Base de dados : MEDLINE
Pesquisa : dopamina [Palavras]
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[PMID]:29382572
[Au] Autor:Lv C; Mo C; Liu H; Wu C; Li Z; Li J; Wang Y
[Ad] Endereço:Key Laboratory of Bio-resources and Eco-environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu 610065, PR China.
[Ti] Título:Dopamine D2-like receptors (DRD2 and DRD4) in chickens: Tissue distribution, functional analysis, and their involvement in dopamine inhibition of pituitary prolactin expression.
[So] Source:Gene;651:33-43, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Dopamine (DA) D2-like (and D1-like) receptors are suggested to mediate the dopamine actions in the anterior pituitary and/or CNS of birds. However, the information regarding the structure, functionality, and expression of avian D2-like receptors have not been fully characterized. In this study, we cloned two D2-like receptors (cDRD2, cDRD4) from chicken brain using RACE PCR. The cloned cDRD4 is a 378-amino acid receptor, which shows 57% amino acid (a.a.) identity with mouse DRD4. As in mammals, two cDRD2 isoforms, cDRD2L (long isoform, 437 a.a.) and cDRD2S (short isoform, 408 a.a.), which differ in their third intracellular loop, were identified in chickens. Using cell-based luciferase reporter assays or Western blot, we demonstrated that cDRD4, cDRD2L and cDRD2S could be activated by dopamine and quinpirole (a D2-like receptor agonist) dose-dependently, and their activation inhibits cAMP signaling pathway and stimulates MAPK/ERK signaling cascade, indicating that they are functional receptors capable of mediating dopamine actions. Quantitative real-time PCR revealed that cDRD2 and cDRD4 are widely expressed in chicken tissues with abundant expression noted in anterior pituitary, and their expressions are likely controlled by their promoters near exon 1, as demonstrated by dual-luciferase reporter assays in DF-1 cells. In accordance with cDRD2/cDRD4 expression in the pituitary, DA or quinpirole could partially inhibit vasoactive intestinal peptide-induced prolactin expression in cultured chick pituitary cells. Together, our data proves the functionality of DRD2 and DRD4 in birds and aids to uncover the conserved roles of DA/D2-like receptor system in vertebrates, such as its action on the pituitary.
[Mh] Termos MeSH primário: Galinhas/metabolismo
Dopamina/metabolismo
Hipófise/metabolismo
Prolactina/biossíntese
Receptores de Dopamina D2/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Galinhas/genética
Clonagem Molecular
DNA Complementar
Feminino
Regulação da Expressão Gênica
Células HEK293
Seres Humanos
Masculino
Prolactina/antagonistas & inibidores
Regiões Promotoras Genéticas
Receptores de Dopamina D2/genética
Receptores de Dopamina D2/fisiologia
Transdução de Sinais
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Receptors, Dopamine D2); 9002-62-4 (Prolactin); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE


  2 / 101078 MEDLINE  
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[PMID]:28471062
[Au] Autor:Rao AN; Patil A; Brodnik ZD; Qiang L; España RA; Sullivan KA; Black MM; Baas PW
[Ad] Endereço:Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, Pennsylvania.
[Ti] Título:Pharmacologically increasing microtubule acetylation corrects stress-exacerbated effects of organophosphates on neurons.
[So] Source:Traffic;18(7):433-441, 2017 Jul.
[Is] ISSN:1600-0854
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Many veterans of the 1990-1991 Gulf War contracted Gulf War Illness (GWI), a multisymptom disease that primarily affects the nervous system. Here, we treated cultures of human or rat neurons with diisopropyl fluorophosphate (DFP), an analog of sarin, one of the organophosphate (OP) toxicants to which the military veterans were exposed. All observed cellular defects produced by DFP were exacerbated by pretreatment with corticosterone or cortisol, which, in rat and human neurons, respectively, serves in our experiments to mimic the physical stress endured by soldiers during the war. To best mimic the disease, DFP was used below the level needed to inhibit acetylcholinesterase. We observed a diminution in the ratio of acetylated to total tubulin that was correctable by treatment with tubacin, a drug that inhibits HDAC6, the tubulin deacetylase. The reduction in microtubule acetylation was coupled with deficits in microtubule dynamics, which were correctable by HDAC6 inhibition. Deficits in mitochondrial transport and dopamine release were also improved by tubacin. Thus, various negative effects of the toxicant/stress exposures were at least partially correctable by restoring microtubule acetylation to a more normal status. Such an approach may have therapeutic benefit for individuals suffering from GWI or other neurological disorders linked to OP exposure.
[Mh] Termos MeSH primário: Anilidas/farmacologia
Substâncias para a Guerra Química/toxicidade
Ácidos Hidroxâmicos/farmacologia
Isoflurofato/toxicidade
Microtúbulos/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Estresse Fisiológico
[Mh] Termos MeSH secundário: Acetilação
Animais
Transporte Biológico
Células Cultivadas
Corticosterona/farmacologia
Dopamina/secreção
Relação Dose-Resposta a Droga
Seres Humanos
Hidrocortisona/farmacologia
Microtúbulos/metabolismo
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Síndrome do Golfo Pérsico
Ratos
Tubulina (Proteína)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anilides); 0 (Chemical Warfare Agents); 0 (Hydroxamic Acids); 0 (Tubulin); 02C2G1D30D (tubacin); 12UHW9R67N (Isoflurophate); VTD58H1Z2X (Dopamine); W980KJ009P (Corticosterone); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1111/tra.12489


  3 / 101078 MEDLINE  
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[PMID]:28462393
[Au] Autor:Pathak D; Berthet A; Bendor JT; Yu K; Sellnow RC; Orr AL; Nguyen MK; Edwards RH; Manfredsson FP; Nakamura K
[Ad] Endereço:Gladstone Institute of Neurological Disease, San Francisco, CA 94158.
[Ti] Título:Loss of α-Synuclein Does Not Affect Mitochondrial Bioenergetics in Rodent Neurons.
[So] Source:eNeuro;4(2), 2017 Mar-Apr.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Increased α-synuclein (αsyn) and mitochondrial dysfunction play central roles in the pathogenesis of Parkinson's disease (PD), and lowering αsyn is under intensive investigation as a therapeutic strategy for PD. Increased αsyn levels disrupt mitochondria and impair respiration, while reduced αsyn protects against mitochondrial toxins, suggesting that interactions between αsyn and mitochondria influences the pathologic and physiologic functions of αsyn. However, we do not know if αsyn affects normal mitochondrial function or if lowering αsyn levels impacts bioenergetic function, especially at the nerve terminal where αsyn is enriched. To determine if αsyn is required for normal mitochondrial function in neurons, we comprehensively evaluated how lowering αsyn affects mitochondrial function. We found that αsyn knockout (KO) does not affect the respiration of cultured hippocampal neurons or cortical and dopaminergic synaptosomes, and that neither loss of αsyn nor all three (α, ß and γ) syn isoforms decreased mitochondria-derived ATP levels at the synapse. Similarly, neither αsyn KO nor knockdown altered the capacity of synaptic mitochondria to meet the energy requirements of synaptic vesicle cycling or influenced the localization of mitochondria to dopamine (DA) synapses . Finally, αsyn KO did not affect overall energy metabolism in mice assessed with a Comprehensive Lab Animal Monitoring System. These studies suggest either that αsyn has little or no significant physiological effect on mitochondrial bioenergetic function, or that any such functions are fully compensated for when lost. These results implicate that αsyn levels can be reduced in neurons without impairing (or improving) mitochondrial bioenergetics or distribution.
[Mh] Termos MeSH primário: Mitocôndrias/metabolismo
Neurônios/metabolismo
Sinapses/metabolismo
alfa-Sinucleína/metabolismo
[Mh] Termos MeSH secundário: Animais
Dopamina/metabolismo
Hipocampo/metabolismo
Camundongos Knockout
Doença de Parkinson/metabolismo
alfa-Sinucleína/deficiência
alfa-Sinucleína/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Snca protein, mouse); 0 (alpha-Synuclein); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


  4 / 101078 MEDLINE  
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[PMID]:27778639
[Au] Autor:Arnold AC; Garland EM; Celedonio JE; Raj SR; Abumrad NN; Biaggioni I; Robertson D; Luther JM; Shibao CA
[Ad] Endereço:Department of Neural and Behavioral Sciences, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033.
[Ti] Título:Hyperinsulinemia and Insulin Resistance in Dopamine ß-Hydroxylase Deficiency.
[So] Source:J Clin Endocrinol Metab;102(1):10-14, 2017 Jan 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Dopamine ß-hydroxylase (DBH) deficiency is a rare genetic disorder characterized by failure to convert dopamine to norepinephrine. DBH-deficient patients lack sympathetic adrenergic function and are therefore predisposed to orthostatic hypotension. DBH-deficient mice exhibit hyperinsulinemia, lower plasma glucose levels, and insulin resistance due to loss of tonic sympathetic inhibition of insulin secretion. The impact of DBH deficiency on glucose homeostasis in humans is unknown. Case Description: We describe the metabolic profile of an adolescent female DBH-deficient patient. The patient underwent genetic testing, cardiovascular autonomic function testing, and evaluation of insulin secretion and sensitivity with hyperglycemic clamp under treatment-naive conditions. All procedures were repeated after 1 year of treatment with the norepinephrine prodrug droxidopa (300 mg, 3 times a day). Genetic testing showed a homozygous mutation in the DBH gene (rs74853476). Under treatment-naive conditions, she had undetectable plasma epinephrine and norepinephrine levels, resulting in sympathetic noradrenergic failure and orthostatic hypotension (-32 mm Hg supine to seated). She had high adiposity (41%) and fasting plasma insulin levels (25 µU/mL), with normal glucose (91 mg/dL). Hyperglycemic clamp revealed increased glucose-stimulated insulin secretion and insulin resistance. Droxidopa restored plasma norepinephrine and improved orthostatic tolerance, with modest effects on glucose homeostasis. Conclusions: We provide evidence for impairment in cardiovascular autonomic regulation, hyperinsulinemia, enhanced glucose-stimulated insulin secretion, and insulin resistance in a DBH-deficient patient. These metabolic derangements were not corrected by chronic droxidopa treatment. These findings provide insight into the pathophysiology and treatment of DBH deficiency and into the importance of catecholaminergic mechanisms to resting metabolism.
[Mh] Termos MeSH primário: Doenças do Sistema Nervoso Autônomo/complicações
Dopamina beta-Hidroxilase/deficiência
Hiperinsulinismo/etiologia
Resistência à Insulina
Norepinefrina/deficiência
[Mh] Termos MeSH secundário: Adolescente
Animais
Droxidopa/uso terapêutico
Feminino
Seres Humanos
Hiperinsulinismo/diagnóstico
Hiperinsulinismo/tratamento farmacológico
Insulina/metabolismo
Camundongos
Prognóstico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insulin); EC 1.14.17.1 (Dopamine beta-Hydroxylase); J7A92W69L7 (Droxidopa); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2016-3274


  5 / 101078 MEDLINE  
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[PMID]:29402888
[Au] Autor:Yano H; Cai NS; Xu M; Verma RK; Rea W; Hoffman AF; Shi L; Javitch JA; Bonci A; Ferré S
[Ad] Endereço:National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, 21224, USA. hideaki.yano@nih.gov.
[Ti] Título:Gs- versus Golf-dependent functional selectivity mediated by the dopamine D receptor.
[So] Source:Nat Commun;9(1):486, 2018 02 05.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The two highly homologous subtypes of stimulatory G proteins Gαs (Gs) and Gαolf (Golf) display contrasting expression patterns in the brain. Golf is predominant in the striatum, while Gs is predominant in the cortex. Yet, little is known about their functional distinctions. The dopamine D receptor (D1R) couples to Gs/olf and is highly expressed in cortical and striatal areas, making it an important therapeutic target for neuropsychiatric disorders. Using novel drug screening methods that allow analysis of specific G-protein subtype coupling, we found that, relative to dopamine, dihydrexidine and N-propyl-apomorphine behave as full D1R agonists when coupled to Gs, but as partial D1R agonists when coupled to Golf. The Gs/Golf-dependent biased agonism by dihydrexidine was consistently observed at the levels of cellular signaling, neuronal function, and behavior. Our findings of Gs/Golf-dependent functional selectivity in D1R ligands open a new avenue for the treatment of cortex-specific or striatum-specific neuropsychiatric dysfunction.
[Mh] Termos MeSH primário: Subunidades alfa Gs de Proteínas de Ligação ao GTP/metabolismo
Subunidades alfa de Proteínas de Ligação ao GTP/metabolismo
Fenantridinas/farmacologia
Receptores de Dopamina D1/agonistas
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sítios de Ligação
Encéfalo/metabolismo
Linhagem Celular Tumoral
Subunidades alfa de Proteínas de Ligação ao GTP/genética
Subunidades alfa Gs de Proteínas de Ligação ao GTP/genética
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Camundongos
Conformação Proteica
Receptores de Dopamina D1/genética
Receptores de Dopamina D1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GTP-Binding Protein alpha Subunits); 0 (Phenanthridines); 0 (Receptors, Dopamine D1); 0 (olfactory G protein subunit alpha olf); 32D64VH037 (dihydrexidine); EC 3.6.5.1 (GTP-Binding Protein alpha Subunits, Gs)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02606-w


  6 / 101078 MEDLINE  
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[PMID]:28448827
[Au] Autor:Broyd A; Balzan RP; Woodward TS; Allen P
[Ad] Endereço:Department of Psychosis Studies, Institute of Psychiatry, Psychology and Neuroscience (IoPPN), King's College, London, UK.
[Ti] Título:Dopamine, cognitive biases and assessment of certainty: A neurocognitive model of delusions.
[So] Source:Clin Psychol Rev;54:96-106, 2017 Jun.
[Is] ISSN:1873-7811
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This paper examines the evidence that delusions can be explained within the framework of a neurocognitive model of how the brain assesses certainty. Here, 'certainty' refers to both low-level interpretations of one's environment and high-level (conscious) appraisals of one's beliefs and experiences. A model is proposed explaining how the brain systems responsible for assigning certainty might dysfunction, contributing to the cause and maintenance of delusional beliefs. It is suggested that delusions arise through a combination of perturbed striatal dopamine and aberrant salience as well as cognitive biases such as the tendency to jump to conclusions (JTC) and hypersalience of evidence-hypothesis matches. The role of emotion, stress, trauma and sociocultural factors in forming and modifying delusions is also considered. Understanding the mechanisms involved in forming and maintaining delusions has important clinical implications, as interventions that improve cognitive flexibility (e.g. cognitive remediation therapy and mindfulness training) could potentially attenuate neurocognitive processes.
[Mh] Termos MeSH primário: Cognição/fisiologia
Delusões/psicologia
Dopamina/metabolismo
Modelos Psicológicos
Psicologia do Esquizofrênico
[Mh] Termos MeSH secundário: Delusões/metabolismo
Seres Humanos
Testes Neuropsicológicos
Incerteza
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE


  7 / 101078 MEDLINE  
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[PMID]:29407591
[Au] Autor:Zajdel P; Kos T; Marciniec K; Satala G; Canale V; Kaminski K; Holuj M; Lenda T; Koralewski R; Bednarski M; Nowinski L; Wójcikowski J; Daniel WA; Nikiforuk A; Nalepa I; Chmielarz P; Kusmierczyk J; Bojarski AJ; Popik P
[Ad] Endereço:Department of Medicinal Chemistry, Jagiellonian University Medical College, 9 Medyczna Street, 30-688 Kraków, Poland. Electronic address: pawel.zajdel@uj.edu.pl.
[Ti] Título:Novel multi-target azinesulfonamides of cyclic amine derivatives as potential antipsychotics with pro-social and pro-cognitive effects.
[So] Source:Eur J Med Chem;145:790-804, 2018 Feb 10.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Currently used antipsychotics are characterized by multireceptor mode of action. While antagonism of dopamine D receptors is responsible for the alleviation of "positive" symptoms of schizophrenia and the effects at other, particularly serotonergic receptors are necessary for their additional therapeutic effects, there is no consensus regarding an "ideal" target engagement. Here, a detailed SAR analysis in a series of 45 novel azinesulfonamides of cyclic amine derivatives, involving the aryl-piperazine/piperidine pharmacophore, central alicyclic amine and azinesulfonamide groups has led to the selection of (S)-4-((2-(2-(4-(benzo[b]thiophen-4-yl)piperazin-1-yl)ethyl)pyrrolidin-1-yl)sulfonyl)isoquinoline (62). The polypharmacology profile of 62, characterized by partial 5-HT R agonism, 5-HT /5-HT /D /D R antagonism, and blockade of SERT, reduced the "positive"-like, and "negative"-like symptoms of psychoses. Compound 62 produced no catalepsy, demonstrated a low hyperprolactinemia liability and displayed pro-cognitive effects in the novel object recognition task and attentional set-shifting test. While association of in vitro features with the promising in vivo profile of 62 is still not fully established, its clinical efficacy should be verified in further stages of development.
[Mh] Termos MeSH primário: Aminas/farmacologia
Antipsicóticos/farmacologia
Cognição/efeitos dos fármacos
Receptores de Dopamina D2/metabolismo
Sulfonamidas/farmacologia
[Mh] Termos MeSH secundário: Aminas/síntese química
Aminas/química
Animais
Antipsicóticos/síntese química
Antipsicóticos/química
Relação Dose-Resposta a Droga
Cobaias
Células HEK293
Seres Humanos
Masculino
Estrutura Molecular
Ratos
Ratos Wistar
Relação Estrutura-Atividade
Sulfonamidas/síntese química
Sulfonamidas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amines); 0 (Antipsychotic Agents); 0 (Receptors, Dopamine D2); 0 (Sulfonamides)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


  8 / 101078 MEDLINE  
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[PMID]:28460583
[Au] Autor:Nielsen BS; Larsen EH; Ladefoged O; Lam HR
[Ad] Endereço:1 Environment and Toxicology, DHI, Hørsholm, Denmark.
[Ti] Título:Subchronic, Low-Level Intraperitoneal Injections of Manganese (IV) Oxide and Manganese (II) Chloride Affect Rat Brain Neurochemistry.
[So] Source:Int J Toxicol;36(3):239-251, 2017 May/Jun.
[Is] ISSN:1092-874X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Manganese (Mn) is neurotoxic and can induce manganism, a Parkinson-like disease categorized as being a serious central nervous system irreversible neurodegenerative disease. An increased risk of developing symptoms of Parkinson disease has been linked to work-related exposure, for example, for workers in agriculture, horticulture, and people living near areas with frequent use of Mn-containing pesticides. In this study, the focus was placed on neurochemical effects of Mn. Rats were dosed intraperitoneally with 0.9% NaCl (control), 1.22 mg Mn (as MnO )/kg bodyweight (bw)/day, or 2.5 mg Mn (as MnCl )/kg bw/day for 7 d/wk for 8 or 12 weeks. This dosing regimen adds relevant new knowledge about Mn neurotoxicity as a consequence of low-dose subchronic Mn dosing. Manganese concentrations increased in the striatum, the rest of the brain, and in plasma, and regional brain neurotransmitter concentrations, including noradrenaline, dopamine (DA), 5-hydroxytrytamine, glutamate, taurine, and γ-amino butyric acid, and the activity of acetylcholinesterase changed. Importantly, a target parameter for Parkinson disease and manganism, the striatal DA concentration, was reduced after 12 weeks of dosing with MnCl . Plasma prolactin concentration was not significantly affected due to a potentially reduced dopaminergic inhibition of the prolactin release from the anterior hypophysis. No effects on the striatal α-synuclein and synaptophysin protein levels were detected.
[Mh] Termos MeSH primário: Química Encefálica/efeitos dos fármacos
Encéfalo/efeitos dos fármacos
Cloretos/toxicidade
Óxidos/toxicidade
[Mh] Termos MeSH secundário: Acetilcolinesterase/metabolismo
Animais
Encéfalo/metabolismo
Cloretos/sangue
Cloretos/farmacocinética
Dopamina/metabolismo
Ácido Glutâmico/metabolismo
Injeções Intraperitoneais
Masculino
Manganês/sangue
Manganês/metabolismo
Compostos de Manganês/sangue
Compostos de Manganês/farmacocinética
Norepinefrina/metabolismo
Óxidos/sangue
Óxidos/farmacocinética
Ratos Sprague-Dawley
Serotonina/metabolismo
Taurina/metabolismo
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chlorides); 0 (Manganese Compounds); 0 (Oxides); 1EQV5MLY3D (Taurine); 333DO1RDJY (Serotonin); 3KX376GY7L (Glutamic Acid); 42Z2K6ZL8P (Manganese); 56-12-2 (gamma-Aminobutyric Acid); 64J2OA7MH3 (manganese oxide); EC 3.1.1.7 (Acetylcholinesterase); QQE170PANO (manganese chloride); VTD58H1Z2X (Dopamine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1177/1091581817704378


  9 / 101078 MEDLINE  
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[PMID]:29338466
[Au] Autor:Sarva H; Henchcliffe C
[Ad] Endereço:a Parkinson's Disease and Movement Disorders Institute , Weill Cornell Medicine/New York Presbyterian Hospital , New York , NY , USA.
[Ti] Título:Valbenazine as the first and only approved treatment for adults with tardive dyskinesia.
[So] Source:Expert Rev Clin Pharmacol;11(3):209-217, 2018 Mar.
[Is] ISSN:1751-2441
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Valbenazine is a selective VMAT2 inhibitor that the FDA approved in April 2017 for the specific treatment of tardive dyskinesia (TD), a movement disorder commonly caused by dopamine blocking agents. Valbenazine acts to decrease dopamine release, reducing excessive movement found in TD. Areas covered: This drug profile reviews the development of valbenazine and the clinical trials that led to its approval as the first treatment specific to TD. The literature search was performed with the PubMed online database. Expert commentary: Two clinical trials assessing the efficacy of valbenazine have shown the reduction of antipsychotic-induced involuntary movement. No life threatening adverse effects were found. Data from a 42-week extension study demonstrated sustained response.
[Mh] Termos MeSH primário: Dopamina/metabolismo
Discinesia Tardia/tratamento farmacológico
Tetrabenazina/análogos & derivados
Valina/análogos & derivados
[Mh] Termos MeSH secundário: Adulto
Animais
Antipsicóticos/administração & dosagem
Antipsicóticos/efeitos adversos
Antipsicóticos/farmacologia
Aprovação de Drogas
Seres Humanos
Discinesia Tardia/induzido quimicamente
Tetrabenazina/efeitos adversos
Tetrabenazina/farmacologia
Tetrabenazina/uso terapêutico
Valina/efeitos adversos
Valina/farmacologia
Valina/uso terapêutico
Proteínas Vesiculares de Transporte de Monoamina/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antipsychotic Agents); 0 (SLC18A2 protein, human); 0 (Vesicular Monoamine Transport Proteins); 54K37P50KH (valbenazine); HG18B9YRS7 (Valine); VTD58H1Z2X (Dopamine); Z9O08YRN8O (Tetrabenazine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1080/17512433.2018.1429264


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[PMID]:29386447
[Au] Autor:Mori T; Sawaguchi T
[Ad] Endereço:Department of Pharmacology, Hoshi University School of Pharmacy and Pharmaceutical Sciences.
[Ti] Título:[Underlying Mechanisms of Methamphetamine-Induced Self-Injurious Behavior and Lethal Effects in Mice].
[So] Source:Nihon Eiseigaku Zasshi;73(1):51-56, 2018.
[Is] ISSN:1882-6482
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Relatively high doses of psychostimulants induce neurotoxicity on the dopaminergic system and self-injurious behavior (SIB) in rodents. However the underlying neuronal mechanisms of SIB remains unclear. Dopamine receptor antagonists, N-methyl-D-aspartic acid (NMDA) receptor antagonists, Nitric Oxide Synthase (NOS) inhibitors and free radical scavengers significantly attenuate methamphetamine-induced SIB. These findings indicate that activation of dopamine as well as NMDA receptors followed by radical formation and oxidative stress, especially when mediated by NOS activation, is associated with methamphetamine-induced SIB. On the other hand, an increase in the incidence of polydrug abuse is a major problem worldwide. Coadministered methamphetamine and morphine induced lethality in more than 80% in mice, accompanied by an increase in the number of poly (ADP-ribose) polymerase (PARP)-immunoreactive cells in the heart, kidney and liver. The lethal effect and the increase in the incidence of rupture or PARP-immunoreactive cells induced by the coadministration of methamphetamine and morphine were significantly attenuated by pretreatment with a phospholipase A2 inhibitor or a radical scavenger, or by cooling of body from 30 to 90 min after drug administration. These results suggest that free radicals play an important role in the increased lethality induced by the coadministration of methamphetamine and morphine. Therefore, free radical scavengers and cooling are beneficial for preventing death that is induced by the coadministration of methamphetamine and morphine. These findings may help us better understand for masochistic behavior, which is a clinical phenomenon on SIB, as well as polydrug-abuse-induced acute toxicity.
[Mh] Termos MeSH primário: Estimulantes do Sistema Nervoso Central/efeitos adversos
Estimulantes do Sistema Nervoso Central/toxicidade
Metanfetamina/efeitos adversos
Metanfetamina/toxicidade
Comportamento Autodestrutivo/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Antagonistas de Dopamina/farmacologia
Antagonistas de Dopamina/uso terapêutico
Neurônios Dopaminérgicos/efeitos dos fármacos
Relação Dose-Resposta a Droga
Interações Medicamentosas
Depuradores de Radicais Livres/farmacologia
Depuradores de Radicais Livres/uso terapêutico
Radicais Livres/efeitos adversos
Radicais Livres/toxicidade
Seres Humanos
Dose Letal Mediana
Metanfetamina/administração & dosagem
Morfina/administração & dosagem
Morfina/efeitos adversos
Morfina/toxicidade
Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
Comportamento Autodestrutivo/etiologia
Transtornos Relacionados ao Uso de Substâncias
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Central Nervous System Stimulants); 0 (Dopamine Antagonists); 0 (Free Radical Scavengers); 0 (Free Radicals); 0 (Receptors, N-Methyl-D-Aspartate); 44RAL3456C (Methamphetamine); 76I7G6D29C (Morphine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180202
[St] Status:MEDLINE
[do] DOI:10.1265/jjh.73.51



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