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Pesquisa : D12.776.157.530.450.162.887.750 [Categoria DeCS]
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[PMID]:28300552
[Au] Autor:Hirono M; Nagao S; Yanagawa Y; Konishi S
[Ad] Endereço:Organization for Research Initiatives and Development, Doshisha University, Kyoto 610-0394, Japan; Laboratory for Motor Learning Control, RIKEN BSI, Wako 351-0198, Japan. Electronic address: mhirono@mail.doshisha.ac.jp.
[Ti] Título:Monoaminergic modulation of GABAergic transmission onto cerebellar globular cells.
[So] Source:Neuropharmacology;118:79-89, 2017 May 15.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cerebellar Purkinje cells (PCs) project their axon collaterals to underneath of the PC layer and make GABAergic synaptic contacts with globular cells, a subgroup of Lugaro cells. GABAergic transmission derived from the PC axon collaterals is so powerful that it could inhibit globular cells and regulate their firing patterns. However, the physiological properties and implications of the GABAergic synapses on globular cells remain unknown. Using whole-cell patch-clamp recordings from globular cells in the mouse cerebellum, we examined the monoaminergic modulation of GABAergic inputs to these cells. Application of either serotonin (5-HT) or noradrenaline (NA) excited globular cells, thereby leading to their firing. The 5-HT- and NA-induced firing was temporally confined and attenuated by GABAergic transmission, although 5-HT and NA exerted an inhibitory effect on the release of GABA from presynaptic terminals of PC axon collaterals. Agonists for 5-HT receptors and α -adrenoceptors mimicked the 5-HT- and NA-induced suppression of GABAergic activity. Through their differential modulatory actions on the cerebellar inhibitory neural circuits, 5-HT facilitated PC firing, whereas NA suppressed it. These results indicate that 5-HT and NA regulate the membrane excitability of globular cells and PCs through their differential modulation of not only the membrane potential but also GABAergic synaptic circuits. Monoaminergic modulation of the neural connections between globular cells and PCs could play a role in cerebellar motor coordination.
[Mh] Termos MeSH primário: Monoaminas Biogênicas/farmacologia
Cerebelo/citologia
Neurônios GABAérgicos/fisiologia
Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos
Transmissão Sináptica/efeitos dos fármacos
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Animais Recém-Nascidos
Proteínas de Bactérias/genética
Proteínas de Bactérias/metabolismo
Fármacos atuantes sobre Aminoácidos Excitatórios/farmacologia
GABAérgicos/farmacologia
Glutamato Descarboxilase/genética
Glutamato Descarboxilase/metabolismo
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Modelos Biológicos
Norepinefrina/farmacologia
Serotonina/farmacologia
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/genética
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Biogenic Monoamines); 0 (Excitatory Amino Acid Agents); 0 (GABA Agents); 0 (Luminescent Proteins); 0 (Sodium Channel Blockers); 0 (Vesicular Inhibitory Amino Acid Transport Proteins); 0 (Viaat protein, mouse); 0 (yellow fluorescent protein, Bacteria); 333DO1RDJY (Serotonin); 4368-28-9 (Tetrodotoxin); EC 4.1.1.15 (Glutamate Decarboxylase); EC 4.1.1.15 (glutamate decarboxylase 1); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170317
[St] Status:MEDLINE


  2 / 375 MEDLINE  
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[PMID]:28192394
[Au] Autor:Shi X; Barchini J; Ledesma HA; Koren D; Jin Y; Liu X; Wei W; Cang J
[Ad] Endereço:Department of Neurobiology, Northwestern University, Evanston, Illinois, USA.
[Ti] Título:Retinal origin of direction selectivity in the superior colliculus.
[So] Source:Nat Neurosci;20(4):550-558, 2017 Apr.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Detecting visual features in the environment, such as motion direction, is crucial for survival. The circuit mechanisms that give rise to direction selectivity in a major visual center, the superior colliculus (SC), are entirely unknown. We optogenetically isolate the retinal inputs that individual direction-selective SC neurons receive and find that they are already selective as a result of precisely converging inputs from similarly tuned retinal ganglion cells. The direction-selective retinal input is linearly amplified by intracollicular circuits without changing its preferred direction or level of selectivity. Finally, using two-photon calcium imaging, we show that SC direction selectivity is dramatically reduced in transgenic mice that have decreased retinal selectivity. Together, our studies demonstrate a retinal origin of direction selectivity in the SC and reveal a central visual deficit as a consequence of altered feature selectivity in the retina.
[Mh] Termos MeSH primário: Percepção de Movimento/fisiologia
Retina/fisiologia
Colículos Superiores/fisiologia
[Mh] Termos MeSH secundário: Animais
Potenciais Pós-Sinápticos Excitadores/fisiologia
Feminino
Glutamato Descarboxilase/genética
Masculino
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Neurônios/fisiologia
Estimulação Luminosa
Células Ganglionares da Retina/fisiologia
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/genética
Vias Visuais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Vesicular Inhibitory Amino Acid Transport Proteins); 0 (Viaat protein, mouse); EC 4.1.1.15 (Glutamate Decarboxylase); EC 4.1.1.15 (glutamate decarboxylase 2)
[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:170214
[St] Status:MEDLINE
[do] DOI:10.1038/nn.4498


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[PMID]:28157737
[Au] Autor:Aresh B; Freitag FB; Perry S; Blümel E; Lau J; Franck MCM; Lagerström MC
[Ad] Endereço:Departments of aNeuroscience and bMedical Cell Biology, Uppsala University, Uppsala, Sweden.
[Ti] Título:Spinal cord interneurons expressing the gastrin-releasing peptide receptor convey itch through VGLUT2-mediated signaling.
[So] Source:Pain;158(5):945-961, 2017 May.
[Is] ISSN:1872-6623
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Itch is a sensation that promotes the desire to scratch, which can be evoked by mechanical and chemical stimuli. In the spinal cord, neurons expressing the gastrin-releasing peptide receptor (GRPR) have been identified as specific mediators of itch. However, our understanding of the GRPR population in the spinal cord, and thus how these neurons exercise their functions, is limited. For this purpose, we constructed a Cre line designed to target the GRPR population of neurons (Grpr-Cre). Our analysis revealed that Grpr-Cre cells in the spinal cord are predominantly excitatory interneurons that are found in the dorsal lamina, especially in laminae II-IV. Application of the specific agonist gastrin-releasing peptide induced spike responses in 43.3% of the patched Grpr-Cre neurons, where the majority of the cells displayed a tonic firing property. Additionally, our analysis showed that the Grpr-Cre population expresses Vglut2 mRNA, and mice ablated of Vglut2 in Grpr-Cre cells (Vglut2-lox;Grpr-Cre mice) displayed less spontaneous itch and attenuated responses to both histaminergic and nonhistaminergic agents. We could also show that application of the itch-inducing peptide, natriuretic polypeptide B, induces calcium influx in a subpopulation of Grpr-Cre neurons. To summarize, our data indicate that the Grpr-Cre spinal cord neural population is composed of interneurons that use VGLUT2-mediated signaling for transmitting chemical and spontaneous itch stimuli to the next, currently unknown, neurons in the labeled line of itch.
[Mh] Termos MeSH primário: Interneurônios/metabolismo
Prurido/patologia
Receptores da Bombesina/metabolismo
Transdução de Sinais/fisiologia
Medula Espinal/citologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Cálcio/metabolismo
Feminino
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Masculino
Potenciais da Membrana/efeitos dos fármacos
Potenciais da Membrana/genética
Camundongos
Camundongos Transgênicos
Medição da Dor
Prurido/induzido quimicamente
Prurido/diagnóstico por imagem
Prurido/genética
Índice de Gravidade de Doença
Transdução de Sinais/efeitos dos fármacos
Proteína Vesicular 2 de Transporte de Glutamato/genética
Proteína Vesicular 2 de Transporte de Glutamato/metabolismo
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/genética
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Bombesin); 0 (Slc17a6 protein, mouse); 0 (Vesicular Glutamate Transport Protein 2); 0 (Vesicular Inhibitory Amino Acid Transport Proteins); 0 (Viaat protein, mouse); 0 (enhanced green fluorescent protein); 147336-22-9 (Green Fluorescent Proteins); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.1097/j.pain.0000000000000861


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[PMID]:28077261
[Au] Autor:Chen MC; Vetrivelan R; Guo CN; Chang C; Fuller PM; Lu J
[Ad] Endereço:Beth Israel Deaconess Medical Center and Harvard Medical School, Department of Neurology, Division of Sleep Medicine, Boston, MA 02115, USA.
[Ti] Título:Ventral medullary control of rapid eye movement sleep and atonia.
[So] Source:Exp Neurol;290:53-62, 2017 Apr.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Discrete populations of neurons at multiple levels of the brainstem control rapid eye movement (REM) sleep and the accompanying loss of postural muscle tone, or atonia. The specific contributions of these brainstem cell populations to REM sleep control remains incompletely understood. Here we show in rats that viral vector-based lesions of the ventromedial medulla at a level rostral to the inferior olive (pSOM) produced violent myoclonic twitches and abnormal electromyographic spikes, but not complete loss of tonic atonia, during REM sleep. Motor tone during non-REM (NREM) sleep was unaffected in these same animals. Acute chemogenetic activation of pSOM neurons in rats robustly and selectively suppressed REM sleep but not NREM sleep. Similar lesions targeting the more rostral ventromedial medulla (RVM) did not affect sleep or atonia, while chemogenetic stimulation of the RVM produced wakefulness and reduced sleep. Finally, selective activation of vesicular GABA transporter (VGAT) pSOM neurons in mice produced complete suppression of REM sleep whereas their loss increased EMG spikes during REM sleep. These results reveal a key contribution of the pSOM and specifically the VGAT+ neurons in this region in REM sleep and motor control.
[Mh] Termos MeSH primário: Bulbo/fisiologia
Sono REM/fisiologia
[Mh] Termos MeSH secundário: Adenoviridae/genética
Animais
Eletroencefalografia
Eletromiografia
Imuno-Histoquímica
Masculino
Camundongos
Mioclonia/fisiopatologia
Neurônios/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/genética
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/metabolismo
Vigília/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Vesicular Inhibitory Amino Acid Transport Proteins); 0 (Viaat protein, mouse)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170113
[St] Status:MEDLINE


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[PMID]:27956032
[Au] Autor:Fogarty MJ; Kanjhan R; Yanagawa Y; Noakes PG; Bellingham MC
[Ad] Endereço:School of Biomedical Sciences, The University of Queensland, St Lucia, QLD 4072, Australia.
[Ti] Título:Alterations in hypoglossal motor neurons due to GAD67 and VGAT deficiency in mice.
[So] Source:Exp Neurol;289:117-127, 2017 Mar.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There is an emerging body of evidence that glycinergic and GABAergic synaptic inputs onto motor neurons (MNs) help regulate the final number of MNs and axonal muscle innervation patterns. Using mutant glutamate decarboxylase 67 (GAD67) and vesicular inhibitory amino acid transporter (VGAT) deficient mice, we describe the effect that deficiencies of presynaptic GABAergic and/or glycinergic release have on the post-synaptic somato-dendritic structure of motor neurons, and the development of excitatory and inhibitory synaptic inputs to MNs. We use whole-cell patch clamp recording of synaptic currents in E18.5 hypoglossal MNs from brainstem slices, combined with dye-filling of these recorded cells with Neurobiotin™, high-resolution confocal imaging and 3-dimensional reconstructions. Hypoglossal MNs from GAD67- and VGAT-deficient mice display decreased inhibitory neurotransmission and increased excitatory synaptic inputs. These changes are associated with increased dendritic arbor length, increased complexity of dendritic branching, and increased density of spiny processes. Our results show that presynaptic release of inhibitory amino acid neurotransmitters are potent regulators of hypoglossal MN morphology and key regulators of synaptic inputs during this critical developmental time point.
[Mh] Termos MeSH primário: Tronco Encefálico/citologia
Glutamato Descarboxilase/deficiência
Neurônios Motores/fisiologia
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/deficiência
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Biotina/análogos & derivados
Biotina/farmacocinética
Espinhas Dendríticas/genética
Estimulação Elétrica
Eletroporação
Embrião de Mamíferos
Feminino
Glutamato Descarboxilase/genética
Técnicas In Vitro
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Plasticidade Neuronal/genética
Técnicas de Patch-Clamp
Gravidez
Potenciais Sinápticos/genética
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/genética
Ácido gama-Aminobutírico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Vesicular Inhibitory Amino Acid Transport Proteins); 0 (Viaat protein, mouse); 0 (neurobiotin); 56-12-2 (gamma-Aminobutyric Acid); 6SO6U10H04 (Biotin); EC 4.1.1.15 (Glutamate Decarboxylase); EC 4.1.1.15 (glutamate decarboxylase 1)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161214
[St] Status:MEDLINE


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[PMID]:27923637
[Au] Autor:Lee EY; Hwang YG; Lee HS
[Ad] Endereço:Department of Anatomy, School of Medicine, Konkuk University, 05029 Seoul, Republic of Korea.
[Ti] Título:Hypothalamic neuronal origin of neuropeptide Y (NPY) or cocaine- and amphetamine-regulated transcript (CART) fibers projecting to the tuberomammillary nucleus of the rat.
[So] Source:Brain Res;1657:16-28, 2017 Feb 15.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Based on the importance of tuberomammillary nucleus (TMN) as a target for feeding/arousal-related functions, we aimed in the present study to investigate hypothalamic neuronal origin of neuropeptide Y (NPY) and cocaine- and amphetamine-regulated transcript (CART) fibers projecting to the histaminergic nucleus. In the first series of experiments, we examined NPY (or CART) fiber distribution within the boundary of adenosine deaminase (ADA)-immunoreactive (ir) TMN regions; extensive NPY (or CART)-ir axon terminals were observed in E4 (TMMd), E3 (TMMv), and E2 (TMVr) subdivisions. NPY varicosities co-contained vesicular GABA transporters (vGAT). CART boutons, however, contained either vGAT or vesicular glutamate transporters (vGLU), which suggested dual (or multiple) origins of CART fibers. Based on the previous observation on melanin-concentrating hormone (MCH)-ir neuronal elements in the TMN, their coexistence with CART peptide was examined in detail. In E subdivision, approximately 40.8% of MCH-ir somata co-contained CART, but the proportion was reduced to 24.1% in E region. In E and E (TMVc) regions, only MCH-ir axon terminals existed without any MCH-ir somata. In the second series of experiments, we investigated hypothalamic neuronal origin of NPY (or CART) fibers projecting to the TMN. The arcuate nucleus (Arc) was the sole source of hypothalamic NPY fibers projecting to the nucleus. In contrast, CART fibers in the TMN originated from the Arc as well as the other hypothalamic nuclei including the retrochiasmatic nucleus, paraventricular nucleus, lateral hypothalamus (LH), zona incerta (ZI), and dorsal hypothalamic area. Quantitative analysis showed that arcuate CART projection to the TMN occupied approximately 23.5% of the total hypothalamic CART input to the nucleus, while the rest originated mainly from the LH and ZI. The present observations suggested that the TMN might play a key role in energy balance and arousal, by receiving periphery-derived, first-order NPY (or CART) inputs from the Arc as well as second-order (and downstream) CART inputs from the other hypothalamic nuclei.
[Mh] Termos MeSH primário: Hipotálamo/citologia
Hipotálamo/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Neurônios/citologia
Neurônios/metabolismo
Neuropeptídeo Y/metabolismo
[Mh] Termos MeSH secundário: Adenosina Desaminase/metabolismo
Animais
Contagem de Células
Imunofluorescência
Hormônios Hipotalâmicos/metabolismo
Masculino
Melaninas/metabolismo
Microscopia Confocal
Vias Neurais/citologia
Vias Neurais/metabolismo
Técnicas de Rastreamento Neuroanatômico
Hormônios Hipofisários/metabolismo
Ratos Sprague-Dawley
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hypothalamic Hormones); 0 (Melanins); 0 (Nerve Tissue Proteins); 0 (Neuropeptide Y); 0 (Pituitary Hormones); 0 (Vesicular Inhibitory Amino Acid Transport Proteins); 0 (Viaat protein, rat); 0 (cocaine- and amphetamine-regulated transcript protein); 67382-96-1 (melanin-concentrating hormone); EC 3.5.4.4 (Adenosine Deaminase)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161208
[St] Status:MEDLINE


  7 / 375 MEDLINE  
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[PMID]:27866231
[Au] Autor:Ramos-Miguel A; Sawada K; Jones AA; Thornton AE; Barr AM; Leurgans SE; Schneider JA; Bennett DA; Honer WG
[Ad] Endereço:BC Mental Health and Addictions Research Institute, 938 West 28th Avenue, Vancouver, BC, V5Z 4H4, Canada.
[Ti] Título:Presynaptic proteins complexin-I and complexin-II differentially influence cognitive function in early and late stages of Alzheimer's disease.
[So] Source:Acta Neuropathol;133(3):395-407, 2017 Mar.
[Is] ISSN:1432-0533
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Progressive accumulation of Alzheimer's disease-related pathology is associated with cognitive dysfunction. Differences in cognitive reserve may contribute to individual differences in cognitive function in the presence of comparable neuropathology. The protective effects of cognitive reserve could contribute differentially in early versus late stages of the disease. We investigated presynaptic proteins as measures of brain reserve (a subset of total cognitive reserve), and used Braak staging to estimate the progression of Alzheimer's disease. Antemortem evaluations of cognitive function, postmortem assessments of pathologic indices, and presynaptic protein analyses, including the complexins I and II as respective measures of inhibitory and excitatory terminal function, were assayed in multiple key brain regions in 418 deceased participants from a community study. After covarying for demographic variables, pathologic indices, and overall synapse density, lower brain complexin-I and -II levels contributed to cognitive dysfunction (P < 0.01). Each complexin appeared to be dysregulated at a different Braak stage. Inhibitory complexin-I explained 14.4% of the variance in global cognition in Braak 0-II, while excitatory complexin-II explained 7.3% of the variance in Braak V-VI. Unlike other presynaptic proteins, complexins did not colocalize with pathologic tau within neuritic plaques, suggesting that these functional components of the synaptic machinery are cleared early from dystrophic neurites. Moreover, complexin levels showed distinct patterns of change related to memory challenges in a rat model, supporting the functional specificity of these proteins. The present results suggest that disruption of inhibitory synaptic terminals may trigger early cognitive impairment, while excitatory terminal disruption may contribute relatively more to later cognitive impairment.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transporte Vesicular/metabolismo
Doença de Alzheimer/complicações
Encéfalo/metabolismo
Transtornos Cognitivos/etiologia
Transtornos Cognitivos/patologia
Proteínas do Tecido Nervoso/metabolismo
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Envelhecimento/patologia
Animais
Autopsia
Encéfalo/patologia
Transtornos Cognitivos/metabolismo
Progressão da Doença
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Masculino
Aprendizagem em Labirinto
Terminações Pré-Sinápticas/metabolismo
Ratos
Ratos Long-Evans
Distribuição Espacial da População
Proteína Vesicular 1 de Transporte de Glutamato/metabolismo
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Vesicular Transport); 0 (Nerve Tissue Proteins); 0 (SLC17A7 protein, human); 0 (SLC32A1 protein, human); 0 (Vesicular Glutamate Transport Protein 1); 0 (Vesicular Inhibitory Amino Acid Transport Proteins); 0 (complexin I); 0 (complexin II)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161121
[St] Status:MEDLINE
[do] DOI:10.1007/s00401-016-1647-9


  8 / 375 MEDLINE  
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[PMID]:27587266
[Au] Autor:Papale A; d'Isa R; Menna E; Cerovic M; Solari N; Hardingham N; Cambiaghi M; Cursi M; Barbacid M; Leocani L; Fasano S; Matteoli M; Brambilla R
[Ad] Endereço:Neuroscience and Mental Health Research Institute, Division of Neuroscience, School of Biosciences, Cardiff University, Cardiff, United Kingdom.
[Ti] Título:Severe Intellectual Disability and Enhanced Gamma-Aminobutyric Acidergic Synaptogenesis in a Novel Model of Rare RASopathies.
[So] Source:Biol Psychiatry;81(3):179-192, 2017 Feb 01.
[Is] ISSN:1873-2402
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Dysregulation of Ras-extracellular signal-related kinase (ERK) signaling gives rise to RASopathies, a class of neurodevelopmental syndromes associated with intellectual disability. Recently, much attention has been directed at models bearing mild forms of RASopathies whose behavioral impairments can be attenuated by inhibiting the Ras-ERK cascade in the adult. Little is known about the brain mechanisms in severe forms of these disorders. METHODS: We performed an extensive characterization of a new brain-specific model of severe forms of RASopathies, the KRAS mutant mouse. RESULTS: The KRAS mutation results in a severe form of intellectual disability, which parallels mental deficits found in patients bearing mutations in this gene. KRAS mice show a severe impairment of both short- and long-term memory in a number of behavioral tasks. At the cellular level, an upregulation of ERK signaling during early phases of postnatal development, but not in the adult state, results in a selective enhancement of synaptogenesis in gamma-aminobutyric acidergic interneurons. The enhancement of ERK activity in interneurons at this critical postnatal time leads to a permanent increase in the inhibitory tone throughout the brain, manifesting in reduced synaptic transmission and long-term plasticity in the hippocampus. In the adult, the behavioral and electrophysiological phenotypes in KRAS mice can be temporarily reverted by inhibiting gamma-aminobutyric acid signaling but not by a Ras-ERK blockade. Importantly, the synaptogenesis phenotype can be rescued by a treatment at the developmental stage with Ras-ERK inhibitors. CONCLUSIONS: These data demonstrate a novel mechanism underlying inhibitory synaptogenesis and provide new insights in understanding mental dysfunctions associated to RASopathies.
[Mh] Termos MeSH primário: Encéfalo/fisiologia
Neurônios GABAérgicos/fisiologia
Deficiência Intelectual/metabolismo
Sistema de Sinalização das MAP Quinases
Proteínas Proto-Oncogênicas p21(ras)/metabolismo
Sinapses/fisiologia
[Mh] Termos MeSH secundário: Animais
Ansiedade/metabolismo
Ansiedade/fisiopatologia
Comportamento Animal/fisiologia
Encéfalo/metabolismo
Modelos Animais de Doenças
Neurônios GABAérgicos/metabolismo
Hipocampo/metabolismo
Hipocampo/fisiologia
Potenciais Pós-Sinápticos Inibidores
Potenciação de Longa Duração
Transtornos da Memória/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Mutação
Proteínas Proto-Oncogênicas p21(ras)/genética
Receptores de GABA/metabolismo
Comportamento Social
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, GABA); 0 (Vesicular Inhibitory Amino Acid Transport Proteins); 0 (Viaat protein, mouse); EC 3.6.5.2 (Kras2 protein, mouse); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras))
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160903
[St] Status:MEDLINE


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[PMID]:27866798
[Au] Autor:Ruder L; Takeoka A; Arber S
[Ad] Endereço:Biozentrum, Department of Cell Biology, University of Basel, Klingelbergstrasse 70, 4056 Basel, Switzerland; Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, 4058 Basel, Switzerland.
[Ti] Título:Long-Distance Descending Spinal Neurons Ensure Quadrupedal Locomotor Stability.
[So] Source:Neuron;92(5):1063-1078, 2016 Dec 07.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Locomotion is an essential animal behavior used for translocation. The spinal cord acts as key executing center, but how it coordinates many body parts located across distance remains poorly understood. Here we employed mouse genetic and viral approaches to reveal organizational principles of long-projecting spinal circuits and their role in quadrupedal locomotion. Using neurotransmitter identity, developmental origin, and projection patterns as criteria, we uncover that spinal segments controlling forelimbs and hindlimbs are bidirectionally connected by symmetrically organized direct synaptic pathways that encompass multiple genetically tractable neuronal subpopulations. We demonstrate that selective ablation of descending spinal neurons linking cervical to lumbar segments impairs coherent locomotion, by reducing postural stability and speed during exploratory locomotion, as well as perturbing interlimb coordination during reinforced high-speed stepping. Together, our results implicate a highly organized long-distance projection system of spinal origin in the control of postural body stabilization and reliability during quadrupedal locomotion.
[Mh] Termos MeSH primário: Interneurônios Comissurais/fisiologia
Marcha/fisiologia
Locomoção/fisiologia
Neurônios/fisiologia
Equilíbrio Postural/fisiologia
Medula Espinal/fisiologia
[Mh] Termos MeSH secundário: Animais
Vértebras Cervicais
Membro Anterior
Membro Posterior
Vértebras Lombares
Camundongos
Neurônios/metabolismo
Medula Espinal/citologia
Proteína Vesicular 2 de Transporte de Glutamato/metabolismo
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Slc17a6 protein, mouse); 0 (Vesicular Glutamate Transport Protein 2); 0 (Vesicular Inhibitory Amino Acid Transport Proteins); 0 (Viaat protein, mouse)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161122
[St] Status:MEDLINE


  10 / 375 MEDLINE  
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[PMID]:27844057
[Au] Autor:Catuara-Solarz S; Espinosa-Carrasco J; Erb I; Langohr K; Gonzalez JR; Notredame C; Dierssen M
[Ad] Endereço:Cellular and Systems Neurobiology, Systems Biology Program, the Barcelona Institute of Science and Technology, Centre for Genomic Regulation (CRG), 08003, Barcelona, Spain; Universitat Pompeu Fabra (UPF), Barcelona, 08003, Spain; Human Pharmacology and Clinical Neurosciences Research Group, Neurosci
[Ti] Título:Combined Treatment With Environmental Enrichment and (-)-Epigallocatechin-3-Gallate Ameliorates Learning Deficits and Hippocampal Alterations in a Mouse Model of Down Syndrome.
[So] Source:eNeuro;3(5), 2016 Sep-Oct.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intellectual disability in Down syndrome (DS) is accompanied by altered neuro-architecture, deficient synaptic plasticity, and excitation-inhibition imbalance in critical brain regions for learning and memory. Recently, we have demonstrated beneficial effects of a combined treatment with green tea extract containing (-)-epigallocatechin-3-gallate (EGCG) and cognitive stimulation in young adult DS individuals. Although we could reproduce the cognitive-enhancing effects in mouse models, the underlying mechanisms of these beneficial effects are unknown. Here, we explored the effects of a combined therapy with environmental enrichment (EE) and EGCG in the Ts65Dn mouse model of DS at young age. Our results show that combined EE-EGCG treatment improved corticohippocampal-dependent learning and memory. Cognitive improvements were accompanied by a rescue of cornu ammonis 1 (CA1) dendritic spine density and a normalization of the proportion of excitatory and inhibitory synaptic markers in CA1 and dentate gyrus.
[Mh] Termos MeSH primário: Região CA1 Hipocampal/patologia
Catequina/análogos & derivados
Síndrome de Down/terapia
Abrigo para Animais
Aprendizagem
Nootrópicos/farmacologia
[Mh] Termos MeSH secundário: Animais
Região CA1 Hipocampal/efeitos dos fármacos
Região CA1 Hipocampal/metabolismo
Catequina/farmacologia
Espinhas Dendríticas/efeitos dos fármacos
Espinhas Dendríticas/metabolismo
Espinhas Dendríticas/patologia
Modelos Animais de Doenças
Síndrome de Down/metabolismo
Síndrome de Down/patologia
Aprendizagem/efeitos dos fármacos
Camundongos Transgênicos
Extratos Vegetais/farmacologia
Distribuição Aleatória
Recognição (Psicologia)/efeitos dos fármacos
Sinapses/efeitos dos fármacos
Sinapses/metabolismo
Sinapses/patologia
Chá
Proteína Vesicular 1 de Transporte de Glutamato/metabolismo
Proteínas Vesiculares de Transporte de Aminoácidos Inibidores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nootropic Agents); 0 (Plant Extracts); 0 (Slc17a7 protein, mouse); 0 (Tea); 0 (Vesicular Glutamate Transport Protein 1); 0 (Vesicular Inhibitory Amino Acid Transport Proteins); 0 (Viaat protein, mouse); 8R1V1STN48 (Catechin); BQM438CTEL (epigallocatechin gallate)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161116
[St] Status:MEDLINE



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