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  1 / 2621 MEDLINE  
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[PMID]:28450542
[Au] Autor:Wright R; Newey SE; Ilie A; Wefelmeyer W; Raimondo JV; Ginham R; Mcllhinney RAJ; Akerman CJ
[Ad] Endereço:Department of Pharmacology and.
[Ti] Título:Neuronal Chloride Regulation via KCC2 Is Modulated through a GABA Receptor Protein Complex.
[So] Source:J Neurosci;37(22):5447-5462, 2017 May 31.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:GABA receptors are G-protein-coupled receptors that mediate inhibitory synaptic actions through a series of downstream target proteins. It is increasingly appreciated that the GABA receptor forms part of larger signaling complexes, which enable the receptor to mediate multiple different effects within neurons. Here we report that GABA receptors can physically associate with the potassium-chloride cotransporter protein, KCC2, which sets the driving force for the chloride-permeable ionotropic GABA receptor in mature neurons. Using biochemical, molecular, and functional studies in rodent hippocampus, we show that activation of GABA receptors results in a decrease in KCC2 function, which is associated with a reduction in the protein at the cell surface. These findings reveal a novel "crosstalk" between the GABA receptor systems, which can be recruited under conditions of high GABA release and which could be important for the regulation of inhibitory synaptic transmission. Synaptic inhibition in the brain is mediated by ionotropic GABA receptors (GABA Rs) and metabotropic GABA receptors (GABA Rs). To fully appreciate the function and regulation of these neurotransmitter receptors, we must understand their interactions with other proteins. We describe a novel association between the GABA R and the potassium-chloride cotransporter protein, KCC2. This association is significant because KCC2 sets the intracellular chloride concentration found in mature neurons and thereby establishes the driving force for the chloride-permeable GABA R. We demonstrate that GABA R activation can regulate KCC2 at the cell surface in a manner that alters intracellular chloride and the reversal potential for the GABA R. Our data therefore support an additional mechanism by which GABA Rs are able to modulate fast synaptic inhibition.
[Mh] Termos MeSH primário: Membrana Celular/metabolismo
Cloro/metabolismo
Ativação do Canal Iônico/fisiologia
Neurônios/metabolismo
Receptores de GABA-B/metabolismo
Simportadores/metabolismo
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Células Cultivadas
Cloro/química
Masculino
Ligação Proteica
Ratos
Ratos Sprague-Dawley
Receptor Cross-Talk/fisiologia
Receptores de GABA-B/química
Simportadores/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, GABA-B); 0 (Symporters); 0 (potassium-chloride symporters); 4R7X1O2820 (Chlorine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180125
[Lr] Data última revisão:
180125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2164-16.2017


  2 / 2621 MEDLINE  
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[PMID]:28878050
[Au] Autor:Escudero D; Guasp M; Ariño H; Gaig C; Martínez-Hernández E; Dalmau J; Graus F
[Ad] Endereço:From the Service of Neurology (D.E., M.G., C.G., J.D., F.G.), Hospital Clinic, University of Barcelona; Neuroimmunology Program (H.A., C.G., E.M.-H., J.D., F.G.), Institut d'Investigació Biomèdica August Pi i Sunyer; Institució Catalana de Recerca i Estudis Avançats (J.D.), Barcelona, Spain; and Dep
[Ti] Título:Antibody-associated CNS syndromes without signs of inflammation in the elderly.
[So] Source:Neurology;89(14):1471-1475, 2017 Oct 03.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To report the CNS syndromes of patients ≥60 years of age with antibodies against neuronal surface antigens but no evidence of brain MRI and CSF inflammatory changes. METHODS: This was a retrospective clinical analysis of patients with antibodies against neuronal surface antigens who fulfilled 3 criteria: age ≥60 years, no inflammatory abnormalities in brain MRI, and no CSF pleocytosis. Antibodies were determined with reported techniques. RESULTS: Among 155 patients ≥60 years of age with neurologic syndromes related to antibodies against neuronal surface antigens, 35 (22.6%) fulfilled the indicated criteria. The median age of these 35 patients was 68 years (range 60-88 years). Clinical manifestations included faciobrachial dystonic seizures (FBDS) in 11 of 35 (31.4%) patients, all with LGI1 antibodies; a combination of gait instability, brainstem dysfunction, and sleep disorder associated with IgLON5 antibodies in 10 (28.6%); acute confusion, memory loss, and behavioral changes suggesting autoimmune encephalitis (AE) in 9 (25.7%; 2 patients with AMPAR, 2 with NMDAR, 2 with GABAbR, 2 with LGI1, and 1 with CASPR2 antibodies); and rapidly progressive cognitive deterioration in 5 (14.3%; 3 patients with IgLON5 antibodies, 1 with chorea; 1 with DPPX antibody-associated cerebellar ataxia and arm rigidity; and 1 with CASPR2 antibodies). CONCLUSIONS: In patients ≥60 years of age, the correct identification of characteristic CNS syndromes (FBDS, anti-IgLON5 syndrome, AE) should prompt antibody testing even without evidence of inflammation in MRI and CSF studies. Up to 15% of the patients developed rapidly progressive cognitive deterioration, which further complicated the differential diagnosis with a neurodegenerative disorder.
[Mh] Termos MeSH primário: Anticorpos/metabolismo
Sistema Nervoso Central/imunologia
Sistema Nervoso Central/metabolismo
Doenças do Sistema Nervoso/imunologia
Doenças do Sistema Nervoso/patologia
[Mh] Termos MeSH secundário: Fatores Etários
Idoso
Idoso de 80 Anos ou mais
Envelhecimento
Moléculas de Adesão Celular Neuronais/imunologia
Feminino
Células HEK293
Seres Humanos
Inflamação
Masculino
Meia-Idade
Proteínas/imunologia
Receptores de GABA-B/imunologia
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Cell Adhesion Molecules, Neuronal); 0 (IgLON5 protein, human); 0 (LGI1 protein, human); 0 (Proteins); 0 (Receptors, GABA-B)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000004541


  3 / 2621 MEDLINE  
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[PMID]:28856709
[Au] Autor:Yoo Y; Jung J; Lee YN; Lee Y; Cho H; Na E; Hong J; Kim E; Lee JS; Lee JS; Hong C; Park SY; Wie J; Miller K; Shur N; Clow C; Ebel RS; DeBrosse SD; Henderson LB; Willaert R; Castaldi C; Tikhonova I; Bilgüvar K; Mane S; Kim KJ; Hwang YS; Lee SG; So I; Lim BC; Choi HJ; Seong JY; Shin YB; Jung H; Chae JH; Choi M
[Ad] Endereço:Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea.
[Ti] Título:GABBR2 mutations determine phenotype in rett syndrome and epileptic encephalopathy.
[So] Source:Ann Neurol;82(3):466-478, 2017 Sep.
[Is] ISSN:1531-8249
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Rett syndrome (RTT) and epileptic encephalopathy (EE) are devastating neurodevelopmental disorders with distinct diagnostic criteria. However, highly heterogeneous and overlapping clinical features often allocate patients into the boundary of the two conditions, complicating accurate diagnosis and appropriate medical interventions. Therefore, we investigated the specific molecular mechanism that allows an understanding of the pathogenesis and relationship of these two conditions. METHODS: We screened novel genetic factors from 34 RTT-like patients without MECP2 mutations, which account for ∼90% of RTT cases, by whole-exome sequencing. The biological function of the discovered variants was assessed in cell culture and Xenopus tropicalis models. RESULTS: We identified a recurring de novo variant in GABAB receptor R2 (GABBR2) that reduces the receptor function, whereas different GABBR2 variants in EE patients possess a more profound effect in reducing receptor activity and are more responsive to agonist rescue in an animal model. INTERPRETATION: GABBR2 is a genetic factor that determines RTT- or EE-like phenotype expression depending on the variant positions. GABBR2-mediated γ-aminobutyric acid signaling is a crucial factor in determining the severity and nature of neurodevelopmental phenotypes. Ann Neurol 2017;82:466-478.
[Mh] Termos MeSH primário: Mutação
Receptores de GABA-B/genética
Síndrome de Rett/genética
Espasmos Infantis/genética
[Mh] Termos MeSH secundário: Exoma
Genótipo
Células HEK293
Seres Humanos
Proteína 2 de Ligação a Metil-CpG/genética
Fenótipo
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABBR2 protein, human); 0 (MECP2 protein, human); 0 (Methyl-CpG-Binding Protein 2); 0 (Receptors, GABA-B)
[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:170901
[St] Status:MEDLINE
[do] DOI:10.1002/ana.25032


  4 / 2621 MEDLINE  
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[PMID]:28778447
[Au] Autor:André A; Félix A; Shamasna M; Nzwalo H; Basílio C
[Ad] Endereço:Neurology Department, Algarve Hospital Center, Portugal. Electronic address: alandre@chalgarve.min-saude.pt.
[Ti] Título:Neuroendocrine tumour metastatic brain disease during immunosuppressive treatment for paraneoplastic GABA receptor antibodies encephalitis: Is immunosuppression always beneficial?
[So] Source:J Neuroimmunol;310:66-68, 2017 Sep 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Limbic autoimmune encephalitis (LE) should be considered in any patient with acute or subacute neuropsychiatric manifestations, without other common causes of encephalitis. Y-Aminobutyric-acid-B-receptor (anti-GABA R) antibodies are rarely encountered in association with LE. CASE REPORT: A 74-year-old patient presented with a progressive cognitive degradation and generalized tonic-clonic seizures, with positive anti-GABA R. He declined under immunosuppression treatment. Control magnetic resonance revealed brain lesions, which became positive for pulmonary neuroendocrine tumour metastatic disease. CONCLUSION: The occurrence of diversified neurological manifestations of an underling tumour is difficult to manage. We speculate if in some cases, immunosuppression can itself facilitate tumour progression.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Imunossupressores/uso terapêutico
Encefalite Límbica
Neoplasias Pulmonares/patologia
Receptores de GABA-B/imunologia
[Mh] Termos MeSH secundário: Adenocarcinoma/patologia
Adenocarcinoma/cirurgia
Idoso
Encéfalo/diagnóstico por imagem
Encéfalo/patologia
Neoplasias Encefálicas/patologia
Neoplasias Encefálicas/cirurgia
Transtornos Cognitivos/etiologia
Epilepsia Tônico-Clônica/diagnóstico por imagem
Epilepsia Tônico-Clônica/etiologia
Seres Humanos
Encefalite Límbica/diagnóstico por imagem
Encefalite Límbica/etiologia
Encefalite Límbica/patologia
Sistema Límbico/diagnóstico por imagem
Imagem por Ressonância Magnética
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Immunosuppressive Agents); 0 (Receptors, GABA-B)
[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:170806
[St] Status:MEDLINE


  5 / 2621 MEDLINE  
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[PMID]:28724189
[Au] Autor:Kahanovitch U; Berlin S; Dascal N
[Ad] Endereço:Department of Physiology and Pharmacology, Sackler School of Medicine, Tel Aviv University, Israel.
[Ti] Título:Collision coupling in the GABA receptor-G protein-GIRK signaling cascade.
[So] Source:FEBS Lett;591(18):2816-2825, 2017 Sep.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The signaling cascade comprising the 4-aminobutyrate(B) receptor (GABA R), G protein and the G protein-gated K channel (GIRK) mediates neuronal inhibition in the brain. Precoupling between components of the pathway (within a permanent macromolecular complex) has been proposed, but this remains debatable. We investigated this mechanism in Xenopus oocytes by varying the expression of the GABA R. Increased expression of GABA R accelerates activation of GIRK by agonist, implying that some of the components in this cascade interact by a classical collision mechanism. We also find that GABA R has a bidirectional effect on the basal activity of the GIRK channel. Our results suggest a complex mechanism of coupling between GABA R and GIRK which involves elements of both precoupling and collision coupling.
[Mh] Termos MeSH primário: Canais de Potássio Corretores do Fluxo de Internalização Acoplados a Proteínas G/metabolismo
Proteínas de Ligação ao GTP/metabolismo
Receptores de GABA-B/metabolismo
[Mh] Termos MeSH secundário: Animais
Anuros
Eletrofisiologia
Feminino
Imunoquímica
Oócitos
Transdução de Sinais/efeitos dos fármacos
Xenopus
Ácido gama-Aminobutírico/farmacologia
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (G Protein-Coupled Inwardly-Rectifying Potassium Channels); 0 (Receptors, GABA-B); 56-12-2 (gamma-Aminobutyric Acid); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12756


  6 / 2621 MEDLINE  
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[PMID]:28662175
[Au] Autor:Cai S; Fischer QS; He Y; Zhang L; Liu H; Daw NW; Yang Y
[Ad] Endereço:CAS Key Laboratory of Brain Function and Diseases, School of Life Sciences, University of Science and Technology of China, Hefei, China.
[Ti] Título:GABAB receptor-dependent bidirectional regulation of critical period ocular dominance plasticity in cats.
[So] Source:PLoS One;12(6):e0180162, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gama amino butyric acid (GABA) inhibition plays an important role in the onset and offset of the critical period for ocular dominance (OD) plasticity in the primary visual cortex. Previous studies have focused on the involvement of GABAA receptors, while the potential contribution of GABAB receptors to OD plasticity has been neglected. In this study, the GABAB receptor antagonist SCH50911 or agonist baclofen was infused into the primary visual cortex of cats concurrently with a period of monocular deprivation (MD). Using single-unit recordings we found that the OD shift induced by four days of MD during the critical period was impaired by infusion of the antagonist SCH50911, but enhanced by infusion of the agonist baclofen. In contrast, seven days of MD in adult cats did not induce any significant OD shift, even when combined with the infusion of SCH50911 or baclofen. Together, these findings indicate that an endogenous GABAB receptor-mediated inhibition contributes to juvenile, but not adult, OD plasticity.
[Mh] Termos MeSH primário: Dominância Ocular/fisiologia
Plasticidade Neuronal/fisiologia
Receptores de GABA-B/fisiologia
[Mh] Termos MeSH secundário: Animais
Baclofeno/farmacologia
Gatos
Feminino
Agonistas dos Receptores de GABA-B/farmacologia
Antagonistas de Receptores de GABA-B
Masculino
Morfolinas/farmacologia
Receptores de GABA-B/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((+)-(S)-5,5-dimethylmorpholinyl-2-acetic acid); 0 (GABA-B Receptor Agonists); 0 (GABA-B Receptor Antagonists); 0 (Morpholines); 0 (Receptors, GABA-B); H789N3FKE8 (Baclofen)
[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:170630
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180162


  7 / 2621 MEDLINE  
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[PMID]:28424220
[Au] Autor:Xia S; He C; Zhu Y; Wang S; Li H; Zhang Z; Jiang X; Liu J
[Ad] Endereço:Cell Signaling Laboratory, College of Life Science and Technology, Collaborative Innovation Center for Genetics and Development, and Key Laboratory of Molecular Biophysics of Ministry of Education, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.
[Ti] Título:GABA R-Induced EGFR Transactivation Promotes Migration of Human Prostate Cancer Cells.
[So] Source:Mol Pharmacol;92(3):265-277, 2017 Sep.
[Is] ISSN:1521-0111
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:G protein-coupled receptors (GPCRs) and receptor tyrosine kinases (RTKs) act in concert to regulate cell growth, proliferation, survival, and migration. Metabotropic GABA receptor (GABA R) is the GPCR for the main inhibitory neurotransmitter GABA in the central nervous system. Increased expression of GABA R has been detected in human cancer tissues and cancer cell lines, but the role of GABA R in these cells is controversial and the underlying mechanism remains poorly understood. Here, we investigated whether GABA R hijacks RTK signaling to modulate the fates of human prostate cancer cells. RTK array analysis revealed that the GABA R-specific agonist baclofen selectively induced the transactivation of EGFR in PC-3 cells. EGFR transactivation resulted in the activation of ERK1/2 by a mechanism that is dependent on G protein and that requires matrix metalloproteinase-mediated proligand shedding. Positive allosteric modulators (PAMs) of GABA R, such as CGP7930, rac-BHFF, and GS39783, can function as PAM agonists to induce EGFR transactivation and subsequent ERK1/2 activation. Moreover, both baclofen and CGP7930 promoted cell migration and invasion through EGFR signaling. In summary, our observations demonstrated that GABA R transactivated EGFR in a ligand-dependent mechanism to promote prostate cancer cell migration and invasion, thus providing new insights into developing a novel strategy for prostate cancer treatment by targeting neurotransmitter signaling.
[Mh] Termos MeSH primário: Neoplasias da Próstata/patologia
Receptor do Fator de Crescimento Epidérmico/genética
Ativação Transcricional
[Mh] Termos MeSH secundário: Regulação Alostérica
Linhagem Celular Tumoral
Movimento Celular
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Subunidades alfa Gi-Go de Proteínas de Ligação ao GTP/fisiologia
Seres Humanos
Masculino
Invasividade Neoplásica
Receptores de GABA-B/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, GABA-B); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.6.5.1 (GTP-Binding Protein alpha Subunits, Gi-Go)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.1124/mol.116.107854


  8 / 2621 MEDLINE  
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[PMID]:28323850
[Au] Autor:Freyd T; Warszycki D; Mordalski S; Bojarski AJ; Sylte I; Gabrielsen M
[Ad] Endereço:Department of Medical Biology, Faculty of Health Sciences, UiT - the Arctic University of Norway, Tromsø, Norway.
[Ti] Título:Ligand-guided homology modelling of the GABAB2 subunit of the GABAB receptor.
[So] Source:PLoS One;12(3):e0173889, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:γ-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the central nervous system, and disturbances in the GABAergic system have been implicated in numerous neurological and neuropsychiatric diseases. The GABAB receptor is a heterodimeric class C G protein-coupled receptor (GPCR) consisting of GABAB1a/b and GABAB2 subunits. Two GABAB receptor ligand binding sites have been described, namely the orthosteric GABA binding site located in the extracellular GABAB1 Venus fly trap domain and the allosteric binding site found in the GABAB2 transmembrane domain. To date, the only experimentally solved three-dimensional structures of the GABAB receptor are of the Venus fly trap domain. GABAB receptor allosteric modulators, however, show great therapeutic potential, and elucidating the structure of the GABAB2 transmembrane domain may lead to development of novel drugs and increased understanding of the allosteric mechanism of action. Despite the lack of x-ray crystal structures of the GABAB2 transmembrane domain, multiple crystal structures belonging to other classes of GPCRs than class A have been released within the last years. More closely related template structures are now available for homology modelling of the GABAB receptor. Here, multiple homology models of the GABAB2 subunit of the GABAB receptor have been constructed using templates from class A, B and C GPCRs, and docking of five clusters of positive allosteric modulators and decoys has been undertaken to select models that enrich the active compounds. Using this ligand-guided approach, eight GABAB2 homology models have been chosen as possible structural representatives of the transmembrane domain of the GABAB2 subunit. To the best of our knowledge, the present study is the first to describe homology modelling of the transmembrane domain of the GABAB2 subunit and the docking of positive allosteric modulators in the receptor.
[Mh] Termos MeSH primário: Receptores de GABA-B/química
[Mh] Termos MeSH secundário: Sítio Alostérico
Seres Humanos
Ligantes
Modelos Moleculares
Domínios Proteicos
Subunidades Proteicas
Homologia Estrutural de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABBR2 protein, human); 0 (Ligands); 0 (Protein Subunits); 0 (Receptors, GABA-B)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0173889


  9 / 2621 MEDLINE  
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[PMID]:28322793
[Au] Autor:Kondo Y; Yada Y; Haga T; Takayama Y; Isomura T; Jimbo Y; Fukayama O; Hoshino T; Mabuchi K
[Ad] Endereço:Department of Information Physics and Computing, The University of Tokyo, Tokyo 113-8656, Japan.
[Ti] Título:Temporal relation between neural activity and neurite pruning on a numerical model and a microchannel device with micro electrode array.
[So] Source:Biochem Biophys Res Commun;486(2):539-544, 2017 Apr 29.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Synapse elimination and neurite pruning are essential processes for the formation of neuronal circuits. These regressive events depend on neural activity and occur in the early postnatal days known as the critical period, but what makes this temporal specificity is not well understood. One possibility is that the neural activities during the developmentally regulated shift of action of GABA inhibitory transmission lead to the critical period. Moreover, it has been reported that the shifting action of the inhibitory transmission on immature neurons overlaps with synapse elimination and neurite pruning and that increased inhibitory transmission by drug treatment could induce temporal shift of the critical period. However, the relationship among these phenomena remains unclear because it is difficult to experimentally show how the developmental shift of inhibitory transmission influences neural activities and whether the activities promote synapse elimination and neurite pruning. In this study, we modeled synapse elimination in neuronal circuits using the modified Izhikevich's model with functional shifting of GABAergic transmission. The simulation results show that synaptic pruning within a specified period like the critical period is spontaneously generated as a function of the developmentally shifting inhibitory transmission and that the specific firing rate and increasing synchronization of neural circuits are seen at the initial stage of the critical period. This temporal relationship was experimentally supported by an in vitro primary culture of rat cortical neurons in a microchannel on a multi-electrode array (MEA). The firing rate decreased remarkably between the 18-25 days in vitro (DIV), and following these changes in the firing rate, the neurite density was slightly reduced. Our simulation and experimental results suggest that decreasing neural activity due to developing inhibitory synaptic transmission could induce synapse elimination and neurite pruning at particular time such as the critical period. Additionally, these findings indicate that we can estimate the maturity level of inhibitory transmission and the critical period by measuring the firing rate and the degree of synchronization in engineered neural networks.
[Mh] Termos MeSH primário: Potenciais de Ação/fisiologia
Modelos Neurológicos
Rede Nervosa/fisiologia
Plasticidade Neuronal/fisiologia
Transmissão Sináptica/fisiologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Axônios/fisiologia
Córtex Cerebral/citologia
Córtex Cerebral/fisiologia
Cérebro/citologia
Cérebro/fisiologia
Simulação por Computador
Microeletrodos
Neuritos/fisiologia
Cultura Primária de Células
Ratos
Receptores de GABA-A/fisiologia
Receptores de GABA-B/fisiologia
Sinapses/fisiologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, GABA-A); 0 (Receptors, GABA-B)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE


  10 / 2621 MEDLINE  
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[PMID]:28275709
[Au] Autor:Hamel L; Thangarasa T; Samadi O; Ito R
[Ad] Endereço:Department of Psychology (Scarborough), University of Toronto , 1265 Military Trail , Toronto, Ontario M1C 1A4, Canada.
[Ti] Título:Caudal Nucleus Accumbens Core Is Critical in the Regulation of Cue-Elicited Approach-Avoidance Decisions.
[So] Source:eNeuro;4(1), 2017 Jan-Feb.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The nucleus accumbens (NAc) is thought to be a site of integration of positively and negatively valenced information and action selection. Functional differentiation in valence processing has previously been found along the rostrocaudal axis of the shell region of the NAc in assessments of unconditioned motivation. Given that the core region of the NAc has been implicated in the elicitation of motivated behavior in response to conditioned cues, we sought to assess the role of caudal, intermediate, and rostral sites within this subregion in cue-elicited approach-avoidance decisions. Rats were trained to associate visuo-tactile cues with appetitive, aversive, and neutral outcomes. Following the successful acquisition of the cue-outcome associations, rats received microinfusions of GABA and GABA receptor agonists (muscimol/baclofen) or saline into the caudal, intermediate, or rostral NAc core and were then exposed to a superimposition of appetitively and aversively valenced cues versus neutral cues in a "conflict test," as well as to the appetitive versus neutral cues, and aversive cues versus neutral cues, in separate conditioned preference/avoidance tests. Disruption of activity in the intermediate to caudal parts of the NAc core resulted in a robust avoidance bias in response to motivationally conflicting cues, as well as a potentiated avoidance of aversive cues as compared with control animals, coupled with an attenuated conditioned preference for the appetitive cue. These results suggest that the caudal NAc core may have the capacity to exert bidirectional control over appetitively and aversively motivated responses to valence signals.
[Mh] Termos MeSH primário: Aprendizagem da Esquiva/fisiologia
Comportamento de Escolha/fisiologia
Sinais (Psicologia)
Núcleo Accumbens/fisiologia
[Mh] Termos MeSH secundário: Animais
Aprendizagem por Associação/efeitos dos fármacos
Aprendizagem por Associação/fisiologia
Aprendizagem da Esquiva/efeitos dos fármacos
Baclofeno/farmacologia
Comportamento de Escolha/efeitos dos fármacos
Condicionamento (Psicologia)/efeitos dos fármacos
Condicionamento (Psicologia)/fisiologia
Conflito (Psicologia)
Agonistas GABAérgicos/farmacologia
Masculino
Motivação/efeitos dos fármacos
Motivação/fisiologia
Muscimol/farmacologia
Núcleo Accumbens/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-fos/metabolismo
Ratos Long-Evans
Receptores de GABA-A/metabolismo
Receptores de GABA-B/metabolismo
Percepção do Tato/efeitos dos fármacos
Percepção do Tato/fisiologia
Percepção Visual/efeitos dos fármacos
Percepção Visual/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA Agonists); 0 (Proto-Oncogene Proteins c-fos); 0 (Receptors, GABA-A); 0 (Receptors, GABA-B); 2763-96-4 (Muscimol); H789N3FKE8 (Baclofen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE



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