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  1 / 2627 MEDLINE  
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[PMID]:28945222
[Au] Autor:Martin-Fernandez M; Jamison S; Robin LM; Zhao Z; Martin ED; Aguilar J; Benneyworth MA; Marsicano G; Araque A
[Ad] Endereço:Department of Neuroscience, University of Minnesota, Minneapolis, Minnesota, USA.
[Ti] Título:Synapse-specific astrocyte gating of amygdala-related behavior.
[So] Source:Nat Neurosci;20(11):1540-1548, 2017 Nov.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The amygdala plays key roles in fear and anxiety. Studies of the amygdala have largely focused on neuronal function and connectivity. Astrocytes functionally interact with neurons, but their role in the amygdala remains largely unknown. We show that astrocytes in the medial subdivision of the central amygdala (CeM) determine the synaptic and behavioral outputs of amygdala circuits. To investigate the role of astrocytes in amygdala-related behavior and identify the underlying synaptic mechanisms, we used exogenous or endogenous signaling to selectively activate CeM astrocytes. Astrocytes depressed excitatory synapses from basolateral amygdala via A adenosine receptor activation and enhanced inhibitory synapses from the lateral subdivision of the central amygdala via A receptor activation. Furthermore, astrocytic activation decreased the firing rate of CeM neurons and reduced fear expression in a fear-conditioning paradigm. Therefore, we conclude that astrocyte activity determines fear responses by selectively regulating specific synapses, which indicates that animal behavior results from the coordinated activity of neurons and astrocytes.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/fisiologia
Astrócitos/fisiologia
Medo/fisiologia
Aprendizagem em Labirinto/fisiologia
Rede Nervosa/fisiologia
Sinapses/fisiologia
[Mh] Termos MeSH secundário: 6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Antagonistas do Receptor A2 de Adenosina/farmacologia
Tonsila do Cerebelo/citologia
Tonsila do Cerebelo/efeitos dos fármacos
Animais
Astrócitos/efeitos dos fármacos
Medo/efeitos dos fármacos
Medo/psicologia
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Rede Nervosa/citologia
Rede Nervosa/efeitos dos fármacos
Técnicas de Cultura de Órgãos
Receptor A2A de Adenosina/fisiologia
Sinapses/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adenosine A2 Receptor Antagonists); 0 (Receptor, Adenosine A2A); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE
[do] DOI:10.1038/nn.4649


  2 / 2627 MEDLINE  
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[PMID]:28559374
[Au] Autor:Sullivan SJ; Farrant M; Cull-Candy SG
[Ad] Endereço:Department of Neuroscience, Physiology and Pharmacology, University College London, London WC1E 6BT, United Kingdom.
[Ti] Título:TARP γ-2 Is Required for Inflammation-Associated AMPA Receptor Plasticity within Lamina II of the Spinal Cord Dorsal Horn.
[So] Source:J Neurosci;37(25):6007-6020, 2017 Jun 21.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the brain, transmembrane AMPAR regulatory proteins (TARPs) critically influence the distribution, gating, and pharmacology of AMPARs, but the contribution of these auxiliary subunits to AMPAR-mediated signaling in the spinal cord remains unclear. We found that the Type I TARP γ-2 (stargazin) is present in lamina II of the superficial dorsal horn, an area involved in nociception. Consistent with the notion that γ-2 is associated with surface AMPARs, CNQX, a partial agonist at AMPARs associated with Type I TARPs, evoked whole-cell currents in lamina II neurons, but such currents were severely attenuated in γ-2-lacking ( ) mice. Examination of EPSCs revealed the targeting of γ-2 to be synapse-specific; the amplitude of spontaneously occurring miniature EPSCs (mEPSCs) was reduced in neurons from mice, but the amplitude of capsaicin-induced mEPSCs from C-fiber synapses was unaltered. This suggests that γ-2 is associated with AMPARs at synapses in lamina II but excluded from those at C-fiber inputs, a view supported by our immunohistochemical colabeling data. Following induction of peripheral inflammation, a model of hyperalgesia, there was a switch in the current-voltage relationships of capsaicin-induced mEPSCs, from linear to inwardly rectifying, indicating an increased prevalence of calcium-permeable (CP) AMPARs. This effect was abolished in mice. Our results establish that, although γ-2 is not typically associated with calcium-impermeable AMPARs at C-fiber synapses, it is required for the translocation of CP-AMPARs to these synapses following peripheral inflammation. In the brain, transmembrane AMPAR regulatory proteins (TARPs) critically determine the functional properties of AMPARs, but the contribution of these auxiliary subunits to AMPAR-mediated signaling in the spinal cord remains unclear. An increase in the excitability of neurons within the superficial dorsal horn (SDH) of the spinal cord is thought to underlie heighted pain sensitivity. One mechanism considered to contribute to such long-lived changes is the remodeling of the ionotropic AMPA-type glutamate receptors that underlie fast excitatory synaptic transmission in the SDH. Here we show that the TARP γ-2 (stargazin) is present in SDH neurons and is necessary in a form of inflammatory pain-induced plasticity, which involves an increase in the prevalence of synaptic calcium-permeable AMPARs.
[Mh] Termos MeSH primário: Canais de Cálcio/metabolismo
Inflamação/metabolismo
Plasticidade Neuronal/fisiologia
Células do Corno Posterior/metabolismo
Receptores de AMPA/fisiologia
[Mh] Termos MeSH secundário: 6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Animais
Canais de Cálcio/genética
Capsaicina/farmacologia
Agonistas de Aminoácidos Excitatórios/farmacologia
Potenciais Pós-Sinápticos Excitadores/fisiologia
Feminino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Fibras Nervosas Amielínicas/efeitos dos fármacos
Doenças do Sistema Nervoso Periférico/genética
Doenças do Sistema Nervoso Periférico/metabolismo
Receptores de AMPA/agonistas
Transmissão Sináptica/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cacng2 protein, mouse); 0 (Calcium Channels); 0 (Excitatory Amino Acid Agonists); 0 (Receptors, AMPA); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione); S07O44R1ZM (Capsaicin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170601
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0772-16.2017


  3 / 2627 MEDLINE  
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[PMID]:28413822
[Au] Autor:Wang X; Hong H; Brown DH; Sanchez JT; Wang Y
[Ad] Endereço:Department of Biomedical Sciences, Florida State University College of Medicine, Tallahassee, FL 32306.
[Ti] Título:Distinct Neural Properties in the Low-Frequency Region of the Chicken Cochlear Nucleus Magnocellularis.
[So] Source:eNeuro;4(2), 2017 Mar-Apr.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Topography in the avian cochlear nucleus magnocellularis (NM) is represented as gradually increasing characteristic frequency (CF) along the caudolateral-to-rostromedial axis. In this study, we characterized the organization and cell biophysics of the caudolateral NM (NMc) in chickens ( ). Examination of cellular and dendritic architecture first revealed that NMc contains small neurons and extensive dendritic processes, in contrast to adendritic, large neurons located more rostromedially. Individual dye-filling study further demonstrated that NMc is divided into two subregions, with NMc2 neurons having larger and more complex dendritic fields than NMc1. Axonal tract tracing studies confirmed that NMc1 and NMc2 neurons receive afferent inputs from the auditory nerve and the superior olivary nucleus, similar to the adendritic NM. However, the auditory axons synapse with NMc neurons via small bouton-like terminals, unlike the large end bulb synapses on adendritic NM neurons. Immunocytochemistry demonstrated that most NMc2 neurons express cholecystokinin but not calretinin, distinct from NMc1 and adendritic NM neurons that are cholecystokinin negative and mostly calretinin positive. Finally, whole-cell current clamp recordings revealed that NMc neurons require significantly lower threshold current for action potential generation than adendritic NM neurons. Moreover, in contrast to adendritic NM neurons that generate a single-onset action potential, NMc neurons generate multiple action potentials to suprathreshold sustained depolarization. Taken together, our data indicate that NMc contains multiple neuron types that are structurally, connectively, molecularly, and physiologically different from traditionally defined NM neurons, emphasizing specialized neural properties for processing low-frequency sounds.
[Mh] Termos MeSH primário: Vias Auditivas/fisiologia
Núcleo Coclear/citologia
Neurônios/citologia
Neurônios/fisiologia
[Mh] Termos MeSH secundário: 2-Amino-5-fosfonovalerato/farmacologia
6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Animais
Animais Recém-Nascidos
Calbindina 2/metabolismo
Embrião de Galinha
Galinhas
Colecistocinina/metabolismo
Núcleo Coclear/embriologia
Núcleo Coclear/crescimento & desenvolvimento
Dendritos/fisiologia
Antagonistas de Aminoácidos Excitatórios/farmacologia
Feminino
Antagonistas GABAérgicos/farmacologia
Imagem Tridimensional
Técnicas In Vitro
Masculino
Potenciais da Membrana/efeitos dos fármacos
Potenciais da Membrana/fisiologia
Proteínas Associadas aos Microtúbulos/metabolismo
Parvalbuminas/metabolismo
Técnicas de Patch-Clamp
Picrotoxina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calbindin 2); 0 (Excitatory Amino Acid Antagonists); 0 (GABA Antagonists); 0 (Microtubule-Associated Proteins); 0 (Parvalbumins); 124-87-8 (Picrotoxin); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione); 76726-92-6 (2-Amino-5-phosphonovalerate); 9011-97-6 (Cholecystokinin)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170418
[St] Status:MEDLINE


  4 / 2627 MEDLINE  
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[PMID]:28408325
[Au] Autor:Valtcheva S; Paillé V; Dembitskaya Y; Perez S; Gangarossa G; Fino E; Venance L
[Ad] Endereço:Dynamics and Pathophysiology of Neuronal Networks Team, Center for Interdisciplinary Research in Biology, Collège de France, CNRS UMR7241/INSERM U1050, MemoLife Labex Paris, France.
[Ti] Título:Developmental control of spike-timing-dependent plasticity by tonic GABAergic signaling in striatum.
[So] Source:Neuropharmacology;121:261-277, 2017 Jul 15.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Activity-dependent long-term potentiation (LTP) and depression (LTD) of synaptic strength underlie multiple forms of learning and memory. Spike-timing-dependent plasticity (STDP) has been described as a Hebbian synaptic learning rule that could account for experience-dependent changes in neural networks, but little is known about whether and how STDP evolves during development. We previously showed that GABAergic signaling governs STDP polarity and thus operates as a Hebbian/anti-Hebbian switch in the striatum. Although GABAergic networks are subject to important developmental maturation, it remains unclear whether STDP is developmentally shaped by GABAergic signaling. Here, we investigated whether STDP rules are developmentally regulated at corticostriatal synapses in the dorsolateral striatum. We found that striatal STDP displays unidirectional plasticity (Hebbian tLTD) in young rats (P ) whereas STDP is bidirectional and anti-Hebbian in juvenile (P ) and adult (P ) rats. We also provide evidence that the appearance of tonic (extrasynaptic) GABAergic signaling from the juvenile stage is a crucial factor in shaping STDP rules during development, establishing bidirectional anti-Hebbian STDP in the adult striatum. Thus, developmental maturation of GABAergic signaling tightly drives the polarity of striatal plasticity.
[Mh] Termos MeSH primário: Potenciais de Ação/fisiologia
Corpo Estriado/citologia
Corpo Estriado/crescimento & desenvolvimento
Neurônios GABAérgicos/fisiologia
Potenciação de Longa Duração/fisiologia
Depressão Sináptica de Longo Prazo/fisiologia
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: 2-Amino-5-fosfonovalerato/farmacologia
6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Fatores Etários
Animais
Animais Recém-Nascidos
Biofísica
Estimulação Elétrica
Antagonistas de Aminoácidos Excitatórios/farmacologia
Antagonistas GABAérgicos/farmacologia
Técnicas In Vitro
Técnicas de Patch-Clamp
Picrotoxina/farmacologia
Ratos
Ácido gama-Aminobutírico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Excitatory Amino Acid Antagonists); 0 (GABA Antagonists); 124-87-8 (Picrotoxin); 56-12-2 (gamma-Aminobutyric Acid); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione); 76726-92-6 (2-Amino-5-phosphonovalerate)
[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:170415
[St] Status:MEDLINE


  5 / 2627 MEDLINE  
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[PMID]:28350885
[Au] Autor:Iwakura Y; Wang R; Inamura N; Araki K; Higashiyama S; Takei N; Nawa H
[Ad] Endereço:Department of Molecular Neurobiology, Brain Research Institute, Niigata University, Niigata, Japan.
[Ti] Título:Glutamate-dependent ectodomain shedding of neuregulin-1 type II precursors in rat forebrain neurons.
[So] Source:PLoS One;12(3):e0174780, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The neurotrophic factor neuregulin 1 (NRG1) regulates neuronal development, glial differentiation, and excitatory synapse maturation. NRG1 is synthesized as a membrane-anchored precursor and is then liberated by proteolytic processing or exocytosis. Mature NRG1 then binds to its receptors expressed by neighboring neurons or glial cells. However, the molecular mechanisms that govern this process in the nervous system are not defined in detail. Here we prepared neuron-enriched and glia-enriched cultures from embryonic rat neocortex to investigate the role of neurotransmitters that regulate the liberation/release of NRG1 from the membrane of neurons or glial cells. Using a two-site enzyme immunoassay to detect soluble NRG1, we show that, of various neurotransmitters, glutamate was the most potent inducer of NRG1 release in neuron-enriched cultures. NRG1 release in glia-enriched cultures was relatively limited. Furthermore, among glutamate receptor agonists, N-Methyl-D-Aspartate (NMDA) and kainate (KA), but not AMPA or tACPD, mimicked the effects of glutamate. Similar findings were acquired from analysis of the hippocampus of rats with KA-induced seizures. To evaluate the contribution of members of a disintegrin and metalloproteinase (ADAM) families to NRG1 release, we transfected primary cultures of neurons with cDNA vectors encoding NRG1 types I, II, or III precursors, each tagged with the alkaline phosphatase reporter. Analysis of alkaline phosphatase activity revealed that the NRG1 type II precursor was subjected to tumor necrosis factor-α-converting enzyme (TACE) / a Disintegrin And Metalloproteinase 17 (ADAM17) -dependent ectodomain shedding in a protein kinase C-dependent manner. These results suggest that glutamatergic neurotransmission positively regulates the ectodomain shedding of NRG1 type II precursors and liberates the active NRG1 domain in an activity-dependent manner.
[Mh] Termos MeSH primário: Glutamatos/farmacologia
Neuregulina-1/metabolismo
Neurônios/efeitos dos fármacos
Precursores de Proteínas/metabolismo
[Mh] Termos MeSH secundário: 6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Proteína ADAM17/metabolismo
Acetilcolina/farmacologia
Animais
Western Blotting
Membrana Celular/efeitos dos fármacos
Membrana Celular/metabolismo
Células Cultivadas
Dipeptídeos/farmacologia
Relação Dose-Resposta a Droga
Ensaio de Imunoadsorção Enzimática
Ácido Caínico/farmacologia
N-Metilaspartato/farmacologia
Neurônios/metabolismo
Prosencéfalo/citologia
Proteína Quinase C/metabolismo
Proteólise/efeitos dos fármacos
Ratos Sprague-Dawley
Serotonina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dipeptides); 0 (Glutamates); 0 (N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide); 0 (Neuregulin-1); 0 (Protein Precursors); 333DO1RDJY (Serotonin); 6384-92-5 (N-Methylaspartate); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione); EC 2.7.11.13 (Protein Kinase C); EC 3.4.24.86 (ADAM17 Protein); N9YNS0M02X (Acetylcholine); SIV03811UC (Kainic Acid)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170831
[Lr] Data última revisão:
170831
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170329
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174780


  6 / 2627 MEDLINE  
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[PMID]:28250271
[Au] Autor:Ishida K; Kotake Y; Sanoh S; Ohta S
[Ad] Endereço:Graduate School of Biomedical and Health Sciences, Hiroshima University.
[Ti] Título:Lead-Induced ERK Activation Is Mediated by GluR2 Non-containing AMPA Receptor in Cortical Neurons.
[So] Source:Biol Pharm Bull;40(3):303-309, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Lead is a persistent environmental pollutant and exposure to high environmental levels causes various deleterious toxicities, especially to the central nervous system (CNS). The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor that is devoid of the glutamate receptor 2 (GluR2) subunit is Ca -permeable, which increases the neuronal vulnerability to excitotoxicity. We have previously reported that long-term exposure of rat cortical neurons to lead acetate induces decrease of GluR2 expression. However, it is not clarified whether lead-induced GluR2 decrease is involved in neurotoxicity. Therefore, we investigated the contribution of GluR2 non-containing AMPA receptor to lead-induced neurotoxic events. Although the expression of four AMPA receptor subunits (GluR1, GluR2, GluR3, and GluR4) was decreased by lead exposure, the decrease in GluR2 expression was remarkable among four subunits. Lead-induced neuronal cell death was rescued by three glutamate receptor antagonists, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, a non-selective AMPA receptor blocker), MK-801 (N-methyl-D-aspartate (NMDA) receptor blocker), and 1-naphthyl acetyl spermine (NAS, a specific Ca -permeable AMPA receptor blocker). Lead exposure activated extracellular signal-regulated protein kinase (ERK) 1/2, which was significantly ameliorated by CNQX. In addition, lead exposure activated p38 mitogen-activated protein kinase (MAPK p38), and protein kinase C (PKC), which was partially ameliorated by CNQX. Our findings indicate that Ca -permeable AMPA receptors resulting from GluR2 decrease may be involved in lead-induced neurotoxicity.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Ácido Glutâmico/metabolismo
Intoxicação do Sistema Nervoso por Chumbo/metabolismo
Chumbo/efeitos adversos
Receptores de AMPA/metabolismo
Ácido alfa-Amino-3-hidroxi-5-metil-4-isoxazol Propiônico/metabolismo
[Mh] Termos MeSH secundário: 6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Animais
Encéfalo/citologia
Cálcio/metabolismo
Células Cultivadas
Poluentes Ambientais/efeitos adversos
Antagonistas de Aminoácidos Excitatórios/farmacologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Proteína Quinase C/metabolismo
Subunidades Proteicas
Ratos
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Environmental Pollutants); 0 (Excitatory Amino Acid Antagonists); 0 (Protein Subunits); 0 (Receptors, AMPA); 0 (glutamate receptor ionotropic, AMPA 2); 2P299V784P (Lead); 3KX376GY7L (Glutamic Acid); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione); 77521-29-0 (alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid); EC 2.7.11.13 (Protein Kinase C); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170328
[Lr] Data última revisão:
170328
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-00784


  7 / 2627 MEDLINE  
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[PMID]:28161374
[Au] Autor:Ramírez-Jarquín UN; Tapia R
[Ad] Endereço:División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, 04510 Ciudad de México, Mexico.
[Ti] Título:Chronic GABAergic blockade in the spinal cord in vivo induces motor alterations and neurodegeneration.
[So] Source:Neuropharmacology;117:85-92, 2017 May 01.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Inhibitory GABAergic and glycinergic neurotransmission in the spinal cord play a central role in the regulation of neuronal excitability, by maintaining a balance with the glutamate-mediated excitatory transmission. Glutamatergic agonists infusion in the spinal cord induce motor neuron death by excitotoxicity, leading to motor deficits and paralysis, but little is known on the effect of the blockade of inhibitory transmission. In this work we studied the effects of GABAergic and glycinergic blockade, by means of microdialysis perfusion (acute administration) and osmotic minipumps infusion (chronic administration) of GABA and glycine receptors antagonists directly in the lumbar spinal cord. We show that acute glycinergic blockade with strychnine or GABAergic blockade with bicuculline had no significant effects on motor activity and on motor neuron survival. However, chronic bicuculline infusion, but not strychnine, induced ipsilateral gait alterations, phalange flaccidity and significant motor neuron loss, and these effects were prevented by AMPA receptor blockade with CNQX but not by NMDA receptor blockade with MK801. In addition, we demonstrate that the chronic infusion of bicuculline enhanced the excitotoxic effect of AMPA, causing faster bilateral paralysis and increasing motor neuron loss. These findings indicate a relevant role of GABAergic inhibitory circuits in the regulation of motor neuron excitability and suggest that their alterations may be involved in the neurodegeneration processes characteristic of motor neuron diseases such as amyotrophic lateral sclerosis.
[Mh] Termos MeSH primário: Bicuculina/toxicidade
Antagonistas GABAérgicos/toxicidade
Atividade Motora/efeitos dos fármacos
Neurônios Motores/efeitos dos fármacos
Degeneração Neural/induzido quimicamente
Medula Espinal/efeitos dos fármacos
Estricnina/toxicidade
[Mh] Termos MeSH secundário: 6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Animais
Atrofia/induzido quimicamente
Bicuculina/antagonistas & inibidores
Maleato de Dizocilpina/farmacologia
Interações Medicamentosas
Marcha/efeitos dos fármacos
Masculino
Hipotonia Muscular/induzido quimicamente
Ratos
Receptores da Glicina/antagonistas & inibidores
Estricnina/antagonistas & inibidores
Ácido alfa-Amino-3-hidroxi-5-metil-4-isoxazol Propiônico/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA Antagonists); 0 (Receptors, Glycine); 6LR8C1B66Q (Dizocilpine Maleate); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione); 77521-29-0 (alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid); H9Y79VD43J (Strychnine); Y37615DVKC (Bicuculline)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170206
[St] Status:MEDLINE


  8 / 2627 MEDLINE  
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[PMID]:28077663
[Au] Autor:Stüttgen MC; Nonkes LJP; Geis HRAP; Tiesinga PH; Houweling AR
[Ad] Endereço:Department of Neuroscience, Erasmus University Medical Center, Rotterdam, The Netherlands; maik.stuettgen@uni-mainz.de.
[Ti] Título:Temporally precise control of single-neuron spiking by juxtacellular nanostimulation.
[So] Source:J Neurophysiol;117(3):1363-1378, 2017 Mar 01.
[Is] ISSN:1522-1598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Temporal patterns of action potentials influence a variety of activity-dependent intra- and intercellular processes and play an important role in theories of neural coding. Elucidating the mechanisms underlying these phenomena requires imposing spike trains with precisely defined patterns, but this has been challenging due to the limitations of existing stimulation techniques. Here we present a new nanostimulation method providing control over the action potential output of individual cortical neurons. Spikes are elicited through the juxtacellular application of short-duration fluctuating currents ("kurzpulses"), allowing for the sub-millisecond precise and reproducible induction of arbitrary patterns of action potentials at all physiologically relevant firing frequencies (<120 Hz), including minute-long spike trains recorded in freely moving animals. We systematically compared our method to whole cell current injection, as well as optogenetic stimulation, and show that nanostimulation performance compares favorably with these techniques. This new nanostimulation approach is easily applied, can be readily performed in awake behaving animals, and thus promises to be a powerful tool for systematic investigations into the temporal elements of neural codes, as well as the mechanisms underlying a wide variety of activity-dependent cellular processes. Assessing the impact of temporal features of neuronal spike trains requires imposing arbitrary patterns of spiking on individual neurons during behavior, but this has been difficult to achieve due to limitations of existing stimulation methods. We present a technique that overcomes these limitations by using carefully designed short-duration fluctuating juxtacellular current injections, which allow for the precise and reliable evocation of arbitrary patterns of neuronal spikes in single neurons in vivo.
[Mh] Termos MeSH primário: Potenciais de Ação/fisiologia
Modelos Neurológicos
Neurônios/fisiologia
Córtex Somatossensorial/citologia
[Mh] Termos MeSH secundário: 6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Potenciais de Ação/efeitos dos fármacos
Animais
Biofísica
Proteínas do Citoesqueleto/genética
Proteínas do Citoesqueleto/metabolismo
Estimulação Elétrica
Antagonistas de Aminoácidos Excitatórios/farmacologia
Feminino
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Masculino
Camundongos
Camundongos Transgênicos
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Neurônios/efeitos dos fármacos
Optogenética
Técnicas de Patch-Clamp
Sinapsinas/genética
Sinapsinas/metabolismo
Fatores de Tempo
Valina/análogos & derivados
Valina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytoskeletal Proteins); 0 (Excitatory Amino Acid Antagonists); 0 (Luminescent Proteins); 0 (Nerve Tissue Proteins); 0 (Synapsins); 0 (activity regulated cytoskeletal-associated protein); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione); 76326-31-3 (2-amino-5-phosphopentanoic acid); HG18B9YRS7 (Valine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170113
[St] Status:MEDLINE
[do] DOI:10.1152/jn.00479.2016


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[PMID]:28073939
[Au] Autor:Pennacchietti F; Vascon S; Nieus T; Rosillo C; Das S; Tyagarajan SK; Diaspro A; Del Bue A; Petrini EM; Barberis A; Cella Zanacchi F
[Ad] Endereço:Nanoscopy Department.
[Ti] Título:Nanoscale Molecular Reorganization of the Inhibitory Postsynaptic Density Is a Determinant of GABAergic Synaptic Potentiation.
[So] Source:J Neurosci;37(7):1747-1756, 2017 Feb 15.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gephyrin is a key scaffold protein mediating the anchoring of GABAA receptors at inhibitory synapses. Here, we exploited superresolution techniques combined with proximity-based clustering analysis and model simulations to investigate the single-molecule gephyrin reorganization during plasticity of inhibitory synapses in mouse hippocampal cultured neurons. This approach revealed that, during the expression of inhibitory LTP, the increase of gephyrin density at postsynaptic sites is associated with the promoted formation of gephyrin nanodomains. We demonstrate that the gephyrin rearrangement in nanodomains stabilizes the amplitude of postsynaptic currents, indicating that, in addition to the number of synaptic GABAA receptors, the nanoscale distribution of GABAA receptors in the postsynaptic area is a crucial determinant for the expression of inhibitory synaptic plasticity. In addition, the methodology implemented here clears the way to the application of the graph-based theory to single-molecule data for the description and quantification of the spatial organization of the synapse at the single-molecule level. The mechanisms of inhibitory synaptic plasticity are poorly understood, mainly because the size of the synapse is below the diffraction limit, thus reducing the effectiveness of conventional optical and imaging techniques. Here, we exploited superresolution approaches combined with clustering analysis to study at unprecedented resolution the distribution of the inhibitory scaffold protein gephyrin in response to protocols inducing LTP of inhibitory synaptic responses (iLTP). We found that, during the expression of iLTP, the increase of synaptic gephyrin is associated with the fragmentation of gephyrin in subsynaptic nanodomains. We demonstrate that such synaptic gephyrin nanodomains stabilize the amplitude of inhibitory postsynaptic responses, thus identifying the nanoscale gephyrin rearrangement as a key determinant for inhibitory synaptic plasticity.
[Mh] Termos MeSH primário: Proteínas de Transporte/metabolismo
Neurônios GABAérgicos/citologia
Depressão Sináptica de Longo Prazo/fisiologia
Proteínas de Membrana/metabolismo
Densidade Pós-Sináptica/metabolismo
[Mh] Termos MeSH secundário: 6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Algoritmos
Animais
Células Cultivadas
Simulação por Computador
Agonistas de Aminoácidos Excitatórios/farmacologia
Antagonistas de Aminoácidos Excitatórios/farmacologia
Feminino
Neurônios GABAérgicos/efeitos dos fármacos
Hipocampo/citologia
Depressão Sináptica de Longo Prazo/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Modelos Neurológicos
N-Metilaspartato/farmacologia
Peptídeos/metabolismo
Densidade Pós-Sináptica/efeitos dos fármacos
Receptores de GABA-A/metabolismo
Valina/análogos & derivados
Valina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Excitatory Amino Acid Agonists); 0 (Excitatory Amino Acid Antagonists); 0 (Membrane Proteins); 0 (Peptides); 0 (Receptors, GABA-A); 0 (gephyrin); 31325-29-8 (GAT); 6384-92-5 (N-Methylaspartate); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione); 76326-31-3 (2-amino-5-phosphopentanoic acid); HG18B9YRS7 (Valine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170112
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0514-16.2016


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[PMID]:28041911
[Au] Autor:Chrobok L; Palus K; Jeczmien-Lazur JS; Chrzanowska A; Kepczynski M; Lewandowski MH
[Ad] Endereço:Department of Neurophysiology and Chronobiology, Institute of Zoology, Jagiellonian University in Krakow, Krakow, Poland. Electronic address: lukasz.chrobok@uj.edu.pl.
[Ti] Título:Disinhibition of the intergeniculate leaflet network in the WAG/Rij rat model of absence epilepsy.
[So] Source:Exp Neurol;289:103-116, 2017 Mar.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The intergeniculate leaflet (IGL) of the thalamus is a retinorecipient structure implicated in orchestrating circadian rhythmicity. The IGL network is highly GABAergic and consists mainly of neuropeptide Y-synthesising and enkephalinergic neurons. A high density of GFAP-immunoreactive astrocytes has been observed in the IGL, with a probable function in guarding neuronal inhibition. Interestingly, putatively enkephalinergic IGL neurons generate action potentials with an infra-slow oscillatory (ISO) pattern in vivo in urethane anesthetised Wistar rats, under light-on conditions only. Absence epilepsy (AE) is a disease characterised by spike-wave discharges present in the encephalogram, directly caused by hypersynchronous thalamo-cortical oscillations. Many pathologies connected with the arousal system, such as abnormalities in sleep architecture and an insufficient brain sleep-promoting system accompany the epileptic phenotype. We hypothesise that disturbances in the function of biological clock structures, controlling this rhythmic physiological process, may be responsible for the observed pathomechanism. To test this hypothesis, we performed an in vitro patch-clamp study on WAG/Rij rats, a well-validated genetic model of AE, in order to assess dampened GABAergic synaptic transmission in the IGL expressed as a lower IPSC amplitude and reduced sIPSC frequency. Moreover, our in vivo extracellular recordings showed higher firing rate of ISO IGL neurons with an abnormal reaction to a change in constant illumination (maintenance of rhythmic neuronal activity in darkness) in the AE model. Additional immunohistochemical experiments indicated astrogliosis in the area of the IGL, which may partially underlie the observed changes in inhibition. Altogether, the data presented here show for the first time the disinhibition of IGL neurons in a model of AE, thereby proposing the possible involvement of circadian-related brain structures in the epileptic phenotype.
[Mh] Termos MeSH primário: Epilepsia Tipo Ausência/patologia
Corpos Geniculados/patologia
Potenciais Pós-Sinápticos Inibidores/fisiologia
Rede Nervosa/patologia
Inibição Neural/fisiologia
[Mh] Termos MeSH secundário: 6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Fatores Etários
Animais
Animais Recém-Nascidos
Modelos Animais de Doenças
Epilepsia Tipo Ausência/genética
Antagonistas de Aminoácidos Excitatórios/farmacologia
GABAérgicos/farmacologia
Potenciais Pós-Sinápticos Inibidores/efeitos dos fármacos
Masculino
Inibição Neural/genética
Neuropeptídeo Y/metabolismo
Ratos
Ratos Mutantes
Ratos Wistar
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
Valina/análogos & derivados
Valina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Excitatory Amino Acid Antagonists); 0 (GABA Agents); 0 (Neuropeptide Y); 0 (Sodium Channel Blockers); 4368-28-9 (Tetrodotoxin); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione); 76326-31-3 (2-amino-5-phosphopentanoic acid); HG18B9YRS7 (Valine)
[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:170103
[St] Status:MEDLINE



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