GSSG. In the presence of clorgyline or pargyline (two monoamine oxidase inhibitors), the rise in GSSG was suppressed by 88-92%, as was the formation of DOPAC. NSD-1055 and carbidopa (two inhibitors of dopa-decarboxylase) also significantly suppressed (50-60%) the rise in GSSG. These data show that the synthesis of dopamine from L-dopa, with subsequent catabolism of dopamine, can evoke a significant rise in the level of GSSG, which reflects the oxidant stress associated with monoamine oxidase activity.
[Mh] Termos MeSH primário: Glutationa/análogos & derivados
Levodopa/farmacologia
Sinaptossomos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Ácido 3,4-Di-Hidroxifenilacético/metabolismo
Animais
Brocresina/farmacologia
Carbidopa/farmacologia
Catalase/metabolismo
Cromatografia Líquida de Alta Pressão
Glutationa/metabolismo
Dissulfeto de Glutationa
Peróxido de Hidrogênio/farmacologia
Masculino
Peróxidos/farmacologia
Ratos
Ratos Endogâmicos
Reserpina/farmacologia
terc-Butil Hidroperóxido
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Peroxides); 102-32-9 (3,4-Dihydroxyphenylacetic Acid); 11F6O06WN0 (Brocresine); 46627O600J (Levodopa); 8B1QWR724A (Reserpine); 955VYL842B (tert-Butylhydroperoxide); BBX060AN9V (Hydrogen Peroxide); EC 1.11.1.6 (Catalase); GAN16C9B8O (Glutathione); MNX7R8C5VO (Carbidopa); ULW86O013H (Glutathione Disulfide)
[Em] Mês de entrada:8812
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:881101
[St] Status:MEDLINE


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[PMID]:2439033
[Au] Autor:Kittner B; Bräutigam M; Herken H
[Ti] Título:PC12 cells: a model system for studying drug effects on dopamine synthesis and release.
[So] Source:Arch Int Pharmacodyn Ther;286(2):181-94, 1987 Apr.
[Is] ISSN:0003-9780
[Cp] País de publicação:Belgium
[La] Idioma:eng
[Ab] Resumo:PC12 cells were used as a model system to examine drug effects on dopamine synthesis and release. It could be demonstrated that KCl treatment induced release of endogenous dopamine, simultaneously DOPA synthesis was increased. Despite of the increase in DOPA synthesis the intracellular concentration of tetrahydrobiopterin (the co-factor of tyrosine hydroxylase) remained stable, indicating that the catalytic recycling of the used tetrahydrobiopterin is much more rapid than the tetrahydrobiopterin consumption by tyrosine hydroxylation. Reserpine induced a decrease of intracellular dopamine but no dopamine reached the extracellular space, instead all dopamine was depleted into the cytoplasma and metabolized to DOPAC. Nitrendipine had no effect on intracellular dopamine storage, Bay K 8644 induced a small decrease of intracellular dopamine and a small increase in DOPA production. N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide (W7) induced a reserpine-like depletion at concentrations above 1 X 10(-6) M. The KCl-induced dopamine release and the stimulation of DOPA production were blocked by 1 X 10(-7) M nitrendipine and enhanced by 1 X 10(-7) M Bay K 8466, whereas 1 X 10(-6) M W7 had no effect on both parameters. These findings were compared to data obtained in other tissues reported in the literature indicating that PC12 cells are a useful model for studying drug effects on catecholamine synthesis and release.
[Mh] Termos MeSH primário: Brocresina/farmacologia
Cresóis/farmacologia
Di-Hidroxifenilalanina/biossíntese
Dopamina/metabolismo
Cloreto de Potássio/farmacologia
Reserpina/farmacologia
[Mh] Termos MeSH secundário: Éster Metílico do Ácido 3-Piridinacarboxílico, 1,4-Di-Hidro-2,6-Dimetil-5-Nitro-4-(2-(Trifluormetil)fenil)/farmacologia
Animais
Células Cultivadas/efeitos dos fármacos
Dopamina/biossíntese
Modelos Biológicos
Nitrendipino/farmacologia
Feocromocitoma/metabolismo
Ratos
Sulfonamidas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cresols); 0 (Sulfonamides); 11F6O06WN0 (Brocresine); 63-84-3 (Dihydroxyphenylalanine); 65595-90-6 (W 7); 660YQ98I10 (Potassium Chloride); 71145-03-4 (3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester); 8B1QWR724A (Reserpine); 9B627AW319 (Nitrendipine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:8707
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:870401
[St] Status:MEDLINE


  9 / 33 MEDLINE  
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[PMID]:3808473
[Au] Autor:Misu Y; Goshima Y; Kubo T
[Ti] Título:Biphasic actions of L-DOPA on the release of endogenous dopamine via presynaptic receptors in rat striatal slices.
[So] Source:Neurosci Lett;72(2):194-8, 1986 Dec 12.
[Is] ISSN:0304-3940
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:In rat striatal slices, 30 nM of L-DOPA increased the impulse (5 Hz)-evoked release of dopamine (DA), without increasing the spontaneous release and tissue content of DA. The minimum dose required to increase spontaneous DA release was 0.1 microM and the dose which led to an accumulation of DA was 100 microM. In the presence of NSD-1055, a DOPA-decarboxylase inhibitor, L-DOPA-induced increases in spontaneous DA release were prevented and L-DOPA produced dual actions on the evoked release of DA, a stereoselective propranolol-sensitive increase at 30 nM and a stereoselective sulpiride-sensitive decrease at 1 microM. L-DOPA produces dual presynaptic regulatory actions on DA release, via facilitatory beta-adrenoceptors at 30 nM and inhibitory DA receptors at 1 microM. The primary action of L-DOPA appears to be the facilitation of release of DA rather than the conversion to DA.
[Mh] Termos MeSH primário: Corpo Estriado/efeitos dos fármacos
Dopamina/secreção
Levodopa/farmacologia
[Mh] Termos MeSH secundário: Animais
Brocresina/farmacologia
Cocaína/farmacologia
Interações Medicamentosas
Técnicas In Vitro
Masculino
Propranolol/farmacologia
Ratos
Ratos Endogâmicos
Sulpirida/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
11F6O06WN0 (Brocresine); 46627O600J (Levodopa); 7MNE9M8287 (Sulpiride); 9Y8NXQ24VQ (Propranolol); I5Y540LHVR (Cocaine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:8703
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:861212
[St] Status:MEDLINE


  10 / 33 MEDLINE  
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[PMID]:3801773
[Au] Autor:Goshima Y; Kubo T; Misu Y
[Ti] Título:Biphasic actions of L-DOPA on the release of endogenous noradrenaline and dopamine from rat hypothalamic slices.
[So] Source:Br J Pharmacol;89(1):229-34, 1986 Sep.
[Is] ISSN:0007-1188
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Effects of L-DOPA on the release of endogenous noradrenaline and dopamine from rat hypothalamic slices evoked by electrical field stimulation at 5 Hz were investigated in the absence and presence of p-bromobenzyloxyamine (NSD-1055), a DOPA-decarboxylase inhibitor. In the absence of NSD-1055, L-DOPA produced a facilitation of impulse-evoked release of noradrenaline at 0.1 microM but not at 1 and 10 microM, and had no effect on the spontaneous release. On the other hand, L-DOPA 0.1 to 10 microM dose-dependently increased the spontaneous release of dopamine and the highest concentration only increased the evoked release and tissue content of dopamine. In the presence of NSD-1055 10 microM, the increase in the spontaneous release of dopamine was prevented and L-DOPA produced biphasic regulatory effects on the evoked release of noradrenaline and dopamine, a facilitation at 0.1 microM and an inhibition at 1 microM. The facilitation was antagonized by (-)-propranolol 0.1 microM, but not by the (+)-isomer, whereas the inhibition was antagonized by S-sulpiride 1 nM, but not by the R-isomer. In conclusion, L-DOPA appears to produce biphasic actions on the release of endogenous noradrenaline and dopamine from rat hypothalamic slices, not through its conversion to dopamine but through presynaptic regulatory mechanisms, an inhibition via dopamine receptors at a micromolar concentration and a facilitation via beta-adrenoceptors at the lower concentration.
[Mh] Termos MeSH primário: Brocresina/farmacologia
Cresóis/farmacologia
Dopamina/metabolismo
Hipotálamo/metabolismo
Levodopa/farmacologia
Norepinefrina/metabolismo
[Mh] Termos MeSH secundário: Animais
Inibidores das Descarboxilases de Aminoácidos Aromáticos
Estimulação Elétrica
Feminino
Hipotálamo/efeitos dos fármacos
Técnicas In Vitro
Ratos
Ratos Endogâmicos
Sulpirida/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aromatic Amino Acid Decarboxylase Inhibitors); 0 (Cresols); 11F6O06WN0 (Brocresine); 46627O600J (Levodopa); 7MNE9M8287 (Sulpiride); VTD58H1Z2X (Dopamine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:8703
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:860901
[St] Status:MEDLINE



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