Base de dados : MEDLINE
Pesquisa : A08.186.211.132.810.428.600.650.374 [Categoria DeCS]
Referências encontradas : 13 [refinar]
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  1 / 13 MEDLINE  
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[PMID]:27663135
[Au] Autor:Li C; Fitzgerald ME; Del Mar N; Reiner A
[Ad] Endereço:Department of Anatomy and Neurobiology, University of Tennessee, Memphis, TN, 38163, United States. Electronic address: chli@uthsc.edu.
[Ti] Título:Disinhibition of neurons of the nucleus of solitary tract that project to the superior salivatory nucleus causes choroidal vasodilation: Implications for mechanisms underlying choroidal baroregulation.
[So] Source:Neurosci Lett;633:106-111, 2016 10 28.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Preganglionic neurons in the superior salivatory nucleus (SSN) that mediate parasympathetic vasodilation of choroidal blood vessels receive a major excitatory input from the baroresponsive part of the nucleus of the solitary tract (NTS). This input appears likely to mediate choroidal vasodilation during systemic hypotension, which prevents decreases in choroidal blood flow (ChBF) due to reduced perfusion pressure. It is uncertain, however, how low blood pressure signals to NTS from the aortic depressor nerve (ADN), which fires at a low rate during systemic hypotension, could yield increased firing in the NTS output to SSN. The simplest hypothesis is that SSN-projecting NTS neurons are under the inhibitory control of ADN-receptive GABAergic NTS neurons. As part of evaluating this hypothesis, we assessed if SSN-projecting NTS neurons, in fact, receive prominent inhibitory input and if blocking GABAergic modulation of them increases ChBF. We found that SSN-projecting NTS neuronal perikarya identified by retrograde labeling are densely coated with GABAergic terminals, but lightly coated with excitatory terminals. We also found that, infusion of the GABA-A receptor antagonist GABAzine into NTS increased ChBF. Our results are consistent with the possibility that low blood pressure signals from the ADN produce vasodilation in choroid by causing diminished activity in ADN-receptive NTS neurons that tonically suppress SSN-projecting NTS neurons.
[Mh] Termos MeSH primário: Corioide/irrigação sanguínea
Núcleo do Nervo Facial/fisiologia
Neurônios/fisiologia
Núcleo Solitário/citologia
[Mh] Termos MeSH secundário: Animais
Pressão Sanguínea
Antagonistas de Receptores de GABA-A/farmacologia
Masculino
Terminações Pré-Sinápticas/metabolismo
Piridazinas/farmacologia
Ratos Sprague-Dawley
Fluxo Sanguíneo Regional
Vasodilatação
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GABA-A Receptor Antagonists); 0 (Pyridazines); 56-12-2 (gamma-Aminobutyric Acid); 99460MG420 (gabazine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160925
[St] Status:MEDLINE


  2 / 13 MEDLINE  
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[PMID]:27423319
[Au] Autor:Shi S; Xu L; Li J; Han Y; Wang H
[Ad] Endereço:Department of Otolaryngology-Head and Neck Surgery, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, PR China; Shandong Provincial Key Laboratory of Otology, Jinan 250022, PR China.
[Ti] Título:Different discharge properties of facial nucleus motoneurons following neurotmesis in a rat model.
[So] Source:Neurosci Lett;629:180-185, 2016 08 26.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Facial nucleus motoneurons innervating the facial expressive muscles are involved in a wide range of motor activities, however, the types of movement related neurons and their electrophysiological transformation after peripheral facial nerve injury haven't been revealed. This study was designed to elucidate the types of facial nucleus motoneurons and their alterations of discharge parameters following peripheral facial nerve injury in vivo. Here we set up a rat model by implanting electrode arrays into the brainstem and recorded the electrophysiological signals of facial nucleus neurons in the intact rats for 5 days, then transected the trunk of facial nerve (TF), and continued the record for 4 weeks. At the 4th week post-surgery, the morphological changes of TFs were analyzed. In this paper, we described two types of putative facial nucleus motoneurons based on their electrophysiological properties and their firing frequency adaptation. Type I motoneurons (n=57.6%) were characterized by a sustained spike adaptation, Type II motoneurons (n=26.2%) were identified by a phasic fast spike firing. Facial palsy and synkinesia, caused by neurotmesis of TF, were accompanied by firing rates reduction and firing pattern alteration of motoneurons. Our findings suggest the presence of two types of facial nucleus motorneurons, and their response patterns after neurotmesis support the notion that the discharge pattern of motorneurons may play an important role in the facial nerve function.
[Mh] Termos MeSH primário: Potenciais de Ação
Traumatismos do Nervo Facial/fisiopatologia
Nervo Facial/fisiopatologia
Núcleo do Nervo Facial/fisiopatologia
Neurônios Motores/fisiologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Paralisia Facial/fisiopatologia
Feminino
Ratos
Ratos Wistar
Sincinesia/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160718
[St] Status:MEDLINE


  3 / 13 MEDLINE  
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[PMID]:27345027
[Au] Autor:Sun D; Zhou R; Dong A; Sun W; Zhang H; Tang L
[Ad] Endereço:* Affiliated Hospital of Qingdao University, Qingdao 266000, People's Republic of China.
[Ti] Título:Nicotine effects on muscarinic receptor-mediated free Ca[Formula: see text] level changes in the facial nucleus following facial nerve injury.
[So] Source:J Integr Neurosci;15(2):175-90, 2016 Jun.
[Is] ISSN:0219-6352
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:It was suggested that muscarinic, and nicotinic receptors increase free Ca[Formula: see text] levels in the facial nerve nucleus via various channels following facial nerve injury. However, intracellular Ca[Formula: see text] overload can trigger either necrotic or apoptotic cell death. It is assumed that, following facial nerve injury, the interactions of nicotinic and muscarinic acetylcholine receptors in facial nerve nucleus may negatively regulate free Ca[Formula: see text] concentrations in the facial nerve nucleus, which provide important information for the repair and regeneration of the facial nerve. The present study investigated the regulatory effects of nicotine on muscarinic receptor-mediated free calcium ion level changes in the facial nucleus in a rat model of facial nerve injury at 7, 30, and 90 days following facial nerve injury using laser confocal microscopy. The dose-dependent regulation of nicotine on muscarinic receptor-mediated free calcium ion level changes in the facial nucleus may decrease the range of free Ca[Formula: see text] increases following facial nerve injury, which is important for nerve cell regeneration. It is concluded that the negative effects of nicotine on muscarinic receptors are related to the [Formula: see text] subtype of nicotinic receptors.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Traumatismos do Nervo Facial/tratamento farmacológico
Núcleo do Nervo Facial/efeitos dos fármacos
Nicotina/farmacologia
Agonistas Nicotínicos/farmacologia
Receptores Muscarínicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Cátions Bivalentes/metabolismo
Modelos Animais de Doenças
Progressão da Doença
Relação Dose-Resposta a Droga
Traumatismos do Nervo Facial/metabolismo
Traumatismos do Nervo Facial/patologia
Núcleo do Nervo Facial/metabolismo
Núcleo do Nervo Facial/patologia
Feminino
Masculino
Regeneração Nervosa/efeitos dos fármacos
Distribuição Aleatória
Ratos Sprague-Dawley
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cations, Divalent); 0 (Nicotinic Agonists); 0 (Receptors, Muscarinic); 6M3C89ZY6R (Nicotine); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170203
[Lr] Data última revisão:
170203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160628
[St] Status:MEDLINE
[do] DOI:10.1142/S0219635216500114


  4 / 13 MEDLINE  
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[PMID]:26910341
[Au] Autor:Sun W; Feng W; Lu H; Gong S
[Ad] Endereço:Department of Otolaryngology, Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, 100730, China.
[Ti] Título:Synaptic plasticity in the facial nucleus in rats following infraorbital nerve manipulation after facial nerve injury.
[So] Source:Eur Arch Otorhinolaryngol;273(10):3135-42, 2016 Oct.
[Is] ISSN:1434-4726
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The aim of this study is to investigate the effect of sensory input on the neural plasticity in the facial nucleus following facial nerve injury. Adult male Wistar rats were randomly assigned to four groups: (1) sham control; (2) facial nerve crush (FNC); (3) nerve crush plus daily manual vibrissal stimulation (FMS); and (4) nerve crush with infraorbital nerve transection plus daily manual stimulation (FIMS). Plasticity related proteins in the facial nucleus were evaluated by western blot at 7, 14, and 28 days postsurgery (n = 6/group per timepoint). Synaptophysin-positive terminals were evaluated by immunohistochemistry in a second set of animals (n = 6/group) at 14 days. Quantitation of synaptophysin immunostaining showed that rats in the FNC group had a significantly lower mean number of pixels compared to control animals (29.1 ± 2.6 × 10(6) vs. 34.2 ± 2.3 × 10(6); P < 0.05). Values in the FMS group (33.2 ± 1.7 × 10(6)) were similar to that of the control group, while the mean number in the FIMS group (26.5 ± 2.4 × 10(6)) was significantly lower than in the control group. Synapsin I phosphorylation was reduced to 70-83 % in FNC rats, but increased to 121-132 % in the FMS group (P < 0.05 vs. controls). Phosphorylation of cAMP response element-binding protein was similarly reduced by facial nerve crush, which was delayed in FMS animals (P < 0.05 vs. controls at 28 days). Expression and phosphorylation of all proteins were reduced to the lowest in the FIMS group (all P < 0.05). Sensory input from the IoN have a strong effect on synaptic plasticity within the facial nucleus, which is necessary to achieve the benefit of manual stimulation.
[Mh] Termos MeSH primário: Lesões por Esmagamento/fisiopatologia
Traumatismos do Nervo Facial/fisiopatologia
Núcleo do Nervo Facial/fisiopatologia
Plasticidade Neuronal/fisiologia
Recuperação de Função Fisiológica/fisiologia
[Mh] Termos MeSH secundário: Animais
Lesões por Esmagamento/terapia
Traumatismos do Nervo Facial/terapia
Masculino
Regeneração Nervosa/fisiologia
Estimulação Física
Distribuição Aleatória
Ratos
Ratos Wistar
Vibrissas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160225
[St] Status:MEDLINE
[do] DOI:10.1007/s00405-016-3939-z


  5 / 13 MEDLINE  
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[PMID]:26224546
[Au] Autor:Faunes M; Oñate-Ponce A; Fernández-Collemann S; Henny P
[Ad] Endereço:Laboratorio de Neuroanatomía, Departamento de Anatomía Normal, Escuela de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile.
[Ti] Título:Excitatory and inhibitory innervation of the mouse orofacial motor nuclei: A stereological study.
[So] Source:J Comp Neurol;524(4):738-58, 2016 Mar 01.
[Is] ISSN:1096-9861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neurons in the trigeminal (Mo5), facial (Mo7), ambiguus (Amb), and hypoglossal (Mo12) motor nuclei innervate jaw, facial, pharynx/larynx/esophagus, and tongue muscles, respectively. They are essential for movements subserving feeding, exploration of the environment, and social communication. These neurons are largely controlled by sensory afferents and premotor neurons of the reticular formation, where central pattern generator circuits controlling orofacial movements are located. To provide a description of the orofacial nuclei of the adult mouse and to ascertain the influence of excitatory and inhibitory afferents upon them, we used stereology to estimate the number of motoneurons as well as of varicosities immunopositive for glutamate (VGluT1+, VGluT2+) and GABA/glycine (known as VIAAT+ or VGAT+) vesicular transporters in the Mo5, Mo7, Amb, and Mo12. Mo5, Mo7, Amb, and Mo12 contain ∼1,000, ∼3,000, ∼600, and ∼1,700 cells, respectively. VGluT1+, VGluT2+, and VIAAT+ varicosities respectively represent: 28%, 41%, and 31% in Mo5; 2%, 49%, and 49% in Mo7; 12%, 42%, and 46% in Amb; and 4%, 54%, and 42% in Mo12. The Mo5 jaw-closing subdivision shows the highest VGluT1+ innervation. Noticeably, the VGluT2+ and VIAAT+ varicosity density in Mo7 is 5-fold higher than in Mo5 and 10-fold higher than in Amb and Mo12. The high density of terminals in Mo7 likely reflects the convergence and integration of numerous inputs to motoneurons subserving the wide range of complex behaviors to which this nucleus contributes. Also, somatic versus neuropil location of varicosities suggests that most of these afferents are integrated in the dendritic trees of Mo7 neurons.
[Mh] Termos MeSH primário: Face/inervação
Núcleo do Nervo Facial/citologia
Bulbo/citologia
Neurônios Motores/citologia
Boca/inervação
Núcleo Motor do Nervo Trigêmeo/citologia
[Mh] Termos MeSH secundário: Animais
Contagem de Células
Núcleo do Nervo Facial/metabolismo
Ácido Glutâmico/metabolismo
Glicina/metabolismo
Nervo Hipoglosso/citologia
Nervo Hipoglosso/metabolismo
Imuno-Histoquímica
Masculino
Bulbo/metabolismo
Camundongos Endogâmicos C57BL
Neurônios Motores/metabolismo
Inibição Neural/fisiologia
Tamanho do Órgão
Núcleo Motor do Nervo Trigêmeo/metabolismo
Proteínas de Transporte Vesicular/metabolismo
Ácido gama-Aminobutírico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Vesicular Transport Proteins); 3KX376GY7L (Glutamic Acid); 56-12-2 (gamma-Aminobutyric Acid); TE7660XO1C (Glycine)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150731
[St] Status:MEDLINE
[do] DOI:10.1002/cne.23862


  6 / 13 MEDLINE  
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[PMID]:26156498
[Au] Autor:Rosin JM; Kurrasch DM; Cobb J
[Ad] Endereço:Department of Biological Sciences, University of Calgary, 2500 University Drive N.W., BI286D, Calgary, AB, T2N 1N4, Canada. jmrosin2013@gmail.com.
[Ti] Título:Shox2 is required for the proper development of the facial motor nucleus and the establishment of the facial nerves.
[So] Source:BMC Neurosci;16:39, 2015 Jul 09.
[Is] ISSN:1471-2202
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Axons from the visceral motor neurons (vMNs) project from nuclei in the hindbrain to innervate autonomic ganglia and branchial arch-derived muscles. Although much is known about the events that govern specification of somatic motor neurons, the genetic pathways responsible for the development of vMNs are less well characterized. We know that vMNs, like all motor neurons, depend on sonic hedgehog signaling for their generation. Similarly, the paired-like homeobox 2b (Phox2b) gene, which is expressed in both proliferating progenitors and post-mitotic motor neurons, is essential for the development of vMNs. Given that our previous study identified a novel role for the short stature homeobox 2 (Shox2) gene in the hindbrain, and since SHOX2 has been shown to regulate transcription of islet 1 (Isl1), an important regulator of vMN development, we sought to determine whether Shox2 is required for the proper development of the facial motor nucleus. RESULTS: Using a Nestin-Cre driver, we show that elimination of Shox2 throughout the brain results in elevated cell death in the facial motor nucleus at embryonic day 12.5 (E12.5) and E14.5, which correlates with impaired axonal projection properties of vMNs. We also observed changes in the spatial expression of the vMN cell fate factors Isl1 and Phox2b, and concomitant defects in Shh and Ptch1 expression in Shox2 mutants. Furthermore, we demonstrate that elimination of Shox2 results in the loss of dorsomedial and ventromedial subnuclei by postnatal day 0 (P0), which may explain the changes in physical activity and impaired feeding/nursing behavior in Shox2 mutants. CONCLUSIONS: Combined, our data show that Shox2 is required for development of the facial motor nucleus and its associated facial (VII) nerves, and serves as a new molecular tool to probe the genetic programs of this understudied hindbrain region.
[Mh] Termos MeSH primário: Nervo Facial/embriologia
Núcleo do Nervo Facial/embriologia
Proteínas de Homeodomínio/metabolismo
Neurônios Motores/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Apoptose/fisiologia
Nervo Facial/metabolismo
Nervo Facial/patologia
Núcleo do Nervo Facial/metabolismo
Núcleo do Nervo Facial/patologia
Comportamento Alimentar/fisiologia
Proteínas Hedgehog/metabolismo
Proteínas de Homeodomínio/genética
Imuno-Histoquímica
Hibridização In Situ
Filamentos Intermediários/metabolismo
Proteínas com Homeodomínio LIM/metabolismo
Camundongos da Linhagem 129
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Neurônios Motores/patologia
Receptores Patched
Receptor Patched-1
RNA Mensageiro/metabolismo
Receptores de Superfície Celular/metabolismo
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hedgehog Proteins); 0 (Homeodomain Proteins); 0 (LIM-Homeodomain Proteins); 0 (NBPhox protein); 0 (Patched Receptors); 0 (Patched-1 Receptor); 0 (Ptch1 protein, mouse); 0 (RNA, Messenger); 0 (Receptors, Cell Surface); 0 (Shh protein, mouse); 0 (Shox2 protein, mouse); 0 (Transcription Factors); 0 (insulin gene enhancer binding protein Isl-1)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150710
[St] Status:MEDLINE
[do] DOI:10.1186/s12868-015-0176-0


  7 / 13 MEDLINE  
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[PMID]:25820785
[Au] Autor:Chen H; Liu C; Yin J; Chen Z; Xu J; Wang D; Zhu J; Zhang Z; Sun Y; Li A
[Ad] Endereço:Department of Neurosurgery, The First People's Hospital of Lianyungang, 182 Tong Guan North Road, Lianyungang, Jiangsu, 222002, People's Republic of China.
[Ti] Título:Mitochondrial Cyclophilin D as a Potential Therapeutic Target for Ischemia-Induced Facial Palsy in Rats.
[So] Source:Cell Mol Neurobiol;35(7):931-41, 2015 Oct.
[Is] ISSN:1573-6830
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many studies have demonstrated that ischemia could induce facial nerve (FN) injury. However, there is a lack of a suitable animal model for FN injury study and thus little knowledge is available about the precise mechanism for FN injury. The aims of this study were to establish a reliable FN injury model induced by blocking the petrosal artery and to investigate whether dysfunctional interaction between cyclophilin D (CypD) and mitochondrial permeability transition pore (MPTP) can mediate cell dysfunction in ischemic FN injury. The outcomes of ischemia-induced FN injury rat model were evaluated by behavioral assessment, histological observation, electrophysiology, and electron microscopy. Then the levels of CypD and protein that forms the MPTP were evaluated under the conditions with or without the treatment of Cyclosporin A (CsA), which has been found to disrupt MPTP through the binding of CypD. The blocking of petrosal artery caused significant facial palsy signs in the ischemia group but not in the sham group. Furthermore, ischemia can induce the dysfunction of facial nucleus neurons and destruction of the myelin sheath and increase the protein levels of CypD and MPTP protein compared with sham group. Interestingly, treatment with CsA significantly improved neurological function and reversed the ischemia-induced increase of CypD and MPTP proteins in ischemia group. These results demonstrated that blocking of petrosal artery in rats can induce FN injury and the mechanism may be related to the disruption of MPTP by CypD.
[Mh] Termos MeSH primário: Ciclofilinas/metabolismo
Sistemas de Liberação de Medicamentos
Núcleo do Nervo Facial/irrigação sanguínea
Núcleo do Nervo Facial/metabolismo
Paralisia Facial/metabolismo
Isquemia/metabolismo
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
[Mh] Termos MeSH secundário: Animais
Ciclosporina/administração & dosagem
Sistemas de Liberação de Medicamentos/métodos
Nervo Facial/irrigação sanguínea
Nervo Facial/efeitos dos fármacos
Núcleo do Nervo Facial/efeitos dos fármacos
Paralisia Facial/tratamento farmacológico
Paralisia Facial/etiologia
Isquemia/complicações
Isquemia/tratamento farmacológico
Masculino
Mitocôndrias/metabolismo
Condução Nervosa/efeitos dos fármacos
Condução Nervosa/fisiologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mitochondrial Membrane Transport Proteins); 0 (mitochondrial permeability transition pore); 83HN0GTJ6D (Cyclosporine); EC 5.2.1.- (Cyclophilins); EC 5.2.1.8 (cyclophilin D)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150331
[St] Status:MEDLINE
[do] DOI:10.1007/s10571-015-0188-4


  8 / 13 MEDLINE  
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[PMID]:25581872
[Au] Autor:Takezawa Y; Baba O; Kohsaka S; Nakajima K
[Ad] Endereço:Department of Bioinformatics, Faculty of Engineering, Soka University, Tokyo, Japan.
[Ti] Título:Accumulation of glycogen in axotomized adult rat facial motoneurons.
[So] Source:J Neurosci Res;93(6):913-21, 2015 Jun.
[Is] ISSN:1097-4547
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study biochemically determined glycogen content in the axotomized facial nucleus of adult rats up to 35 days postinsult. The amounts of glycogen in the transected facial nucleus were significantly increased at 5 days postinsult, peaked at 7 days postinsult, and declined to the control levels at 21-35 days postinsult. Immunohistochemical analysis with antiglycogen antibody revealed that the quantity of glycogen granules in the axotomized facial nucleus was greater than that in the control nucleus at 7 days postinjury. Dual staining methods with antiglycogen antibody and a motoneuron marker clarified that the glycogen was localized mainly in motoneurons. Immunoblotting and quantification analysis revealed that the ratio of inactive glycogen synthase (GS) to total GS was significantly decreased in the injured nucleus at about 1-3 days postinsult and significantly increased from 7 to 14 days postinsult, suggesting that glycogen is actively synthesized in the early period postinjury but suppressed after 7 days postinsult. The enhanced glycogen at about 5-7 days postinsult is suggested to be responsible for the decrease in inactive GS levels, and the decrease of glycogen after 7 days postinsult is considered to be caused by increased inactive GS levels and possibly the increase in active glycogen phosphorylase.
[Mh] Termos MeSH primário: Núcleo do Nervo Facial/lesões
Núcleo do Nervo Facial/patologia
Glicogênio/metabolismo
Neurônios Motores/metabolismo
[Mh] Termos MeSH secundário: Animais
Axotomia
Modelos Animais de Doenças
Proteína Glial Fibrilar Ácida/metabolismo
Glucose/metabolismo
Glicogênio Sintase/metabolismo
Masculino
Neurônios Motores/classificação
Ratos
Ratos Wistar
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glial Fibrillary Acidic Protein); 9005-79-2 (Glycogen); EC 2.4.1.11 (Glycogen Synthase); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:150414
[Lr] Data última revisão:
150414
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150113
[St] Status:MEDLINE
[do] DOI:10.1002/jnr.23546


  9 / 13 MEDLINE  
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[PMID]:24911596
[Au] Autor:Mesnard-Hoaglin NA; Xin J; Haulcomb MM; Batka RJ; Sanders VM; Jones KJ
[Ad] Endereço:Neuroscience Institute, Loyola University Medical Center, Maywood, IL 60153, USA; Research and Development Service, Hines VAMC, Hines, IL 60141, USA; Dept. of Anatomy and Cell Biology, Indiana University, Indianapolis, IN 46202, USA. Electronic address: namh.phd@gmail.com.
[Ti] Título:SOD1(G93A) transgenic mouse CD4(+) T cells mediate neuroprotection after facial nerve axotomy when removed from a suppressive peripheral microenvironment.
[So] Source:Brain Behav Immun;40:55-60, 2014 Aug.
[Is] ISSN:1090-2139
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease involving motoneuron (MN) axonal withdrawal and cell death. Previously, we established that facial MN (FMN) survival levels in the SOD1(G93A) transgenic mouse model of ALS are reduced and nerve regeneration is delayed, similar to immunodeficient RAG2(-/-) mice, after facial nerve axotomy. The objective of this study was to examine the functionality of SOD1(G93A) splenic microenvironment, focusing on CD4(+) T cells, with regard to defects in immune-mediated neuroprotection of injured MN. We utilized the RAG2(-/-) and SOD1(G93A) mouse models, along with the facial nerve axotomy paradigm and a variety of cellular adoptive transfers, to assess immune-mediated neuroprotection of FMN survival levels. We determined that adoptively transferred SOD1(G93A) unfractionated splenocytes into RAG2(-/-) mice were unable to support FMN survival after axotomy, but that adoptive transfer of isolated SOD1(G93A) CD4(+) T cells could. Although WT unfractionated splenocytes adoptively transferred into SOD1(G93A) mice were able to maintain FMN survival levels, WT CD4(+) T cells alone could not. Importantly, these results suggest that SOD1(G93A) CD4(+) T cells retain neuroprotective functionality when removed from a dysfunctional SOD1(G93A) peripheral splenic microenvironment. These results also indicate that the SOD1(G93A) central nervous system microenvironment is able to re-activate CD4(+) T cells for immune-mediated neuroprotection when a permissive peripheral microenvironment exists. We hypothesize that a suppressive SOD1(G93A) peripheral splenic microenvironment may compromise neuroprotective CD4(+) T cell activation and/or differentiation, which, in turn, results in impaired immune-mediated neuroprotection for MN survival after peripheral axotomy in SOD1(G93A) mice.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/imunologia
Linfócitos T CD4-Positivos/imunologia
Núcleo do Nervo Facial/imunologia
Neurônios Motores/imunologia
Superóxido Dismutase/genética
[Mh] Termos MeSH secundário: Transferência Adotiva
Esclerose Amiotrófica Lateral/patologia
Animais
Axotomia
Linfócitos T CD4-Positivos/transplante
Proteínas de Ligação a DNA/genética
Traumatismos do Nervo Facial
Núcleo do Nervo Facial/patologia
Feminino
Seres Humanos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Neurônios Motores/patologia
Superóxido Dismutase-1
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Rag2 protein, mouse); 0 (SOD1 protein, human); EC 1.15.1.1 (Sod1 protein, mouse); EC 1.15.1.1 (Superoxide Dismutase); EC 1.15.1.1 (Superoxide Dismutase-1)
[Em] Mês de entrada:1503
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140610
[St] Status:MEDLINE


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[PMID]:24907602
[Au] Autor:Sajjan S; Holsinger RM; Fok S; Ebrahimkhani S; Rollo JL; Banati RB; Graeber MB
[Ad] Endereço:Brain Tumor Research and Molecular Neuroscience & Neuropathology Laboratories, Brain and Mind Research Institute, Faculty of Medicine and Faculty of Health Sciences, The University of Sydney, Camperdown, NSW, Australia.
[Ti] Título:Up-regulation of matrix metallopeptidase 12 in motor neurons undergoing synaptic stripping.
[So] Source:Neuroscience;274:331-40, 2014 Aug 22.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Axotomy of the rodent facial nerve represents a well-established model of synaptic plasticity. Post-traumatic "synaptic stripping" was originally discovered in this system. We report upregulation of matrix metalloproteinase MMP12 in regenerating motor neurons of the mouse and rat facial nucleus. Matrix metalloproteinases (matrix metallopeptidases, MMPs) are zinc-binding proteases capable of degrading components of the extracellular matrix and of regulating extracellular signaling networks including within synapses. MMP12 protein expression in facial motor neurons was enhanced following axotomy and peaked at day 3 after the operation. The peak of neuronal MMP12 expression preceded the peak of experimentally induced synaptic plasticity. At the same time, MMP12 redistributed intracellularly and became predominantly localized beneath the neuronal somatic cytoplasmic membrane. Both findings point to a role of MMP12 in the neuronal initiation of the synaptic stripping process. MMP12 is the first candidate molecule for such a trigger function and has potential as a therapeutic target. Moreover, since statins have been shown to increase the expression of MMP12, interference with synaptic stability may represent one mechanism by which these widely used drugs exert their side effects on higher CNS functions.
[Mh] Termos MeSH primário: Núcleo do Nervo Facial/fisiologia
Metaloproteinase 12 da Matriz/metabolismo
Neurônios Motores/fisiologia
Regeneração Nervosa/fisiologia
Sinapses/fisiologia
[Mh] Termos MeSH secundário: Animais
Membrana Celular/metabolismo
Traumatismos do Nervo Facial/fisiopatologia
Espaço Intracelular/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Neuroglia/fisiologia
Plasticidade Neuronal/fisiologia
Ratos Endogâmicos Lew
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.24.65 (Matrix Metalloproteinase 12); EC 3.4.24.65 (matrix metallopeptidase 12, mouse); EC 3.4.24.65 (matrix metallopeptidase 12, rat)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:140714
[Lr] Data última revisão:
140714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140608
[St] Status:MEDLINE



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