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  1 / 9422 MEDLINE  
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[PMID]:28462391
[Au] Autor:Nishimura M; Casanova JR; Swann JW
[Ad] Endereço:The Cain Foundation Laboratories, The Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, TX 77030.
[Ti] Título:The Impact of Electrographic Seizures on Developing Hippocampal Dendrites Is Calcineurin Dependent.
[So] Source:eNeuro;4(2), 2017 Mar-Apr.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neurobehavioral abnormalities are commonly associated with intractable childhood epilepsy. Studies from numerous labs have demonstrated cognitive and socialization deficits in rats and mice that have experienced early-life seizures. However, the cellular and molecular mechanisms underlying these effects are unknown. Previously, experiments have shown that recurrent seizures in infancy suppress the growth of hippocampal dendrites at the same time they impair learning and memory. Experiments in slice cultures have also demonstrated dendrite growth suppression. Here, we crossed calcineurin B1 (CaNB1) floxed and Thy1GFP-M mice to produce mice that were homozygous for the both the floxed CaNB1 and the Thy1GFP-M transgene. Littermates that were homozygous for wild-type CaNB1 and Thy1GFP-M served as controls. Hippocampal slice cultures from these mice were transfected with an AAV/hSyn-mCherry-Cre virus to eliminate CaNB1 from neurons. Immunohistochemical results showed that CaNB1 was eliminated from at least 90% of the transfected CA1 pyramidal cells. Moreover, the CaN-dependent nuclear translocation of the CREB transcription coactivator, CREB-regulated transcriptional coactivator 1 (CRTC1), was blocked in transfected neurons. Cell attach patch recordings combined with live multiphoton imaging demonstrated that the loss of CaNB1 did not prevent neurons from fully participating in electrographic seizure activity. Finally, dendrite reconstruction showed that the elimination of CaNB1 prevented seizure-induced decreases in both dendrite length and branch number. Results suggest that CaN plays a key role in seizure-induced dendrite growth suppression and may contribute to the neurobehavioral comorbidities of childhood epilepsy.
[Mh] Termos MeSH primário: Calcineurina/metabolismo
Dendritos/metabolismo
Hipocampo/metabolismo
Neurônios/metabolismo
Fosfoproteínas/metabolismo
Convulsões/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Aprendizagem/fisiologia
Memória/fisiologia
Camundongos
Células Piramidais/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cabin1 protein, mouse); 0 (Phosphoproteins); EC 3.1.3.16 (Calcineurin)
[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


  2 / 9422 MEDLINE  
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[PMID]:29335532
[Au] Autor:Brasko C; Smith K; Molnar C; Farago N; Hegedus L; Balind A; Balassa T; Szkalisity A; Sukosd F; Kocsis K; Balint B; Paavolainen L; Enyedi MZ; Nagy I; Puskas LG; Haracska L; Tamas G; Horvath P
[Ad] Endereço:University of Szeged, Szeged, Hungary Közép fasor 52, 6726, Szeged, Hungary.
[Ti] Título:Intelligent image-based in situ single-cell isolation.
[So] Source:Nat Commun;9(1):226, 2018 01 15.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Quantifying heterogeneities within cell populations is important for many fields including cancer research and neurobiology; however, techniques to isolate individual cells are limited. Here, we describe a high-throughput, non-disruptive, and cost-effective isolation method that is capable of capturing individually targeted cells using widely available techniques. Using high-resolution microscopy, laser microcapture microscopy, image analysis, and machine learning, our technology enables scalable molecular genetic analysis of single cells, targetable by morphology or location within the sample.
[Mh] Termos MeSH primário: Separação Celular/métodos
Processamento de Imagem Assistida por Computador/métodos
Microscopia Confocal/métodos
Análise de Célula Única/métodos
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Perfilação da Expressão Gênica
Seres Humanos
Aprendizado de Máquina
Células Piramidais/citologia
Células Piramidais/metabolismo
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[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:180117
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02628-4


  3 / 9422 MEDLINE  
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[PMID]:27773352
[Au] Autor:Torres-Berrío A; Lopez JP; Bagot RC; Nouel D; Dal Bo G; Cuesta S; Zhu L; Manitt C; Eng C; Cooper HM; Storch KF; Turecki G; Nestler EJ; Flores C
[Ad] Endereço:Integrated Program in Neuroscience, Montréal, Québec, Canada; Douglas Mental Health University Institute; Montréal, Québec, Canada.
[Ti] Título:DCC Confers Susceptibility to Depression-like Behaviors in Humans and Mice and Is Regulated by miR-218.
[So] Source:Biol Psychiatry;81(4):306-315, 2017 02 15.
[Is] ISSN:1873-2402
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUD: Variations in the expression of the Netrin-1 guidance cue receptor DCC (deleted in colorectal cancer) appear to confer resilience or susceptibility to psychopathologies involving prefrontal cortex (PFC) dysfunction. METHODS: With the use of postmortem brain tissue, mouse models of defeat stress, and in vitro analysis, we assessed microRNA (miRNA) regulation of DCC and whether changes in DCC levels in the PFC lead to vulnerability to depression-like behaviors. RESULTS: We identified miR-218 as a posttranscriptional repressor of DCC and detected coexpression of DCC and miR-218 in pyramidal neurons of human and mouse PFC. We found that exaggerated expression of DCC and reduced levels of miR-218 in the PFC are consistent traits of mice susceptible to chronic stress and of major depressive disorder in humans. Remarkably, upregulation of Dcc in mouse PFC pyramidal neurons causes vulnerability to stress-induced social avoidance and anhedonia. CONCLUSIONS: These data are the first demonstration of microRNA regulation of DCC and suggest that, by regulating DCC, miR-218 may be a switch of susceptibility versus resilience to stress-related disorders.
[Mh] Termos MeSH primário: Transtorno Depressivo Maior/metabolismo
MicroRNAs/metabolismo
Córtex Pré-Frontal/metabolismo
Células Piramidais/metabolismo
Receptores de Superfície Celular/metabolismo
Proteínas Supressoras de Tumor/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Receptor DCC
Transtorno Depressivo Maior/etiologia
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
RNA Mensageiro/metabolismo
Comportamento Social
Estresse Psicológico/complicações
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (DCC Receptor); 0 (DCC protein, human); 0 (MIRN218 microRNA, human); 0 (MicroRNAs); 0 (RNA, Messenger); 0 (Receptors, Cell Surface); 0 (Tumor Suppressor Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  4 / 9422 MEDLINE  
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[PMID]:29326273
[Au] Autor:Danjo T; Toyoizumi T; Fujisawa S
[Ad] Endereço:Laboratory for Systems Neurophysiology, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako, Saitama, 351-0198, Japan.
[Ti] Título:Spatial representations of self and other in the hippocampus.
[So] Source:Science;359(6372):213-218, 2018 Jan 12.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An animal's awareness of its location in space depends on the activity of place cells in the hippocampus. How the brain encodes the spatial position of others has not yet been identified. We investigated neuronal representations of other animals' locations in the dorsal CA1 region of the hippocampus with an observational T-maze task in which one rat was required to observe another rat's trajectory to successfully retrieve a reward. Information reflecting the spatial location of both the self and the other was jointly and discretely encoded by CA1 pyramidal cells in the observer rat. A subset of CA1 pyramidal cells exhibited spatial receptive fields that were identical for the self and the other. These findings demonstrate that hippocampal spatial representations include dimensions for both self and nonself.
[Mh] Termos MeSH primário: Região CA1 Hipocampal/fisiologia
Células de Lugar/fisiologia
Células Piramidais/fisiologia
Percepção Espacial
Comportamento Espacial
[Mh] Termos MeSH secundário: Potenciais de Ação
Animais
Região CA1 Hipocampal/citologia
Masculino
Aprendizagem em Labirinto
Modelos Biológicos
Ratos
Ratos Long-Evans
Processamento Espacial
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE
[do] DOI:10.1126/science.aao3898


  5 / 9422 MEDLINE  
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[PMID]:29176325
[Au] Autor:Dibué-Adjei M; Kamp MA; Alpdogan S; Tevoufouet EE; Neiss WF; Hescheler J; Schneider T
[Ad] Endereço:Institute for Neurophysiology, Cologne, Germany.
[Ti] Título:Cav2.3 (R-Type) Calcium Channels are Critical for Mediating Anticonvulsive and Neuroprotective Properties of Lamotrigine In Vivo.
[So] Source:Cell Physiol Biochem;44(3):935-947, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Lamotrigine (LTG) is a popular modern antiepileptic drug (AED), however, its mechanism of action has yet to be fully understood, as it is known to modulate many members of several ion channel families. In heterologous systems, LTG inhibits Cav2.3 (R-type) calcium currents, which contribute to kainic-acid- (KA) induced epilepsy in vivo. To gain insight into the role of R-type currents in LTG drug action in vivo, we compared the effects of LTG to topiramate and lacosamide in Cav2.3-deficient mice and controls on KA-induced seizures. METHODS: Behavioral seizure rating and quantitative electrocorticography were performed after injection of 20 mg/kg [and 30 mg/kg] KA. One hour before KA injection, mice were pretreated with either 30 mg/kg LTG, 50 mg/kg topiramate (TPM) or 30 mg/kg lacosamide (LSM). RESULTS: Ablation of Cav2.3 reduced total seizure scores by 28.6% (p=0.0012) and pretreatment with LTG reduced seizure activity of control mice by 23.2% (p=0.02). In Cav2.3-deficient mice LTG pretreatment increased seizure activity by 22.1% (p=0.018) and increased the percentage of degenerated CA1 pyramidal neurons (p=0.02). All three tested AEDs reduced seizure activity in control mice, however only the non-calcium channel modulating AED, LSM had an anticonvulsive effect in Cav2.3-deficient mice. Furthermore LTG altered electrocorticographic parameters differently in the two genotypes, decreasing relative power of ictal spikes in control mice compared to Cav2.3-defcient mice. CONCLUSION: These findings give first in vivo evidence for an essential role for Cav2.3 in LTG pharmacology and shed light on a paradoxical effect of LTG in their absence. Furthermore, LTG appears to promote ictal activity in Cav2.3-deficient mice resulting in increased neurotoxicity in the CA1 region. This paradoxical mechanism, possibly reflecting rebound hyperexcitation of pyramidal CA1 neurons after increased inhibition, may be key in understanding LTG-induced seizure aggravation, observed in clinical practice.
[Mh] Termos MeSH primário: Anticonvulsivantes/farmacologia
Comportamento Animal/efeitos dos fármacos
Canais de Cálcio Tipo R/genética
Epilepsia/patologia
Fármacos Neuroprotetores/farmacologia
Triazinas/farmacologia
[Mh] Termos MeSH secundário: Acetamidas/farmacologia
Acetamidas/uso terapêutico
Animais
Anticonvulsivantes/uso terapêutico
Canais de Cálcio Tipo R/deficiência
Eletrocorticografia
Epilepsia/induzido quimicamente
Epilepsia/prevenção & controle
Frutose/análogos & derivados
Frutose/farmacologia
Frutose/uso terapêutico
Genótipo
Imuno-Histoquímica
Ácido Caínico/toxicidade
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fármacos Neuroprotetores/uso terapêutico
Células Piramidais/efeitos dos fármacos
Células Piramidais/patologia
Triazinas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetamides); 0 (Anticonvulsants); 0 (Calcium Channels, R-Type); 0 (Neuroprotective Agents); 0 (Triazines); 0H73WJJ391 (topiramate); 30237-26-4 (Fructose); 563KS2PQY5 (lacosamide); SIV03811UC (Kainic Acid); U3H27498KS (lamotrigine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485361


  6 / 9422 MEDLINE  
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[PMID]:29244810
[Au] Autor:Bliss DP; D'Esposito M
[Ad] Endereço:Helen Wills Neuroscience Institute, University of California, Berkeley, CA, United States of America.
[Ti] Título:Synaptic augmentation in a cortical circuit model reproduces serial dependence in visual working memory.
[So] Source:PLoS One;12(12):e0188927, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent work has established that visual working memory is subject to serial dependence: current information in memory blends with that from the recent past as a function of their similarity. This tuned temporal smoothing likely promotes the stability of memory in the face of noise and occlusion. Serial dependence accumulates over several seconds in memory and deteriorates with increased separation between trials. While this phenomenon has been extensively characterized in behavior, its neural mechanism is unknown. In the present study, we investigate the circuit-level origins of serial dependence in a biophysical model of cortex. We explore two distinct kinds of mechanisms: stable persistent activity during the memory delay period and dynamic "activity-silent" synaptic plasticity. We find that networks endowed with both strong reverberation to support persistent activity and dynamic synapses can closely reproduce behavioral serial dependence. Specifically, elevated activity drives synaptic augmentation, which biases activity on the subsequent trial, giving rise to a spatiotemporally tuned shift in the population response. Our hybrid neural model is a theoretical advance beyond abstract mathematical characterizations, offers testable hypotheses for physiological research, and demonstrates the power of biological insights to provide a quantitative explanation of human behavior.
[Mh] Termos MeSH primário: Córtex Cerebral/fisiologia
Memória de Curto Prazo/fisiologia
Modelos Neurológicos
Transmissão Sináptica/fisiologia
Vias Visuais/fisiologia
[Mh] Termos MeSH secundário: Córtex Cerebral/citologia
Simulação por Computador
Seres Humanos
Plasticidade Neuronal/fisiologia
Células Piramidais/citologia
Células Piramidais/fisiologia
Receptores de AMPA/fisiologia
Receptores de GABA-A/fisiologia
Receptores de N-Metil-D-Aspartato/fisiologia
Sinapses/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, AMPA); 0 (Receptors, GABA-A); 0 (Receptors, N-Methyl-D-Aspartate)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188927


  7 / 9422 MEDLINE  
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[PMID]:29211992
[Au] Autor:Scheppach C; Robinson HPC
[Ad] Endereço:Physiological Laboratory, Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, United Kingdom; Institute of Physics, University of Freiburg, Freiburg im Breisgau, Germany. Electronic address: christian.scheppach@physik.uni-freiburg.de.
[Ti] Título:Fluctuation Analysis in Nonstationary Conditions: Single Ca Channel Current in Pyramidal Neurons.
[So] Source:Biophys J;113(11):2383-2395, 2017 Dec 05.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fluctuation analysis is a method that allows measurement of the single-channel current of ion channels even when it is too small to be resolved directly with the patch-clamp technique. This is the case for voltage-gated calcium channels. They are present in all mammalian central neurons, controlling presynaptic release of transmitter, postsynaptic signaling, and synaptic integration. The amplitudes of their single-channel currents in a physiological concentration of extracellular calcium, however, are small and not well determined. But measurement of this quantity is essential for estimating numbers of functional voltage-gated calcium channels in the membrane and the size of channel-associated calcium signaling domains, and for understanding the stochastic nature of calcium signaling. Here, we recorded the voltage-gated calcium channel current in nucleated patches from layer 5 pyramidal neurons in rat neocortex, in physiological external calcium (1-2 mM). The ensemble-averaging of current responses required for conventional fluctuation analysis proved impractical because of the rapid rundown of calcium channel currents. We therefore developed a more robust method, using mean current fitting of individual current responses and band-pass filtering. Furthermore, voltage-ramp stimulation proved useful. We validated the accuracy of the method by analyzing simulated data. At an external calcium concentration of 1 mM, and a membrane potential of -20 mV, we found that the average single-channel current amplitude was ∼0.04 pA, increasing to 0.065 pA at 2 mM external calcium, and 0.12 pA at 5 mM. The relaxation time constant of the fluctuations was in the range 0.2-0.8 ms. The results are relevant to understanding the stochastic properties of dendritic Ca spikes in neocortical layer 5 pyramidal neurons. With the reported method, single-channel current amplitude of native voltage-gated calcium channels can be resolved accurately despite conditions of unstable rundown.
[Mh] Termos MeSH primário: Canais de Cálcio/metabolismo
Células Piramidais/metabolismo
[Mh] Termos MeSH secundário: Animais
Cálcio/farmacologia
Relação Dose-Resposta a Droga
Espaço Extracelular/efeitos dos fármacos
Espaço Extracelular/metabolismo
Modelos Neurológicos
Células Piramidais/citologia
Células Piramidais/efeitos dos fármacos
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180103
[Lr] Data última revisão:
180103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


  8 / 9422 MEDLINE  
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[PMID]:29050394
[Au] Autor:Altwegg-Boussac T; Schramm AE; Ballestero J; Grosselin F; Chavez M; Lecas S; Baulac M; Naccache L; Demeret S; Navarro V; Mahon S; Charpier S
[Ad] Endereço:Inserm U 1127, CNRS UMR 7225, Sorbonne Universités, UPMC Univ Paris 06 UMR S 1127, Institut du Cerveau et de la Moelle épinière, ICM, F-75013, Paris, France.
[Ti] Título:Cortical neurons and networks are dormant but fully responsive during isoelectric brain state.
[So] Source:Brain;140(9):2381-2398, 2017 Sep 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A continuous isoelectric electroencephalogram reflects an interruption of endogenously-generated activity in cortical networks and systematically results in a complete dissolution of conscious processes. This electro-cerebral inactivity occurs during various brain disorders, including hypothermia, drug intoxication, long-lasting anoxia and brain trauma. It can also be induced in a therapeutic context, following the administration of high doses of barbiturate-derived compounds, to interrupt a hyper-refractory status epilepticus. Although altered sensory responses can be occasionally observed on an isoelectric electroencephalogram, the electrical membrane properties and synaptic responses of individual neurons during this cerebral state remain largely unknown. The aim of the present study was to characterize the intracellular correlates of a barbiturate-induced isoelectric electroencephalogram and to analyse the sensory-evoked synaptic responses that can emerge from a brain deprived of spontaneous electrical activity. We first examined the sensory responsiveness from patients suffering from intractable status epilepticus and treated by administration of thiopental. Multimodal sensory responses could be evoked on the flat electroencephalogram, including visually-evoked potentials that were significantly amplified and delayed, with a high trial-to-trial reproducibility compared to awake healthy subjects. Using an analogous pharmacological procedure to induce prolonged electro-cerebral inactivity in the rat, we could describe its cortical and subcortical intracellular counterparts. Neocortical, hippocampal and thalamo-cortical neurons were all silent during the isoelectric state and displayed a flat membrane potential significantly hyperpolarized compared with spontaneously active control states. Nonetheless, all recorded neurons could fire action potentials in response to intracellularly injected depolarizing current pulses and their specific intrinsic electrophysiological features were preserved. Manipulations of the membrane potential and intracellular injection of chloride in neocortical neurons failed to reveal an augmented synaptic inhibition during the isoelectric condition. Consistent with the sensory responses recorded from comatose patients, large and highly reproducible somatosensory-evoked potentials could be generated on the inactive electrocorticogram in rats. Intracellular recordings revealed that the underlying neocortical pyramidal cells responded to sensory stimuli by complex synaptic potentials able to trigger action potentials. As in patients, sensory responses in the isoelectric state were delayed compared to control responses and exhibited an elevated reliability during repeated stimuli. Our findings demonstrate that during prolonged isoelectric brain state neurons and synaptic networks are dormant rather than excessively inhibited, conserving their intrinsic properties and their ability to integrate and propagate environmental stimuli.
[Mh] Termos MeSH primário: Córtex Cerebral/citologia
Córtex Cerebral/fisiologia
Neurônios/fisiologia
Estado Epiléptico/fisiopatologia
Tiopental/farmacologia
Inconsciência/fisiopatologia
[Mh] Termos MeSH secundário: Potenciais de Ação/fisiologia
Adolescente
Adulto
Idoso
Animais
Encéfalo/efeitos dos fármacos
Encéfalo/fisiologia
Estudos de Casos e Controles
Estimulação Elétrica
Eletroencefalografia
Potenciais Evocados/fisiologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Vias Neurais/fisiologia
Células Piramidais/fisiologia
Ratos
Estado Epiléptico/tratamento farmacológico
Tiopental/uso terapêutico
Inconsciência/induzido quimicamente
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
JI8Z5M7NA3 (Thiopental)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171021
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx175


  9 / 9422 MEDLINE  
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[PMID]:29024669
[Au] Autor:English DF; McKenzie S; Evans T; Kim K; Yoon E; Buzsáki G
[Ad] Endereço:Neuroscience Institute, New York University, New York, NY 10016, US.
[Ti] Título:Pyramidal Cell-Interneuron Circuit Architecture and Dynamics in Hippocampal Networks.
[So] Source:Neuron;96(2):505-520.e7, 2017 Oct 11.
[Is] ISSN:1097-4199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Excitatory control of inhibitory neurons is poorly understood due to the difficulty of studying synaptic connectivity in vivo. We inferred such connectivity through analysis of spike timing and validated this inference using juxtacellular and optogenetic control of presynaptic spikes in behaving mice. We observed that neighboring CA1 neurons had stronger connections and that superficial pyramidal cells projected more to deep interneurons. Connection probability and strength were skewed, with a minority of highly connected hubs. Divergent presynaptic connections led to synchrony between interneurons. Synchrony of convergent presynaptic inputs boosted postsynaptic drive. Presynaptic firing frequency was read out by postsynaptic neurons through short-term depression and facilitation, with individual pyramidal cells and interneurons displaying a diversity of spike transmission filters. Additionally, spike transmission was strongly modulated by prior spike timing of the postsynaptic cell. These results bridge anatomical structure with physiological function.
[Mh] Termos MeSH primário: Potenciais de Ação/fisiologia
Região CA1 Hipocampal/fisiologia
Interneurônios/fisiologia
Rede Nervosa/fisiologia
Células Piramidais/fisiologia
[Mh] Termos MeSH secundário: Animais
Região CA1 Hipocampal/química
Região CA1 Hipocampal/citologia
Feminino
Interneurônios/química
Masculino
Camundongos
Camundongos Transgênicos
Rede Nervosa/química
Rede Nervosa/citologia
Optogenética/métodos
Células Piramidais/química
Distribuição Aleatória
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE


  10 / 9422 MEDLINE  
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[PMID]:28931075
[Au] Autor:Luque MA; Beltran-Matas P; Marin MC; Torres B; Herrero L
[Ad] Endereço:Department of Physiology. University of Seville, Seville, Spain.
[Ti] Título:Excitability is increased in hippocampal CA1 pyramidal cells of Fmr1 knockout mice.
[So] Source:PLoS One;12(9):e0185067, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fragile X syndrome (FXS) is caused by a failure of neuronal cells to express the gene encoding the fragile mental retardation protein (FMRP). Clinical features of the syndrome include intellectual disability, learning impairment, hyperactivity, seizures and anxiety. Fmr1 knockout (KO) mice do not express FMRP and, as a result, reproduce some FXS behavioral abnormalities. While intrinsic and synaptic properties of excitatory cells in various part of the brain have been studied in Fmr1 KO mice, a thorough analysis of action potential characteristics and input-output function of CA1 pyramidal cells in this model is lacking. With a view to determining the effects of the absence of FMRP on cell excitability, we studied rheobase, action potential duration, firing frequency-current intensity relationship and action potential after-hyperpolarization (AHP) in CA1 pyramidal cells of the hippocampus of wild type (WT) and Fmr1 KO male mice. Brain slices were prepared from 8- to 12-week-old mice and the electrophysiological properties of cells recorded. Cells from both groups had similar resting membrane potentials. In the absence of FMRP expression, cells had a significantly higher input resistance, while voltage threshold and depolarization voltage were similar in WT and Fmr1 KO cell groups. No changes were observed in rheobase. The action potential duration was longer in the Fmr1 KO cell group, and the action potential firing frequency evoked by current steps of the same intensity was higher. Moreover, the gain (slope) of the relationship between firing frequency and injected current was 1.25-fold higher in the Fmr1 KO cell group. Finally, AHP amplitude was significantly reduced in the Fmr1 KO cell group. According to these data, FMRP absence increases excitability in hippocampal CA1 pyramidal cells.
[Mh] Termos MeSH primário: Proteína do X Frágil de Retardo Mental/genética
Células Piramidais/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação/genética
Animais
Proteína do X Frágil de Retardo Mental/metabolismo
Masculino
Camundongos Knockout
Técnicas de Patch-Clamp
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fmr1 protein, mouse); 139135-51-6 (Fragile X Mental Retardation Protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185067



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