Base de dados : MEDLINE
Pesquisa : D12.776.543.750.670.300.400 [Categoria DeCS]
Referências encontradas : 13481 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 1349 ir para página                         

  1 / 13481 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28448718
[Au] Autor:Fransquet PD; Hutchinson D; Olsson CA; Allsop S; Elliott EJ; Burns L; Mattick R; Saffery R; Ryan J
[Ad] Endereço:a Murdoch Childrens Research Institute, The University of Melbourne , Parkville , Victoria , Australia.
[Ti] Título:Cannabis use by women during pregnancy does not influence infant DNA methylation of the dopamine receptor DRD4.
[So] Source:Am J Drug Alcohol Abuse;43(6):671-677, 2017 Nov.
[Is] ISSN:1097-9891
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Maternal cannabis use in pregnancy is linked with long-term adverse behavioral outcomes in offspring. Epigenetic processes established in utero that affect dopaminergic (reward) signaling may mediate risks. Associations between cannabis use and offspring DNA methylation have not been investigated; however, maternal tobacco smoking in pregnancy is associated with distinct patterns of DNA methylation at birth and beyond. OBJECTIVES: To determine whether maternal cannabis use is associated with methylation of the dopamine receptor gene DRD4 promoter in infants. METHODS: Mothers in the Triple B study provided detailed information on drug use in each trimester of pregnancy. Buccal swabs were collected from neonates at 8 weeks (n = 804, 51.7% male, and 48.3% female). DRD4 promoter DNA methylation was measured using SEQUENOM MassARRAY. RESULTS: Fifty-seven of the women in the study reported drug use during pregnancy, of whom 44 used cannabis. Of 19 cytosine-phosphate-guanine dinucleotides (CpG) units tested in DRD4, gestational cannabis use was associated with offspring methylation at 1 CpG unit in multivariate models (ß + 1.48, CI: 0.02 to 2.93, and p = 0.047). At another site there was weak evidence that both cannabis and other drug use were independently associated with increased methylation, while the association with tobacco was in the reverse direction (cannabis use ß + 0.67, CI: -0.12 to 1.46, and p = 0.09; other drug use ß + 1.11, CI: 0.17 to 2.05, and p = 0.02; tobacco use ß -0.41, CI: -0.85 to 0.03, and p = 0.07). None of the associations would remain significant after correction for multiple testing. CONCLUSION: There is no strong evidence that maternal cannabis use in pregnancy is associated with offspring DRD4 methylation.
[Mh] Termos MeSH primário: Metilação de DNA/efeitos dos fármacos
Fumar Maconha/metabolismo
Efeitos Tardios da Exposição Pré-Natal/metabolismo
Receptores Dopaminérgicos/metabolismo
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Lactente
Masculino
Gravidez
Regiões Promotoras Genéticas
Fumar Tabaco/efeitos adversos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Dopamine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE
[do] DOI:10.1080/00952990.2017.1314488


  2 / 13481 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:29283228
[Au] Autor:Bazyan AS
[Ti] Título:Integration the Highest Function of Brain as the Basis of Cognition.
[So] Source:Usp Fiziol Nauk;47(3):17-29, 2016 Jul-Sep.
[Is] ISSN:0301-1798
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Based on the process needs, motivations and emotions, are describing molecular, cellular and systemic mechanisms of goal-direction motivated behavior. Goal-direction behavior is impossible without the orientation in space and forming a cognitive map. This process implements the hippocampus, via the neocortical connections. The hippocampus is linked to the amygdala, which is involved in the implementation of emotional behavior and organizing emotionally intense cognitive map or context of the environment.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/fisiologia
Cognição/fisiologia
Emoções/fisiologia
Hipocampo/fisiologia
Rede Nervosa/fisiologia
[Mh] Termos MeSH secundário: Tonsila do Cerebelo/anatomia & histologia
Mapeamento Encefálico
Corpo Estriado/anatomia & histologia
Corpo Estriado/fisiologia
Hipocampo/anatomia & histologia
Seres Humanos
Motivação/fisiologia
Neocórtex/anatomia & histologia
Neocórtex/fisiologia
Rede Nervosa/anatomia & histologia
Plasticidade Neuronal/fisiologia
Receptores Dopaminérgicos/fisiologia
Receptores de GABA/fisiologia
Receptores de Glutamato Metabotrópico/fisiologia
Transdução de Sinais
Tálamo/anatomia & histologia
Tálamo/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Dopamine); 0 (Receptors, GABA); 0 (Receptors, Metabotropic Glutamate)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171229
[St] Status:MEDLINE


  3 / 13481 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29032150
[Au] Autor:Sundararajan T; Manzardo AM; Butler MG
[Ad] Endereço:Department of Psychiatry and Behavioral Sciences, University of Kansas Medical Center, Kansas City, KS, United States.
[Ti] Título:Functional analysis of schizophrenia genes using GeneAnalytics program and integrated databases.
[So] Source:Gene;641:25-34, 2018 Jan 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Schizophrenia (SCZ) is a chronic debilitating neuropsychiatric disorder with multiple risk factors involving numerous complex genetic influences. We examined and updated a master list of clinically relevant and susceptibility genes associated with SCZ reported in the literature and genomic databases dedicated to gene discovery for characterization of SCZ genes. We used the commercially available GeneAnalytics computer-based gene analysis program and integrated genomic databases to create a molecular profile of the updated list of 608 SCZ genes to model their impact in select categories (tissues and cells, diseases, pathways, biological processes, molecular functions, phenotypes and compounds) using specialized GeneAnalytics algorithms. Genes for schizophrenia were predominantly expressed in the cerebellum, cerebral cortex, medulla oblongata, thalamus and hypothalamus. Psychiatric/behavioral disorders incorporating SCZ genes included ADHD, bipolar disorder, autism spectrum disorder and alcohol dependence as well as cancer, Alzheimer's and Parkinson's disease, sleep disturbances and inflammation. Function based analysis of major biological pathways and mechanisms associated with SCZ genes identified glutaminergic receptors (e.g., GRIA1, GRIN2, GRIK4, GRM5), serotonergic receptors (e.g., HTR2A, HTR2C), GABAergic receptors (e.g., GABRA1, GABRB2), dopaminergic receptors (e.g., DRD1, DRD2), calcium-related channels (e.g., CACNA1H, CACNA1B), solute transporters (e.g., SLC1A1, SLC6A2) and for neurodevelopment (e.g., ADCY1, MEF2C, NOTCH2, SHANK3). Biological mechanisms involving synaptic transmission, regulation of membrane potential and transmembrane ion transport were identified as leading molecular functions associated with SCZ genes. Our approach to interrogate SCZ genes and their interactions at various levels has increased our knowledge and insight into the disease process possibly opening new avenues for therapeutic intervention.
[Mh] Termos MeSH primário: Estudo de Associação Genômica Ampla
Transporte de Íons/genética
Potenciais da Membrana/genética
Esquizofrenia/genética
Transmissão Sináptica/genética
[Mh] Termos MeSH secundário: Sistemas de Transporte de Aminoácidos/genética
Canais de Cálcio/genética
Cerebelo/citologia
Córtex Cerebral/citologia
Bases de Dados Genéticas
Seres Humanos
Hipotálamo/citologia
Bulbo/citologia
Receptores Dopaminérgicos/genética
Receptores de GABA-A/genética
Receptores Ionotrópicos de Glutamato/genética
Receptores de Serotonina/genética
Tálamo/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amino Acid Transport Systems); 0 (Calcium Channels); 0 (Receptors, Dopamine); 0 (Receptors, GABA-A); 0 (Receptors, Ionotropic Glutamate); 0 (Receptors, Serotonin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171017
[St] Status:MEDLINE


  4 / 13481 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28745677
[Au] Autor:Pilipovich AA; Golubev VL
[Ad] Endereço:I.M. Sechenov First Moscow State Medical University, Moscow, Russia.
[Ti] Título:[The agonist of dopamine receptors piribedil in treatment of Parkinson's disease].
[Ti] Título:Agonist dofaminovykh retseptorov piribedil v terapii bolezni Parkinsona..
[So] Source:Zh Nevrol Psikhiatr Im S S Korsakova;117(6):83-90, 2017.
[Is] ISSN:1997-7298
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:In this paper, the authors review the current foreign and domestic literature on a role of the agonist of dopamine receptors piribedil in the treatment of Parkinson's disease. The results of the main studies of the efficacy and safety of piribedil, mechanisms of actions and a comparative characteristics with other dopamine receptors agonist are reviewed.
[Mh] Termos MeSH primário: Antiparkinsonianos/uso terapêutico
Agonistas de Dopamina/uso terapêutico
Doença de Parkinson/tratamento farmacológico
Piribedil/uso terapêutico
[Mh] Termos MeSH secundário: Antiparkinsonianos/farmacologia
Agonistas de Dopamina/farmacologia
Seres Humanos
Atividade Motora/efeitos dos fármacos
Neuroproteção
Piribedil/farmacologia
Receptores Dopaminérgicos/metabolismo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antiparkinson Agents); 0 (Dopamine Agonists); 0 (Receptors, Dopamine); DO22K1PRDJ (Piribedil)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.17116/jnevro20171176183-90


  5 / 13481 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28465234
[Au] Autor:Jung YS; Lee SO
[Ad] Endereço:Department of Food Science and Technology, Keimyung University, Daegu 42601, Republic of Korea.
[Ti] Título:Apomorphine suppresses TNF-α-induced MMP-9 expression and cell invasion through inhibition of ERK/AP-1 signaling pathway in MCF-7 cells.
[So] Source:Biochem Biophys Res Commun;487(4):903-909, 2017 06 10.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent studies have shown that dopamine plays an important role in several types of cancer by inhibiting cell growth and invasion via dopamine receptors (DRs), such as dopamine receptor D2. However, the roles of DR agonists in cancer cell growth and invasion remain unclear. In our study, we found that apomorphine (APO), one of the most commonly prescribed DR agonists, inhibited TNF-α-induced matrix metalloprotease-9 (MMP-9) expression and cell invasion in MCF-7 human breast carcinoma cells through DR-independent pathways. Further mechanistic studies demonstrated that APO suppresses TNF-α-induced transcription of MMP-9 by inhibiting activator protein-1 (AP-1), a well-described transcription factor. This is achieved via extracellular signal-regulated kinases 1 and 2 (ERK1/2). Our study has demonstrated that APO targets human MMP-9 in a DR-independent fashion in MCF-7 cells, suggesting that APO is a potential anticancer agent that can suppress the metastatic progression of cancer cells.
[Mh] Termos MeSH primário: Apomorfina/farmacologia
Movimento Celular/efeitos dos fármacos
MAP Quinases Reguladas por Sinal Extracelular/antagonistas & inibidores
Metaloproteinase 9 da Matriz/genética
Transdução de Sinais/efeitos dos fármacos
Fator de Transcrição AP-1/antagonistas & inibidores
Fator de Necrose Tumoral alfa/antagonistas & inibidores
[Mh] Termos MeSH secundário: Apomorfina/química
Sobrevivência Celular/efeitos dos fármacos
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Seres Humanos
Células MCF-7
Metaloproteinase 9 da Matriz/metabolismo
Invasividade Neoplásica/prevenção & controle
Receptores Dopaminérgicos/metabolismo
Fator de Transcrição AP-1/metabolismo
Fator de Necrose Tumoral alfa/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Dopamine); 0 (Transcription Factor AP-1); 0 (Tumor Necrosis Factor-alpha); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.4.24.35 (Matrix Metalloproteinase 9); N21FAR7B4S (Apomorphine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  6 / 13481 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28652413
[Au] Autor:Lavian H; Almog M; Madar R; Loewenstern Y; Bar-Gad I; Okun E; Korngreen A
[Ad] Endereço:The Leslie and Susan Gonda Interdisciplinary Brain Research Center.
[Ti] Título:Dopaminergic Modulation of Synaptic Integration and Firing Patterns in the Rat Entopeduncular Nucleus.
[So] Source:J Neurosci;37(30):7177-7187, 2017 Jul 26.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dopamine is known to differentially modulate the impact of cortical input to the striatum between the direct and indirect pathways of the basal ganglia (BG). However, the role of extrastriatal dopamine receptors (DRs) in BG information processing is less clear. To investigate the role of extrastriatal DRs, we studied their distribution and function in one of the output nuclei of the BG of the rodent, the entopeduncular nucleus (EP). qRT-PCR indicated that all DR subtypes were expressed by EP neurons, suggesting that both D -like receptors (D1LRs) and D -like receptors (D2LRs) were likely to affect information processing in the EP. Whole-cell recordings revealed that striatal inputs to the EP were potentiated by D1LRs whereas pallidal inputs to the EP were depressed by D2LRs. Changes to the paired-pulse ratio of inputs to the EP suggested that dopaminergic modulation of striatal inputs is mediated by postsynaptic receptors, and that of globus pallidus-evoked inputs is mediated by presynaptic receptors. We show that these changes in synaptic efficacy changed the information content of EP neuron firing. Overall, the findings suggest that the dopaminergic system affects the passage of feedforward information through the BG by modulating input divergence in the striatum and output convergence in the EP. The entopeduncular nucleus (EP), one of the basal ganglia (BG) output nuclei, is an important station in information processing in BG. However, it remains unclear how EP neurons encode information and how dopamine affects this process. This contrasts with the well established role of dopamine in the striatum, which is known to redistribute cortical input between the direct and indirect pathways. Here we show that, in symmetry with the striatum, dopamine controls the rebalancing of information flow between the two pathways in the EP. Specifically, we demonstrate that dopamine regulates EP activity by differentially modulating striatal and pallidal GABAergic inputs. These results call for a reassessment of current perspectives on BG information processing by highlighting the functional role of extrastriatal dopamine receptors.
[Mh] Termos MeSH primário: Potenciais de Ação/fisiologia
Gânglios da Base/fisiologia
Núcleo Entopeduncular/fisiologia
Modelos Neurológicos
Receptores Dopaminérgicos/metabolismo
Transmissão Sináptica/fisiologia
[Mh] Termos MeSH secundário: Animais
Simulação por Computador
Dopamina
Neurônios Dopaminérgicos
Feminino
Rede Nervosa/fisiologia
Vias Neurais/fisiologia
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Dopamine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0639-17.2017


  7 / 13481 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28644892
[Au] Autor:Shanmugasundaram B; Aher YD; Aradska J; Ilic M; Daba Feyissa D; Kalaba P; Aher NY; Dragacevic V; Saber Marouf B; Langer T; Sitte HH; Hoeger H; Lubec G; Korz V
[Ad] Endereço:Department of Pediatrics, Medical University of Vienna, Vienna, Austria.
[Ti] Título:R-Modafinil exerts weak effects on spatial memory acquisition and dentate gyrus synaptic plasticity.
[So] Source:PLoS One;12(6):e0179675, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Modafinil is a wake promoting drug approved for clinical use and also has cognitive enhancing properties. Its enantiomer R-Modafinil (R-MO) is not well studied in regard to cognitive enhancing properties. Hence we studied its effect in a spatial memory paradigm and its possible effects on dentate gyrus long-term potentiation (DG-LTP). Clinically relevant doses of R-MO, vehicle dimethyl sulfoxide (DMSO) or saline were administered for three days during the hole-board test and in in vivo DG-LTP. Synaptic levels of dopamine receptors D1R, D2R, dopamine transporter (DAT), and its phosphorylated form (ph-DAT) in DG tissue 4 h after LTP induction were quantified by western blot analysis. Monoamine reuptake and release assays were performed by using transfected HEK-293 cells. Possible neurotoxic side effects on general behaviour were also studied. R-MO at both doses significantly enhanced spatial reference memory during the last training session and during memory retrieval compared to DMSO vehicle but not when compared to saline treated rats. Similarly, R-MO rescues DG-LTP from impairing effects of DMSO. DMSO reduced memory performance and LTP magnitude when compared to saline treated groups. The synaptic DR1 levels in R-MO groups were significantly decreased compared to DMSO group but were comparable with saline treated animals. We found no effect of R-MO in neurotoxicity tests. Thus, our results support the notion that LTP-like synaptic plasticity processes could be one of the factors contributing to the cognitive enhancing effects of spatial memory traces. D1R may play an important regulatory role in these processes.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/farmacologia
Giro Denteado/efeitos dos fármacos
Aprendizagem/efeitos dos fármacos
Potenciação de Longa Duração/efeitos dos fármacos
Nootrópicos/farmacologia
Memória Espacial/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Giro Denteado/fisiologia
Dimetil Sulfóxido/farmacologia
Dopamina/metabolismo
Proteínas da Membrana Plasmática de Transporte de Dopamina/metabolismo
Avaliação Pré-Clínica de Medicamentos
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Potenciais Pós-Sinápticos Excitadores/fisiologia
Células HEK293
Seres Humanos
Aprendizagem/fisiologia
Potenciação de Longa Duração/fisiologia
Masculino
Ratos Sprague-Dawley
Receptores Dopaminérgicos/metabolismo
Memória Espacial/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzhydryl Compounds); 0 (Dopamine Plasma Membrane Transport Proteins); 0 (Nootropic Agents); 0 (Receptors, Dopamine); R3UK8X3U3D (modafinil); VTD58H1Z2X (Dopamine); YOW8V9698H (Dimethyl Sulfoxide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170624
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179675


  8 / 13481 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:28638920
[Au] Autor:Wei TJ; Chen HY; Huang X; Weng JJ; Qin JY; Su JP
[Ad] Endereço:Department of Otolaryngology Head and Neck Surgery, First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China.
[Ti] Título:[A study on toxic effects of sodium salicylate on rat cochlear spiral ganglion neurons: dopamine receptors mediate expressions of NMDA and GABA receptors].
[So] Source:Sheng Li Xue Bao;69(3):285-290, 2017 Jun 25.
[Is] ISSN:0371-0874
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:The aim of the present study was to observe whether dopamine receptor (DR) was involved in the effects of sodium salicylate (SS) on the expressions of N-methyl-D-aspartic acid (NMDA) and γ-aminobutyric acid (GABA) receptors in rat cochlear spiral ganglion neurons (SGNs). Forty-eight hours after primary culture of rat SGNs, immunofluorescence technique was applied to detect expressions of DR1 and DR2, the two subtypes of dopamine receptors. Western blot was performed to assess NMDA receptor NR1 subunit and GABA receptor subunit α2 (GABRα2) protein expressions in the SGNs after the treatments of SS alone or in combination with DR antagonists. The results demonstrated that: (1) The DR1 and DR2 were expressed in the bodies and axons of the SGN; (2) After the treatment with SS, the surface protein expressions of GABRα2 and NR1 were decreased by 44.69% and 21.57%, respectively, while the total protein expressions showed no significant changes; (3) Neither SS + SCH23390 (DR1 antagonist) group nor SS + Eticlopride (DR2 antagonist) group showed significant differences in GABRα2 and NR1 surface protein expressions compared with the control group. These results suggest that SS regulates the surface GABA and NMDA receptors trafficking on SGN, and the mechanism may involve DR mediation.
[Mh] Termos MeSH primário: Receptores Dopaminérgicos/metabolismo
Receptores de GABA-A/metabolismo
Receptores de N-Metil-D-Aspartato/metabolismo
Salicilato de Sódio/toxicidade
Gânglio Espiral da Cóclea/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Benzazepinas/farmacologia
Células Cultivadas
Cóclea/citologia
Neurônios/efeitos dos fármacos
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzazepines); 0 (Receptors, Dopamine); 0 (Receptors, GABA-A); 0 (Receptors, N-Methyl-D-Aspartate); 0 (SCH 23390); WIQ1H85SYP (Sodium Salicylate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE


  9 / 13481 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28546312
[Au] Autor:Jenni NL; Larkin JD; Floresco SB
[Ad] Endereço:Department of Psychology and Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, British Columbia V6T 1Z4, Canada.
[Ti] Título:Prefrontal Dopamine D and D Receptors Regulate Dissociable Aspects of Decision Making via Distinct Ventral Striatal and Amygdalar Circuits.
[So] Source:J Neurosci;37(26):6200-6213, 2017 Jun 28.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mesocortical dopamine (DA) regulates a variety of cognitive functions via actions on D and/or D receptors. For example, risk/reward decision making is modulated differentially by these two receptors within the prefrontal cortex (PFC), with D receptors enabling flexible decision making and D receptors promoting persistence in choice biases. However, it is unclear how DA mediates opposing patterns of behavior by acting on different receptors within the same terminal region. We explored the possibility that DA may act on separate networks of PFC neurons that are modulated by D or D receptors and in turn interface with divergent downstream structures such as the basolateral amygdala (BLA) or nucleus accumbens (NAc). Decision making was assessed using a probabilistic discounting task in which well trained male rats chose between small/certain or large/risky rewards, with the odds of obtaining the larger reward changing systematically within a session. Selective disruption of D or D modulation of separate PFC output pathways was achieved using unilateral intra-PFC infusions of DA antagonists combined with contralateral inactivation of the BLA or NAc. Disrupting D (but not D ) modulation of PFC→BLA circuitry impaired adjustments in decision biases in response to changes in reward probabilities. In contrast, disrupting D modulation of PFC→NAc networks reduced risky choice, attenuating reward sensitivity and increasing sensitivity to reward omissions. These findings reveal that mesocortical DA can facilitate dissociable components of reward seeking and action selection by acting on different functional networks of PFC neurons that can be distinguished by the subcortical projection targets with which they interface. Prefrontal cortical dopamine regulates a variety of executive functions governed by the frontal lobes via actions on D and D receptors. These receptors can in some instances mediate different patterns of behavior, but the mechanisms underlying these dissociable actions are unclear. Using a selective disconnection approach, we reveal that D and D receptors can facilitate diverse aspects of decision making by acting on separate networks of prefrontal neurons that interface with distinct striatal or amygdalar targets. These findings reveal an additional level of complexity in how mesocortical DA regulates different forms of cognition via actions on different receptors, highlighting how it may act upon distinct cortical microcircuits to drive different patterns of behavior.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/patologia
Tomada de Decisões/fisiologia
Córtex Pré-Frontal/fisiologia
Receptores Dopaminérgicos/metabolismo
Recompensa
Estriado Ventral/fisiologia
[Mh] Termos MeSH secundário: Animais
Função Executiva/fisiologia
Masculino
Rede Nervosa/fisiologia
Vias Neurais/fisiologia
Ratos
Ratos Long-Evans
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Dopamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170527
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0030-17.2017


  10 / 13481 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28474551
[Au] Autor:Chen W; Nong Z; Li Y; Huang J; Chen C; Huang L
[Ad] Endereço:Department of Emergency, the People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, Guangxi 530021, China.
[Ti] Título:Role of Dopamine Signaling in Drug Addiction.
[So] Source:Curr Top Med Chem;17(21):2440-2455, 2017.
[Is] ISSN:1873-4294
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Addiction is a chronic, relapsing disease of the brain that includes drug-induced compulsive seeking behavior and consumption of drugs. Dopamine (DA) is considered to be critical in drug addiction due to reward mechanisms in the midbrain. In this article, we review the major animal models in addictive drug experiments in vivo and in vitro. We discuss the relevance of the structure and pharmacological function of DA receptors. To improve the understanding of the role of DA receptors in reward pathways, specific brain regions, including the Ventral tegmental area, Nucleus accumbens, Prefrontal cortex, and Habenula, are highlighted. These factors contribute to the development of novel therapeutic targets that act at DA receptors. In addiction, the development of neuroimaging method will increase our understanding of the mechanisms underlying drug addiction.
[Mh] Termos MeSH primário: Comportamento Aditivo
Encéfalo/metabolismo
Dopamina/metabolismo
Receptores Dopaminérgicos/metabolismo
Transtornos Relacionados ao Uso de Substâncias/metabolismo
[Mh] Termos MeSH secundário: Animais
Agonistas de Dopamina/química
Agonistas de Dopamina/farmacologia
Antagonistas de Dopamina/química
Antagonistas de Dopamina/farmacologia
Recompensa
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Dopamine Agonists); 0 (Dopamine Antagonists); 0 (Receptors, Dopamine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170506
[St] Status:MEDLINE
[do] DOI:10.2174/1568026617666170504100642



página 1 de 1349 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde