Base de dados : MEDLINE
Pesquisa : G04.580.887 [Categoria DeCS]
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[PMID]:28742093
[Au] Autor:Hermes D; Nguyen M; Winawer J
[Ad] Endereço:Department of Psychology, New York University, New York, New York, United States of America.
[Ti] Título:Neuronal synchrony and the relation between the blood-oxygen-level dependent response and the local field potential.
[So] Source:PLoS Biol;15(7):e2001461, 2017 Jul.
[Is] ISSN:1545-7885
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The most widespread measures of human brain activity are the blood-oxygen-level dependent (BOLD) signal and surface field potential. Prior studies report a variety of relationships between these signals. To develop an understanding of how to interpret these signals and the relationship between them, we developed a model of (a) neuronal population responses and (b) transformations from neuronal responses into the functional magnetic resonance imaging (fMRI) BOLD signal and electrocorticographic (ECoG) field potential. Rather than seeking a transformation between the two measures directly, this approach interprets each measure with respect to the underlying neuronal population responses. This model accounts for the relationship between BOLD and ECoG data from human visual cortex in V1, V2, and V3, with the model predictions and data matching in three ways: across stimuli, the BOLD amplitude and ECoG broadband power were positively correlated, the BOLD amplitude and alpha power (8-13 Hz) were negatively correlated, and the BOLD amplitude and narrowband gamma power (30-80 Hz) were uncorrelated. The two measures provide complementary information about human brain activity, and we infer that features of the field potential that are uncorrelated with BOLD arise largely from changes in synchrony, rather than level, of neuronal activity.
[Mh] Termos MeSH primário: Sincronização Cortical
Hipóxia Encefálica/etiologia
Modelos Neurológicos
Potenciais Sinápticos
Córtex Visual/diagnóstico por imagem
[Mh] Termos MeSH secundário: Adulto
Algoritmos
Monitorização Transcutânea dos Gases Sanguíneos
Simulação por Computador
Eletrocorticografia
Feminino
Neuroimagem Funcional
Seres Humanos
Hipóxia Encefálica/sangue
Imagem por Ressonância Magnética
Masculino
Neurônios/metabolismo
Oxigênio/sangue
Análise de Componente Principal
Reprodutibilidade dos Testes
Córtex Visual/irrigação sanguínea
Córtex Visual/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
S88TT14065 (Oxygen)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pbio.2001461


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[PMID]:28981509
[Au] Autor:Soriano J; Kubo T; Inoue T; Kida H; Yamakawa T; Suzuki M; Ikeda K
[Ad] Endereço:Mathematical Informatics Laboratory, Graduate School of Information Science, Nara Institute of Science and Technology, Ikoma, Japan.
[Ti] Título:Differential temperature sensitivity of synaptic and firing processes in a neural mass model of epileptic discharges explains heterogeneous response of experimental epilepsy to focal brain cooling.
[So] Source:PLoS Comput Biol;13(10):e1005736, 2017 Oct.
[Is] ISSN:1553-7358
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Experiments with drug-induced epilepsy in rat brains and epileptic human brain region reveal that focal cooling can suppress epileptic discharges without affecting the brain's normal neurological function. Findings suggest a viable treatment for intractable epilepsy cases via an implantable cooling device. However, precise mechanisms by which cooling suppresses epileptic discharges are still not clearly understood. Cooling experiments in vitro presented evidence of reduction in neurotransmitter release from presynaptic terminals and loss of dendritic spines at post-synaptic terminals offering a possible synaptic mechanism. We show that termination of epileptic discharges is possible by introducing a homogeneous temperature factor in a neural mass model which attenuates the post-synaptic impulse responses of the neuronal populations. This result however may be expected since such attenuation leads to reduced post-synaptic potential and when the effect on inhibitory interneurons is less than on excitatory interneurons, frequency of firing of pyramidal cells is consequently reduced. While this is observed in cooling experiments in vitro, experiments in vivo exhibit persistent discharges during cooling but suppressed in magnitude. This leads us to conjecture that reduction in the frequency of discharges may be compensated through intrinsic excitability mechanisms. Such compensatory mechanism is modelled using a reciprocal temperature factor in the firing response function in the neural mass model. We demonstrate that the complete model can reproduce attenuation of both magnitude and frequency of epileptic discharges during cooling. The compensatory mechanism suggests that cooling lowers the average and the variance of the distribution of threshold potential of firing across the population. Bifurcation study with respect to the temperature parameters of the model reveals how heterogeneous response of epileptic discharges to cooling (termination or suppression only) is exhibited. Possibility of differential temperature effects on post-synaptic potential generation of different populations is also explored.
[Mh] Termos MeSH primário: Encéfalo/fisiologia
Epilepsia/fisiopatologia
Hipotermia Induzida
Modelos Neurológicos
Transmissão Sináptica/fisiologia
[Mh] Termos MeSH secundário: Animais
Temperatura Corporal/fisiologia
Temperatura Baixa
Biologia Computacional
Modelos Animais de Doenças
Masculino
Ratos
Ratos Sprague-Dawley
Potenciais Sinápticos/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171022
[Lr] Data última revisão:
171022
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171006
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pcbi.1005736


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[PMID]:28915251
[Au] Autor:Canakci S; Toy MF; Inci AF; Liu X; Kuzum D
[Ad] Endereço:Electrical and Computer Engineering Department, Boston University, Boston, Massachusetts, United States of America.
[Ti] Título:Computational analysis of network activity and spatial reach of sharp wave-ripples.
[So] Source:PLoS One;12(9):e0184542, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Network oscillations of different frequencies, durations and amplitudes are hypothesized to coordinate information processing and transfer across brain areas. Among these oscillations, hippocampal sharp wave-ripple complexes (SPW-Rs) are one of the most prominent. SPW-Rs occurring in the hippocampus are suggested to play essential roles in memory consolidation as well as information transfer to the neocortex. To-date, most of the knowledge about SPW-Rs comes from experimental studies averaging responses from neuronal populations monitored by conventional microelectrodes. In this work, we investigate spatiotemporal characteristics of SPW-Rs and how microelectrode size and distance influence SPW-R recordings using a biophysical model of hippocampus. We also explore contributions from neuronal spikes and synaptic potentials to SPW-Rs based on two different types of network activity. Our study suggests that neuronal spikes from pyramidal cells contribute significantly to ripples while high amplitude sharp waves mainly arise from synaptic activity. Our simulations on spatial reach of SPW-Rs show that the amplitudes of sharp waves and ripples exhibit a steep decrease with distance from the network and this effect is more prominent for smaller area electrodes. Furthermore, the amplitude of the signal decreases strongly with increasing electrode surface area as a result of averaging. The relative decrease is more pronounced when the recording electrode is closer to the source of the activity. Through simulations of field potentials across a high-density microelectrode array, we demonstrate the importance of finding the ideal spatial resolution for capturing SPW-Rs with great sensitivity. Our work provides insights on contributions from spikes and synaptic potentials to SPW-Rs and describes the effect of measurement configuration on LFPs to guide experimental studies towards improved SPW-R recordings.
[Mh] Termos MeSH primário: Simulação por Computador
Hipocampo/fisiologia
Modelos Neurológicos
Neocórtex/fisiologia
Rede Nervosa/fisiologia
Potenciais Sinápticos/fisiologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Microeletrodos
Células Piramidais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184542


  4 / 870 MEDLINE  
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[PMID]:28882644
[Au] Autor:Weon H; Kim TW; Youn DH
[Ad] Endereço:Department of Oral Physiology, BioCure Laboratory, School of Dentistry, Kyungpook National University, 2177 Dalgubeol Blvd, Jung-gu, Daegu 41940, Republic of Korea.
[Ti] Título:Postsynaptic N-type or P/Q-type calcium channels mediate long-term potentiation by group I metabotropic glutamate receptors in the trigeminal oralis.
[So] Source:Life Sci;188:110-117, 2017 Nov 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Both N-type and P/Q-type voltage-gated Ca channels (VGCCs) are involved in the induction of long-term potentiation (LTP), the long-lasting increase of synaptic strength, in the central nervous system. To provide further information on the roles of N-type and P/Q-type VGCCs in the induction of LTP at excitatory synapses of trigeminal primary afferents in the spinal trigeminal subnucleus oralis (Vo), we investigated whether they contribute to the induction of LTP by activation of group I metabotropic glutamate receptors (mGluRs). MAIN METHODS: (S)-3,5-Dihydroxyphenylglycine (DHPG; 10µM for 5min), the group I mGluR agonist, was used to induce LTP of excitatory postsynaptic currents that were evoked in the Vo neurons by stimulating the trigeminal track. KEY FINDINGS: Weak blockade of the N-type or P/Q-type VGCCs by ω-conotoxin GVIA or ω-agatoxin IVA, respectively, which inhibited only 20-40% of Ca currents recorded in isolated trigeminal ganglion neurons but had no effect on the basal excitatory synaptic transmission, completely blocked the induction of LTP. In contrast, stronger blockade of the channels, which inhibited >50% of Ca currents and about 30% of basal synaptic transmission, resulted in the development of long-term depression (LTD), the long-lasting decrease of synaptic strength. Interestingly, the postsynaptic mechanism of DHPG-induced LTP, which was determined by paired-pulse ratio, disappeared when LTP was blocked, or LTD occurred, while a presynaptic mechanism still remained. SIGNIFICANCE: Our data suggest that postsynaptic N-type and P/Q-type VGCCs mediate the DHPG-induced LTP at the trigeminal afferent synapses in the Vo.
[Mh] Termos MeSH primário: Canais de Cálcio Tipo N/fisiologia
Canais de Cálcio Tipo P/fisiologia
Canais de Cálcio Tipo Q/fisiologia
Potenciação de Longa Duração/fisiologia
Receptores de Glutamato Metabotrópico/fisiologia
Núcleo Espinal do Trigêmeo/fisiologia
[Mh] Termos MeSH secundário: Agatoxinas/farmacologia
Animais
Agonistas dos Canais de Cálcio/farmacologia
Bloqueadores dos Canais de Cálcio
Cromonas/farmacologia
Feminino
Potenciação de Longa Duração/efeitos dos fármacos
Depressão Sináptica de Longo Prazo/efeitos dos fármacos
Depressão Sináptica de Longo Prazo/fisiologia
Masculino
Terminações Pré-Sinápticas/fisiologia
Ratos
Receptores de Glutamato Metabotrópico/agonistas
Potenciais Sinápticos/fisiologia
Transmissão Sináptica/efeitos dos fármacos
Núcleo Espinal do Trigêmeo/efeitos dos fármacos
ômega-Conotoxinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((S)-3,7-dihydroxychroman-4-one); 0 (Agatoxins); 0 (Calcium Channel Agonists); 0 (Calcium Channel Blockers); 0 (Calcium Channels, N-Type); 0 (Calcium Channels, P-Type); 0 (Calcium Channels, Q-Type); 0 (Chromones); 0 (Receptors, Metabotropic Glutamate); 0 (omega-Conotoxins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


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[PMID]:28871036
[Au] Autor:Cho IH; Panzera LC; Chin M; Hoppa MB
[Ad] Endereço:Department of Biological Sciences, Dartmouth College, Hanover, New Hampshire 03755.
[Ti] Título:Sodium Channel ß2 Subunits Prevent Action Potential Propagation Failures at Axonal Branch Points.
[So] Source:J Neurosci;37(39):9519-9533, 2017 Sep 27.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neurotransmitter release depends on voltage-gated Na channels (Na s) to propagate an action potential (AP) successfully from the axon hillock to a synaptic terminal. Unmyelinated sections of axon are very diverse structures encompassing branch points and numerous presynaptic terminals with undefined molecular partners of Na channels. Using optical recordings of Ca and membrane voltage, we demonstrate here that Na channel ß2 subunits (Na ß2s) are required to prevent AP propagation failures across the axonal arborization of cultured rat hippocampal neurons (mixed male and female). When Na ß2 expression was reduced, we identified two specific phenotypes: (1) membrane excitability and AP-evoked Ca entry were impaired at synapses and (2) AP propagation was severely compromised with >40% of axonal branches no longer responding to AP-stimulation. We went on to show that a great deal of electrical signaling heterogeneity exists in AP waveforms across the axonal arborization independent of axon morphology. Therefore, Na ß2 is a critical regulator of axonal excitability and synaptic function in unmyelinated axons. Voltage-gated Ca channels are fulcrums of neurotransmission that convert electrical inputs into chemical outputs in the form of vesicle fusion at synaptic terminals. However, the role of the electrical signal, the presynaptic action potential (AP), in modulating synaptic transmission is less clear. What is the fidelity of a propagating AP waveform in the axon and what molecules shape it throughout the axonal arborization? Our work identifies several new features of AP propagation in unmyelinated axons: (1) branches of a single axonal arborization have variable AP waveforms independent of morphology, (2) Na channel ß2 subunits modulate AP-evoked Ca -influx, and (3) ß2 subunits maintain successful AP propagation across the axonal arbor. These findings are relevant to understanding the flow of excitation in the brain.
[Mh] Termos MeSH primário: Potenciais de Ação
Axônios/metabolismo
Subunidade beta-2 do Canal de Sódio Disparado por Voltagem/metabolismo
[Mh] Termos MeSH secundário: Animais
Axônios/fisiologia
Região CA1 Hipocampal/citologia
Sinalização do Cálcio
Linhagem Celular
Células Cultivadas
Feminino
Masculino
Potenciais da Membrana
Ratos
Ratos Sprague-Dawley
Potenciais Sinápticos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Voltage-Gated Sodium Channel beta-2 Subunit)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0891-17.2017


  6 / 870 MEDLINE  
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[PMID]:28829781
[Au] Autor:Nagy B; Hovhannisyan A; Barzan R; Chen TJ; Kukley M
[Ad] Endereço:Group of Neuron Glia Interaction, Werner Reichardt Centre for Integrative Neuroscience, University of Tübingen, Tübingen, Germany.
[Ti] Título:Different patterns of neuronal activity trigger distinct responses of oligodendrocyte precursor cells in the corpus callosum.
[So] Source:PLoS Biol;15(8):e2001993, 2017 Aug.
[Is] ISSN:1545-7885
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the developing and adult brain, oligodendrocyte precursor cells (OPCs) are influenced by neuronal activity: they are involved in synaptic signaling with neurons, and their proliferation and differentiation into myelinating glia can be altered by transient changes in neuronal firing. An important question that has been unanswered is whether OPCs can discriminate different patterns of neuronal activity and respond to them in a distinct way. Here, we demonstrate in brain slices that the pattern of neuronal activity determines the functional changes triggered at synapses between axons and OPCs. Furthermore, we show that stimulation of the corpus callosum at different frequencies in vivo affects proliferation and differentiation of OPCs in a dissimilar way. Our findings suggest that neurons do not influence OPCs in "all-or-none" fashion but use their firing pattern to tune the response and behavior of these nonneuronal cells.
[Mh] Termos MeSH primário: Células-Tronco Adultas/fisiologia
Corpo Caloso/fisiologia
Neurogênese
Oligodendroglia/fisiologia
Transmissão Sináptica
[Mh] Termos MeSH secundário: Células-Tronco Adultas/citologia
Animais
Axônios/fisiologia
Sinalização do Cálcio
Proliferação Celular
Corpo Caloso/citologia
Imuno-Histoquímica
Masculino
Camundongos Transgênicos
Microglia/citologia
Microglia/fisiologia
Microscopia Confocal
Oligodendroglia/citologia
Técnicas de Patch-Clamp
Distribuição Aleatória
Sinapses/fisiologia
Potenciais Sinápticos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pbio.2001993


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[PMID]:28821661
[Au] Autor:Maurer AP; Burke SN; Diba K; Barnes CA
[Ad] Endereço:McKnight Brain Institute, Department of Neuroscience.
[Ti] Título:Attenuated Activity across Multiple Cell Types and Reduced Monosynaptic Connectivity in the Aged Perirhinal Cortex.
[So] Source:J Neurosci;37(37):8965-8974, 2017 Sep 13.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The perirhinal cortex (PER), which is critical for associative memory and stimulus discrimination, has been described as a wall of inhibition between the neocortex and hippocampus. With advanced age, rats show deficits on PER-dependent behavioral tasks and fewer PER principal neurons are activated by stimuli, but the role of PER interneurons in these altered circuit properties in old age has not been characterized. In the present study, PER neurons were recorded while rats traversed a circular track bidirectionally in which the track was either empty or contained eight novel objects evenly spaced around the track. Putative interneurons were discriminated from principal cells based on the autocorrelogram, waveform parameters, and firing rate. While object modulation of interneuron firing was observed in both young and aged rats, PER interneurons recorded from old animals had lower firing rates compared with those from young animals. This difference could not be accounted for by differences in running speed, as the firing rates of PER interneurons did not show significant velocity modulation. Finally, in the aged rats, relative to young rats, there was a significant reduction in detected excitatory and inhibitory monosynaptic connections. Together these data suggest that with advanced age there may be reduced afferent drive from excitatory cells onto interneurons that may compromise the wall of inhibition between the hippocampus and cortex. This circuit dysfunction could erode the function of temporal lobe networks and ultimately contribute to cognitive aging. We report that lower firing rates observed in aged perirhinal cortical principal cells are associated with weaker interneuron activity and reduced monosynaptic coupling between excitatory and inhibitory cells. This is likely to affect feedforward inhibition from the perirhinal to the entorhinal cortex that gates the flow of information to the hippocampus. This is significant because cognitive dysfunction in normative and pathological aging has been linked to hyperexcitability in the aged CA3 subregion of the hippocampus in rats, monkeys, and humans. The reduced inhibition in the perirhinal cortex reported here could contribute to this circuit imbalance, and may be a key point to consider for therapeutic interventions aimed at restoring network function to optimize cognition.
[Mh] Termos MeSH primário: Potenciais de Ação/fisiologia
Envelhecimento/fisiologia
Inibição Neural/fisiologia
Neurônios/fisiologia
Córtex Perirrinal/fisiologia
Sinapses/fisiologia
Potenciais Sinápticos/fisiologia
[Mh] Termos MeSH secundário: Animais
Conectoma
Potenciais Pós-Sinápticos Excitadores/fisiologia
Potenciais Pós-Sinápticos Inibidores/fisiologia
Masculino
Neurônios/classificação
Neurônios/citologia
Ratos
Ratos Endogâmicos F344
Transmissão Sináptica/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170820
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0531-17.2017


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[PMID]:28787594
[Au] Autor:Guo J; Otis JM; Higginbotham H; Monckton C; Cheng J; Asokan A; Mykytyn K; Caspary T; Stuber GD; Anton ES
[Ad] Endereço:UNC Neuroscience Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA; Department of Cell Biology and Physiology, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.
[Ti] Título:Primary Cilia Signaling Shapes the Development of Interneuronal Connectivity.
[So] Source:Dev Cell;42(3):286-300.e4, 2017 Aug 07.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Appropriate growth and synaptic integration of GABAergic inhibitory interneurons are essential for functional neural circuits in the brain. Here, we demonstrate that disruption of primary cilia function following the selective loss of ciliary GTPase Arl13b in interneurons impairs interneuronal morphology and synaptic connectivity, leading to altered excitatory/inhibitory activity balance. The altered morphology and connectivity of cilia mutant interneurons and the functional deficits are rescued by either chemogenetic activation of ciliary G-protein-coupled receptor (GPCR) signaling or the selective induction of Sstr3, a ciliary GPCR, in Arl13b-deficient cilia. Our results thus define a specific requirement for primary cilia-mediated GPCR signaling in interneuronal connectivity and inhibitory circuit formation.
[Mh] Termos MeSH primário: Interneurônios/metabolismo
Transdução de Sinais
Sinapses/metabolismo
Potenciais Sinápticos
[Mh] Termos MeSH secundário: Fatores de Ribosilação do ADP/genética
Fatores de Ribosilação do ADP/metabolismo
Animais
Células Cultivadas
Cílios/metabolismo
Interneurônios/citologia
Interneurônios/fisiologia
Camundongos
Neurogênese
Receptores de Somatostatina/genética
Receptores de Somatostatina/metabolismo
Sinapses/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arl13b protein, mouse); 0 (Receptors, Somatostatin); 0 (somatostatin receptor 3); EC 3.6.5.2 (ADP-Ribosylation Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE


  9 / 870 MEDLINE  
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[PMID]:28759616
[Au] Autor:Peng C; Engle SE; Yan Y; Weera MM; Berry JN; Arvin MC; Zhao G; McIntosh JM; Chester JA; Drenan RM
[Ad] Endereço:Department of Pharmacology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, United States of America.
[Ti] Título:Altered nicotine reward-associated behavior following α4 nAChR subunit deletion in ventral midbrain.
[So] Source:PLoS One;12(7):e0182142, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nicotinic acetylcholine receptors containing α4 subunits (α4ß2* nAChRs) are critical for nicotinic cholinergic transmission and the addictive action of nicotine. To identify specific activities of these receptors in the adult mouse brain, we coupled targeted deletion of α4 nAChR subunits with behavioral and and electrophysiological measures of nicotine sensitivity. A viral-mediated Cre/lox approach allowed us to delete α4 from ventral midbrain (vMB) neurons. We used two behavioral assays commonly used to assess the motivational effects of drugs of abuse: home-cage oral self-administration, and place conditioning. Mice lacking α4 subunits in vMB consumed significantly more nicotine at the highest offered nicotine concentration (200 µg/mL) compared to control mice. Deletion of α4 subunits in vMB blocked nicotine-induced conditioned place preference (CPP) without affecting locomotor activity. Acetylcholine-evoked currents as well as nicotine-mediated increases in synaptic potentiation were reduced in mice lacking α4 in vMB. Immunostaining verified that α4 subunits were deleted from both dopamine and non-dopamine neurons in the ventral tegmental area (VTA). These results reveal that attenuation of α4* nAChR function in reward-related brain circuitry of adult animals may increase nicotine intake by enhancing the rewarding effects and/or reducing the aversive effects of nicotine.
[Mh] Termos MeSH primário: Nicotina/metabolismo
Receptores Nicotínicos/metabolismo
Recompensa
Área Tegmentar Ventral/metabolismo
[Mh] Termos MeSH secundário: Animais
Neurônios Dopaminérgicos/metabolismo
Neurônios Dopaminérgicos/fisiologia
Comportamento de Procura de Droga
Feminino
Deleção de Genes
Potenciação de Longa Duração
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Receptores Nicotínicos/genética
Potenciais Sinápticos
Área Tegmentar Ventral/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Nicotinic); 0 (nicotinic acetylcholine receptor alpha4 subunit); 6M3C89ZY6R (Nicotine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170801
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0182142


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[PMID]:28735442
[Au] Autor:Ledda F; Paratcha G
[Ad] Endereço:Division of Molecular and Cellular Neuroscience, Institute of Cell Biology and Neuroscience (IBCN)-CONICET, School of Medicine, University of Buenos Aires (UBA), Paraguay 2155, 3rd Floor, CABA, 1121, Buenos Aires, Argentina.
[Ti] Título:Mechanisms regulating dendritic arbor patterning.
[So] Source:Cell Mol Life Sci;74(24):4511-4537, 2017 Dec.
[Is] ISSN:1420-9071
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The nervous system is populated by diverse types of neurons, each of which has dendritic trees with strikingly different morphologies. These neuron-specific morphologies determine how dendritic trees integrate thousands of synaptic inputs to generate different firing properties. To ensure proper neuronal function and connectivity, it is necessary that dendrite patterns are precisely controlled and coordinated with synaptic activity. Here, we summarize the molecular and cellular mechanisms that regulate the formation of cell type-specific dendrite patterns during development. We focus on different aspects of vertebrate dendrite patterning that are particularly important in determining the neuronal function; such as the shape, branching, orientation and size of the arbors as well as the development of dendritic spine protrusions that receive excitatory inputs and compartmentalize postsynaptic responses. Additionally, we briefly comment on the implications of aberrant dendritic morphology for nervous system disease.
[Mh] Termos MeSH primário: Espinhas Dendríticas/fisiologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Doenças do Sistema Nervoso/patologia
Neurônios/fisiologia
Potenciais Sinápticos/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170724
[St] Status:MEDLINE
[do] DOI:10.1007/s00018-017-2588-8



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