Base de dados : MEDLINE
Pesquisa : D27.505.696.663 [Categoria DeCS]
Referências encontradas : 53 [refinar]
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[PMID]:28445756
[Au] Autor:Kanda H; Gu JG
[Ad] Endereço:Department of Anesthesiology and Perioperative Medicine, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
[Ti] Título:Membrane Mechanics of Primary Afferent Neurons in the Dorsal Root Ganglia of Rats.
[So] Source:Biophys J;112(8):1654-1662, 2017 Apr 25.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Membrane mechanics is an important biological factor regulating many cellular functions including cell motility, intercellular and intracellular signaling, gene expression, and membrane ion channel activity. Primary afferent neurons transduce sensory information about temperature, touch, and pain. These sensory functions may be profoundly affected by the states of primary afferent neuron mechanics. However, membrane mechanics of primary afferent neurons is largely unknown. In this study, we established the optical trapping technique for determining membrane mechanics of cultured primary afferent neurons of the dorsal root ganglia (DRG). We further determined the roles of cytoskeleton and membrane lipids in DRG neuron mechanics. We found that DRG neurons had a plasma membrane tension of ∼54 pN/µm, and the tension was significantly decreased to ∼29 pN/µm by cytochalasin D treatment to disrupt actin cytoskeleton and increased to ∼79 pN/µm by methyl-ß-cyclodextrin treatment to sequester membrane cholesterol. DRG neuron membrane stiffness was not significantly affected by the cytoskeleton disruption but was significantly increased after cholesterol sequestration. Our findings elucidate membrane mechanical properties of primary afferent neurons, which provide, to our knowledge, a new perspective on their sensory functions.
[Mh] Termos MeSH primário: Membrana Celular/fisiologia
Gânglios Espinais/fisiologia
Neurônios Aferentes/fisiologia
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Membrana Celular/efeitos dos fármacos
Células Cultivadas
Citocalasina D/farmacologia
Citoesqueleto/metabolismo
Elasticidade
Feminino
Gânglios Espinais/efeitos dos fármacos
Lipídeos de Membrana/metabolismo
Microscopia Eletrônica de Varredura
Neurônios Aferentes/efeitos dos fármacos
Pinças Ópticas
Fármacos do Sistema Nervoso Periférico/farmacologia
Ratos Sprague-Dawley
beta-Ciclodextrinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Membrane Lipids); 0 (Peripheral Nervous System Agents); 0 (beta-Cyclodextrins); 0 (methyl-beta-cyclodextrin); 22144-77-0 (Cytochalasin D)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE


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[PMID]:28101526
[Au] Autor:Chen W; Lu N; Ding Y; Wang Y; Chan LT; Wang X; Gao X; Jiang S; Liu K
[Ad] Endereço:Division of Life Science, State Key Laboratory of Molecular Neuroscience; Center of Systems Biology and Human Health, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong, China.
[Ti] Título:Rapamycin-Resistant mTOR Activity Is Required for Sensory Axon Regeneration Induced by a Conditioning Lesion.
[So] Source:eNeuro;3(6), 2016 Nov-Dec.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuronal mammalian target of rapamycin (mTOR) activity is a critical determinant of the intrinsic regenerative ability of mature neurons in the adult central nervous system (CNS). However, whether its action also applies to peripheral nervous system (PNS) neurons after injury remains elusive. To address this issue unambiguously, we used genetic approaches to determine the role of mTOR signaling in sensory axon regeneration in mice. We showed that deleting mTOR in dorsal root ganglion (DRG) neurons suppressed the axon regeneration induced by conditioning lesions. To establish whether the impact of mTOR on axon regeneration results from functions of mTOR complex 1 (mTORC1) or 2 (mTORC2), two distinct kinase complexes, we ablated either Raptor or Rictor in DRG neurons. We found that suppressing mTORC1 signaling dramatically decreased the conditioning lesion effect. In addition, an injury to the peripheral branch boosts mTOR activity in DRG neurons that cannot be completely inhibited by rapamycin, a widely used mTOR-specific inhibitor. Unexpectedly, examining several conditioning lesion-induced pro-regenerative pathways revealed that Raptor deletion but not rapamycin suppressed Stat3 activity in neurons. Therefore, our results demonstrate that crosstalk between mTOR and Stat3 signaling mediates the conditioning lesion effect and provide genetic evidence that rapamycin-resistant mTOR activity contributes to the intrinsic axon growth capacity in adult sensory neurons after injury.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Axônios/metabolismo
Proteínas de Transporte/metabolismo
Gânglios Espinais/metabolismo
Regeneração Nervosa/fisiologia
Células Receptoras Sensoriais/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Animais
Axônios/efeitos dos fármacos
Axônios/patologia
Proteínas de Transporte/genética
Células Cultivadas
Feminino
Gânglios Espinais/efeitos dos fármacos
Gânglios Espinais/patologia
Masculino
Alvo Mecanístico do Complexo 1 de Rapamicina
Alvo Mecanístico do Complexo 2 de Rapamicina
Camundongos Transgênicos
Complexos Multiproteicos/metabolismo
Regeneração Nervosa/efeitos dos fármacos
Fármacos do Sistema Nervoso Periférico/farmacologia
Proteína Companheira de mTOR Insensível à Rapamicina
Proteína Associada Regulatória a mTOR
Fator de Transcrição STAT3/metabolismo
Neuropatia Ciática/tratamento farmacológico
Neuropatia Ciática/metabolismo
Neuropatia Ciática/patologia
Células Receptoras Sensoriais/efeitos dos fármacos
Células Receptoras Sensoriais/patologia
Sirolimo/farmacologia
Serina-Treonina Quinases TOR/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Carrier Proteins); 0 (Multiprotein Complexes); 0 (Peripheral Nervous System Agents); 0 (Rapamycin-Insensitive Companion of mTOR Protein); 0 (Regulatory-Associated Protein of mTOR); 0 (Rptor protein, mouse); 0 (STAT3 Transcription Factor); 0 (Stat3 protein, mouse); 0 (rictor protein, mouse); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 2); W36ZG6FT64 (Sirolimus)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE


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[PMID]:27693814
[Au] Autor:Orlowska-Feuer P; Jeczmien-Lazur JS; Szkudlarek HJ; Lewandowski MH
[Ad] Endereço:Department of Neurophysiology and Chronobiology, Institute of Zoology, Jagiellonian University, Gronostajowa 9, 30-387 Krakow, Poland.
[Ti] Título:Retinal gap junctions are involved in rhythmogenesis of neuronal activity at remote locations - Study on infra-slow oscillations in the rat olivary pretectal nucleus.
[So] Source:Neuroscience;339:150-161, 2016 Dec 17.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A subpopulation of olivary pretectal nucleus (OPN) neurons fire action potentials in a rhythmic manner with an eruption of activity occurring approximately every two minutes. These infra-slow oscillations depend critically on functional retinal input and are subject to modulation by light. Interestingly, the activity of photoreceptors is necessary for the emergence of the rhythm and while classic photoreceptors (rods and cones) are necessary in darkness and dim light, melanopsin photoreceptors are indispensable in bright light. Using pharmacological and electrophysiological approaches in vivo, we show that also blocking retinal gap junctions (GJs), which are expressed by multitude of retinal cells, leads to the disruption of oscillatory activity in the rat OPN. Intravitreal injection of carbenoxolone (CBX) quenched oscillations in a concentration-dependent manner with 1mM being ineffective, 5mM showing partial and 20mM showing complete effectiveness in disrupting oscillations. Moreover, the most effective CBX concentration depressed cone-mediated light-induced responses of oscillatory neurons suggesting that CBX is also acting on targets other than GJs. In contrast, intravitreal injection of meclofenamic acid (MFA, 20mM) led to disruption of the rhythm but did not interfere with cone-mediated light-induced responses of oscillatory neurons, implying that MFA is more specific toward GJs than CBX, as suggested before. We conclude that electrical coupling between various types of retinal cells and resultant synchronous firing of retinal ganglion cells is necessary for the generation of infra-slow oscillations in the rat OPN.
[Mh] Termos MeSH primário: Junções Comunicantes/fisiologia
Periodicidade
Área Pré-Tetal/fisiologia
Retina/fisiologia
[Mh] Termos MeSH secundário: Animais
Carbenoxolona/farmacologia
Relação Dose-Resposta a Droga
Junções Comunicantes/efeitos dos fármacos
Injeções Intravítreas
Masculino
Ácido Meclofenâmico/farmacologia
Vias Neurais/efeitos dos fármacos
Vias Neurais/fisiologia
Fármacos do Sistema Nervoso Periférico/farmacologia
Ratos
Ratos Wistar
Retina/efeitos dos fármacos
Visão Ocular/efeitos dos fármacos
Visão Ocular/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peripheral Nervous System Agents); 48I5LU4ZWD (Meclofenamic Acid); MM6384NG73 (Carbenoxolone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE


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[PMID]:27306673
[Au] Autor:Turner SM; ElMallah MK; Hoyt AK; Greer JJ; Fuller DD
[Ad] Endereço:Department of Physical Therapy, College of Public Health and Health Professions, University of Florida, Gainesville, Florida; McKnight Brain Institute, University of Florida, Gainesville, Florida; and Center for Respiratory Research and Rehabilitation, University of Florida, Gainesville, Florida.
[Ti] Título:Ampakine CX717 potentiates intermittent hypoxia-induced hypoglossal long-term facilitation.
[So] Source:J Neurophysiol;116(3):1232-8, 2016 Sep 01.
[Is] ISSN:1522-1598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glutamatergic currents play a fundamental role in regulating respiratory motor output and are partially mediated by α-amino-3-hydroxy-5-methyl-isoxazole-propionic acid (AMPA) receptors throughout the premotor and motor respiratory circuitry. Ampakines are pharmacological compounds that enhance glutamatergic transmission by altering AMPA receptor channel kinetics. Here, we examined if ampakines alter the expression of respiratory long-term facilitation (LTF), a form of neuroplasticity manifested as a persistent increase in inspiratory activity following brief periods of reduced O2 [intermittent hypoxia (IH)]. Current synaptic models indicate enhanced effectiveness of glutamatergic synapses after IH, and we hypothesized that ampakine pretreatment would potentiate IH-induced LTF of respiratory activity. Inspiratory bursting was recorded from the hypoglossal nerve of anesthetized and mechanically ventilated mice. During baseline (BL) recording conditions, burst amplitude was stable for at least 90 min (98 ± 5% BL). Exposure to IH (3 × 1 min, 15% O2) resulted in a sustained increase in burst amplitude (218 ± 44% BL at 90 min following final bout of hypoxia). Mice given an intraperitoneal injection of ampakine CX717 (15 mg/kg) 10 min before IH showed enhanced LTF (500 ± 110% BL at 90 min). Post hoc analyses indicated that CX717 potentiated LTF only when initial baseline burst amplitude was low. We conclude that under appropriate conditions ampakine pretreatment can potentiate IH-induced respiratory LTF. These data suggest that ampakines may have therapeutic value in the context of hypoxia-based neurorehabilitation strategies, particularly in disorders with blunted respiratory motor output such as spinal cord injury.
[Mh] Termos MeSH primário: Nervo Hipoglosso/efeitos dos fármacos
Hipóxia/fisiopatologia
Isoxazóis/farmacologia
Potenciação de Longa Duração/efeitos dos fármacos
Fármacos do Sistema Nervoso Periférico/farmacologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Potenciais de Ação/fisiologia
Animais
Nervo Hipoglosso/fisiopatologia
Potenciação de Longa Duração/fisiologia
Masculino
Camundongos da Linhagem 129
Modelos Animais
Reabilitação Neurológica
Respiração
Respiração Artificial
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CX717); 0 (Isoxazoles); 0 (Peripheral Nervous System Agents)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160617
[St] Status:MEDLINE
[do] DOI:10.1152/jn.00210.2016


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[PMID]:26955781
[Au] Autor:Tello Velasquez J; Nazareth L; Quinn RJ; Ekberg JA; St John JA
[Ad] Endereço:Eskitis Institute for Drug Discovery, Griffith University, Brisbane, Australia.
[Ti] Título:Stimulating the proliferation, migration and lamellipodia of Schwann cells using low-dose curcumin.
[So] Source:Neuroscience;324:140-50, 2016 Jun 02.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transplantation of peripheral glia is being trialled for neural repair therapies, and identification of compounds that enhance the activity of glia is therefore of therapeutic interest. We have previously shown that curcumin potently stimulates the activity of olfactory glia. We have now examined the effect of curcumin on Schwann cell (SC) activities including proliferation, migration and the expression of protein markers. SCs were treated with control media and with different concentrations of curcumin (0.02-20 µM). Cell proliferation was determined by MTS assay and migration changes were determined by single live cell migration tracking. We found that small doses of curcumin (40 nM) dramatically increased the proliferation and migration in SCs within just one day. When compared with olfactory glia, curcumin stimulated SC proliferation more rapidly and at lower concentrations. Curcumin significantly increased the migration of SCs, and also increased the dynamic activity of lamellipodial waves which are essential for SC migration. Expression of the activated form of the MAP kinase p38 (p-p38) was significantly decreased in curcumin-treated SCs. These results show that curcumin's effects on SCs differ remarkably to its effects on olfactory glia, suggesting that subtypes of closely related glia can be differentially stimulated by curcumin. Overall these results demonstrate that the therapeutically beneficial activities of glia can be differentially enhanced by curcumin which could be used to improve outcomes of neural repair therapies.
[Mh] Termos MeSH primário: Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Curcumina/farmacologia
Fármacos do Sistema Nervoso Periférico/farmacologia
Pseudópodes/efeitos dos fármacos
Células de Schwann/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Movimento Celular/fisiologia
Proliferação Celular/fisiologia
Células Cultivadas
Gânglios Espinais/citologia
Gânglios Espinais/efeitos dos fármacos
Gânglios Espinais/fisiologia
Camundongos Transgênicos
Proteína Quinase 1 Ativada por Mitógeno/antagonistas & inibidores
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/antagonistas & inibidores
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Fagocitose/efeitos dos fármacos
Fagocitose/fisiologia
Pseudópodes/fisiologia
Células de Schwann/citologia
Células de Schwann/fisiologia
Medula Espinal/citologia
Medula Espinal/efeitos dos fármacos
Medula Espinal/fisiologia
Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Peripheral Nervous System Agents); EC 2.7.11.24 (Mapk1 protein, mouse); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170111
[Lr] Data última revisão:
170111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160310
[St] Status:MEDLINE


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[PMID]:26840837
[Au] Autor:Dhingra RR; Dutschmann M; Dick TE
[Ad] Endereço:Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, USA; Department of Neurosciences, Case Western Reserve University, Cleveland, OH, USA.
[Ti] Título:Blockade of dorsolateral pontine 5HT1A receptors destabilizes the respiratory rhythm in C57BL6/J wild-type mice.
[So] Source:Respir Physiol Neurobiol;226:110-4, 2016 Jun.
[Is] ISSN:1878-1519
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The neurotransmitter serotonin (5HT) acting via 5HT1a receptors (5HT1aR) is a potent determinant of respiratory rhythm variability. Here, we address the 5HT1aR-dependent control of respiratory rhythm variability in C57BL6/J mice. Using the in situ perfused preparation, we compared the effects of systemic versus focal blockade of 5HT1aRs. Blocking 5HT1aRs in the Kölliker-Fuse nucleus (KFn) increased the occurrence of spontaneous apneas and accounted for the systemic effects of 5HT1aR antagonists. Further, 5HT1aRs of the KFn stabilized the respiratory rhythm's response to arterial chemoreflex perturbations; reducing the recovering time, e.g., the latency to return to the baseline pattern. Together, these results suggest that the KFn regulates both intrinsic and sensory determinants of respiratory rhythm variability.
[Mh] Termos MeSH primário: Cicloexanos/farmacologia
Núcleo de Kölliker-Fuse/efeitos dos fármacos
Núcleo de Kölliker-Fuse/metabolismo
Piperazinas/farmacologia
Receptor 5-HT1A de Serotonina/metabolismo
Respiração/efeitos dos fármacos
Antagonistas do Receptor 5-HT1 de Serotonina/farmacologia
[Mh] Termos MeSH secundário: Animais
Apneia/induzido quimicamente
Apneia/metabolismo
Células Quimiorreceptoras/efeitos dos fármacos
Células Quimiorreceptoras/fisiologia
Feminino
Potenciais da Membrana/efeitos dos fármacos
Camundongos da Linhagem 129
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Fármacos do Sistema Nervoso Periférico/farmacologia
Nervo Frênico/efeitos dos fármacos
Nervo Frênico/fisiologia
Reflexo/efeitos dos fármacos
Reflexo/fisiologia
Cianeto de Sódio/farmacologia
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclohexanes); 0 (Peripheral Nervous System Agents); 0 (Piperazines); 0 (Serotonin 5-HT1 Receptor Antagonists); 0 (WAY 101363); 112692-38-3 (Receptor, Serotonin, 5-HT1A); O5DDB9Z95G (Sodium Cyanide)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160204
[St] Status:MEDLINE


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[PMID]:26254869
[Au] Autor:Bautista TG; Dutschmann M
[Ad] Endereço:Systems Neurophysiology division, Florey Institute of Neuroscience and Mental Health, Gate 11 Royal Parade, University of Melbourne, VIC 3010, Australia. Electronic address: tara.bautista@florey.edu.au.
[Ti] Título:The role of the Kölliker-Fuse nuclei in the determination of abdominal motor output in a perfused brainstem preparation of juvenile rat.
[So] Source:Respir Physiol Neurobiol;226:102-9, 2016 Jun.
[Is] ISSN:1878-1519
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The abdominal muscles are largely quiescent during normal breathing but may exhibit tonic activity or subtle respiratory modulation. The origin of baseline abdominal motor nerve activity (AbNA) if present remains uncharacterised. The contribution of the Kölliker-Fuse nucleus (KF) in the dorsolateral pons in the patterning and amplitude of AbNA was investigated using in situ perfused brainstem preparations of juvenile rats (n=12). Two types of AbNA were observed: Type I - expiratory-modulated (n=7), and Type II - weakly inspiratory/post-inspiratory-modulated (n=5). Despite this, all preparations exhibited the same bi-phasic late expiratory/postinspiratory bursts upon elicitation of the peripheral chemoreflex. Interestingly, the type of AbNA exhibited correlated with postinspiratory duration. Targeted microinjections of GABA-A receptor agonist isoguvacine (10mM; 70nl) into KF however did not significantly modify pattern or amplitude of baseline AbNA in either Type besides the selective abolition of the postinspiratory phase and, consequently, postinspiratory modulation in AbNAwhen present. In sum, the KF is not a major contributorin setting baseline abdominal motor output.
[Mh] Termos MeSH primário: Abdome/fisiologia
Núcleo de Kölliker-Fuse/fisiologia
Movimento/fisiologia
Respiração
[Mh] Termos MeSH secundário: Abdome/inervação
Animais
Animais Recém-Nascidos
Geradores de Padrão Central/efeitos dos fármacos
Geradores de Padrão Central/fisiologia
Células Quimiorreceptoras/efeitos dos fármacos
Células Quimiorreceptoras/fisiologia
Agonistas de Receptores de GABA-A/farmacologia
Ácidos Isonicotínicos/farmacologia
Núcleo de Kölliker-Fuse/efeitos dos fármacos
Potenciais da Membrana/efeitos dos fármacos
Fármacos do Sistema Nervoso Periférico/farmacologia
Nervo Frênico/fisiologia
Ratos Sprague-Dawley
Receptores de GABA-A/metabolismo
Respiração/efeitos dos fármacos
Músculos Respiratórios/fisiologia
Cianeto de Sódio/farmacologia
Taquipneia/fisiopatologia
Técnicas de Cultura de Tecidos
Nervo Vago/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (GABA-A Receptor Agonists); 0 (Isonicotinic Acids); 0 (Peripheral Nervous System Agents); 0 (Receptors, GABA-A); O5DDB9Z95G (Sodium Cyanide); YTF580771Y (isoguvacine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170724
[Lr] Data última revisão:
170724
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150810
[St] Status:MEDLINE


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[PMID]:25797812
[Au] Autor:Kim H; W Caspar T; Shah SB; Hsieh AH
[Ad] Endereço:Fischell Department of Bioengineering, University of Maryland, College Park, Jeong H. Kim Engineering Building, College Park, MD 20742, USA.
[Ti] Título:Effects of proinflammatory cytokines on axonal outgrowth from adult rat lumbar dorsal root ganglia using a novel three-dimensional culture system.
[So] Source:Spine J;15(8):1823-31, 2015 Aug 01.
[Is] ISSN:1878-1632
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND CONTEXT: Degeneration of the intervertebral disc is often associated with low back pain and increased infiltration of nerve fibers originating from dorsal root ganglia (DRG). The degenerated disc is also characterized by the presence of proinflammatory cytokines, which may influence axonal outgrowth. Toward an improved understanding of the growth of DRG neurons into compliant extracellular matrices, we developed a novel experimental system to measure axonal outgrowth of adult rat lumbar DRG neurons within three-dimensional (3D) collagen hydrogels and used this system to examine the effects of interleukin 1ß (IL-1ß) and tumor necrosis factor (TNF)-α treatment. PURPOSE: The aim was to investigate the effects of proinflammatory cytokines on 3D neuronal growth into collagen matrices. STUDY DESIGN: This was an in vitro study of neurite outgrowth from adult rat lumbar DRG into collagen gels in response to IL-1ß and TNF-α. METHODS: Lumbar DRG were obtained from adult Sprague Dawley rats, bisected to expose cell bodies and placed onto collagen gel constructs prepared in 24-well Transwell inserts. Dorsal root ganglia were then treated with nerve growth factor (NGF)-free Neurobasal media (negative control) or NGF-supplemented media containing 0, 1, and 10 ng/mL of IL-1ß and TNF-α. After 7 days, collagen gel-DRG constructs were immunostained for phosphorylated neurofilament, an axonal marker. Simple Neurite Tracer (Fiji/ImageJ) was used to quantify 3D axonal outgrowth from confocal image stacks. Data were analyzed using one-way analysis of variance, with Tukey HSD post hoc correction at a level of p<.05. RESULTS: Immunostaining showed robust axonal outgrowth into collagen gels from all NGF-treated DRG. The negative control demonstrated very few and short neurites. Tumor necrosis factor-α (1 and 10 ng/mL) significantly inhibited axonal outgrowth compared with NGF-only media (p<.026 and p<.02, respectively). After IL-1ß treatment, average axon length was 10% lower at 1 ng/mL and 7.5% higher at 10 ng/mL, but these differences were not statistically significant. Among cytokine treatments, however, average axon length in the IL-1ß (10 ng/mL) group was significantly higher than that in the other groups (p<.05). CONCLUSIONS: A novel 3D collagen gel culture system was used to investigate factors modulating neuronal ingrowth. Our results showed that NGF was necessary to promote neurite growth into collagen gels. In the presence of proinflammatory cytokines, high concentrations of IL-1ß induced significantly higher axonal outgrowth than TNF-α and low levels of IL-1ß.
[Mh] Termos MeSH primário: Citocinas/farmacologia
Gânglios Espinais/efeitos dos fármacos
Interleucina-1beta/farmacologia
Fator de Crescimento Neural/farmacologia
Neuritos/efeitos dos fármacos
Fator de Necrose Tumoral alfa/farmacologia
[Mh] Termos MeSH secundário: Animais
Axônios/efeitos dos fármacos
Técnicas de Cultura de Células
Colágeno
Gânglios Espinais/crescimento & desenvolvimento
Hidrogéis
Região Lombossacral
Modelos Animais
Fármacos do Sistema Nervoso Periférico/farmacologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Hydrogels); 0 (Interleukin-1beta); 0 (Peripheral Nervous System Agents); 0 (Tumor Necrosis Factor-alpha); 9007-34-5 (Collagen); 9061-61-4 (Nerve Growth Factor)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:150727
[Lr] Data última revisão:
150727
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150324
[St] Status:MEDLINE


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[PMID]:25643184
[Au] Autor:Leibig N; Boyle V; Kraus D; Stark GB; Penna V
[Ad] Endereço:From the *Clinic of Hand, Plastic and Reconstructive Surgery, Burn Center, BG Trauma Center, Ludwigshafen; †Clinic for Neurology, Ortenau Klinikum Lahr-Ettenheim, Lahr; and ‡Clinic of Plastic and Hand Surgery, University Medical Center Freiburg, Freiburg, Germany.
[Ti] Título:C3 toxin and poly-DL-lactide-ε-caprolactone conduits in the critically damaged peripheral nervous system: a combined therapeutic approach.
[So] Source:Ann Plast Surg;74(3):350-3, 2015 Mar.
[Is] ISSN:1536-3708
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Peripheral nerve regeneration over longer distances through conduits is limited. In the presented study, critical size nerve gap bridging with a poly-DL-lactide-ε-caprolactone (PLC) conduit was combined with application of C3 toxin to facilitate axonal sprouting. MATERIALS AND METHODS: The PLC filled with fibrin (n = 10) and fibrin gel loaded with 1-µg C3-C2I and 2-µg C2II (n = 10) were compared to autologous nerve grafts (n = 10) in a 15-mm sciatic nerve gap lesion model of the rat. Functional and electrophysiological analyses were performed before histological evaluation. RESULTS: Evaluation of motor function and nerve conduction velocity at 16 weeks revealed no differences between the groups. All histological parameters and muscle weight were significantly elevated in nerve graft group. No differences were observed in both PLC groups. CONCLUSIONS: The PLCs are permissive for nerve regeneration over a 15-mm defect in rats. Intraluminal application of C3 toxin did not lead to significant enhancement of nerve sprouting.
[Mh] Termos MeSH primário: ADP Ribose Transferases/uso terapêutico
Proteínas de Bactérias/uso terapêutico
Toxinas Botulínicas/uso terapêutico
Regeneração Tecidual Guiada/métodos
Fármacos do Sistema Nervoso Periférico/uso terapêutico
Poliésteres
Neuropatia Ciática/terapia
Tecidos Suporte
[Mh] Termos MeSH secundário: Animais
Materiais Biocompatíveis
Terapia Combinada
Feminino
Regeneração Nervosa/fisiologia
Distribuição Aleatória
Ratos
Nervo Isquiático/lesões
Nervo Isquiático/patologia
Nervo Isquiático/fisiopatologia
Nervo Isquiático/cirurgia
Neuropatia Ciática/patologia
Neuropatia Ciática/fisiopatologia
Resultado do Tratamento
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Biocompatible Materials); 0 (Peripheral Nervous System Agents); 0 (Polyesters); 70524-20-8 (lactide-caprolactone copolymer); EC 2.4.2.- (ADP Ribose Transferases); EC 2.4.2.- (exoenzyme C3, Clostridium botulinum); EC 3.4.24.69 (Botulinum Toxins)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:150211
[Lr] Data última revisão:
150211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150203
[St] Status:MEDLINE
[do] DOI:10.1097/SAP.0000000000000415


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[PMID]:25238916
[Au] Autor:Gómez-Caravaca MT; Cáceres-Redondo MT; Huertas-Fernández I; Vargas-González L; Carrillo F; Carballo M; Mir P
[Ad] Endereço:Unidad de Trastornos del Movimiento, Servicio de Neurología y Neurofisiología, Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Avda. Manuel Siurot s/n, 41013, Seville, Spain.
[Ti] Título:The use of botulinum toxin in the treatment of sialorrhea in parkinsonian disorders.
[So] Source:Neurol Sci;36(2):275-9, 2015 Feb.
[Is] ISSN:1590-3478
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Drooling is a common symptom in parkinsonian disorders. Our aim was to assess the safety and effect of botulinum toxin when applied to parotid glands without ultrasound guidance for sialorrhea in parkinsonian disorders in a retrospective study with a long-term follow-up. We evaluated 53 patients (64.2% male and 35.8% female) with a mean age of 70.18 ± 9.25 years who were treated in our centre between 2007 and 2013. We analysed the mean dose, latency, effect duration, response and adverse effects of treating sialorrhea by injecting botulinum toxin type A (Botox) into the parotid glands without ultrasound guidance. A total of 41 patients with Parkinson's disease, 6 with progressive supranuclear palsy, 4 with multiple system atrophy and 2 with corticobasal degeneration were included. The mean duration of the disease at onset was 10.51 ± 6.81 years and the mean sialorrhea duration was 1.99 ± 1.55 years. The initial dose used for each parotid gland was 14.53 ± 3.95 units of Botox, with a mean dose of 22.17 ± 8.76 units. There was an improvement after treatment in 65.22% of patients with an average score of 6.85 ± 1.58 points on a scale from 0 to 10. The duration of the treatment effect was 4.38 ± 2.11 months, with a latency period of 10.06 ± 9.63 days. Adverse effects were mild and infrequent. Botulinum toxin is a safe and effective therapy for the treatment of sialorrhea in parkinsonian disorders and there is no requirement for ultrasound guidance. It has a rapid onset and lasting effect without requiring a high dosage.
[Mh] Termos MeSH primário: Toxinas Botulínicas Tipo A/administração & dosagem
Transtornos Parkinsonianos/fisiopatologia
Glândula Parótida/efeitos dos fármacos
Fármacos do Sistema Nervoso Periférico/administração & dosagem
Sialorreia/tratamento farmacológico
Sialorreia/fisiopatologia
[Mh] Termos MeSH secundário: Idoso
Toxinas Botulínicas Tipo A/efeitos adversos
Feminino
Seguimentos
Seres Humanos
Masculino
Transtornos Parkinsonianos/tratamento farmacológico
Fármacos do Sistema Nervoso Periférico/efeitos adversos
Estudos Retrospectivos
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Peripheral Nervous System Agents); EC 3.4.24.69 (Botulinum Toxins, Type A)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140921
[St] Status:MEDLINE
[do] DOI:10.1007/s10072-014-1950-y



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