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Aim of the study: Dysembryoplastic neuroepithelial tumor (DNET) is a rare glioneuronal tumor usually found in the temporal lobe of children and young adults. DNETs are commonly associated with drug-resistant partial seizures, with most cases diagnosed before age 20. Asymptomatic brain tumors are rare in the general healthy population, and the frequency of incidental DNETs in adults remains unknown.Materials and methods: We report the case of a 34-year-old healthy man who presented with a facial rash but was incidentally found to have a large T1 hypointense lesion in the left temporal cortex on neuroimaging. The patient opted for surgical removal of the mass, which was subsequently identified as a DNET, positive for a fibroblast growth factor receptor (FGFR) mutation.Results: This case report presents the first incidentally discovered DNET in an adult without epilepsy, highlighting its atypical presentation. In addition, the presence of an FGFR mutation emphasizes its role in DNET pathogenesis and potential therapeutic implications. DNETs exhibit varied behavior based on age, tumor location, and cortical dysplasia.Conclusions: In this case, the absence of seizure onset may be attributed to the lack of cortical dysplasia. Further research is needed to understand the incidence of DNETs and their association with seizure onset and cortical dysplasia.
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Cerebral palsy (CP) is characterized by motor disorders, including deficits in locomotor activity, coordination, and balance. Selective serotonin reuptake inhibitors have been shown to play an important role in brain plasticity. This study investigates the effect of neonatal treatment using fluoxetine on locomotor activity and histomorphometric parameters of the primary somatosensory cortex (S1) in rats submitted to an experimental model of CP. CP was found to reduce bodyweight and locomotion parameters and also to increase the glia/neuron index in the S1. Administration of fluoxetine 10 mg/kg reduced bodyweight, impaired locomotor activity parameters, and increased the number of glial cells and the glia/neuron ratio in the S1 in rats with CP. However, treatment with fluoxetine 5 mg/kg was not found to be associated with adverse effects on locomotor activity and seems to improve histomorphometric parameters by way of minor changes in the S1 in animals with CP. These results thus indicate that experimental CP, in combination with the use of a high dose of fluoxetine (10 mg/kg), impairs locomotor and histomorphometric parameters in the S1, while treatment with a low dose of fluoxetine (5 mg/kg) averts the negative outcomes associated with a high dose of fluoxetine in relation to these parameters but produces no protective effect.
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Paralisia Cerebral , Fluoxetina , Ratos , Animais , Fluoxetina/farmacologia , Fluoxetina/uso terapêutico , Paralisia Cerebral/tratamento farmacológico , Atividade Motora , Neurônios , Neuroglia , LocomoçãoRESUMO
ABSTRACT BACKGROUND AND OBJECTIVES: Evidence has highlighted a role of glial cell activation, and their interaction with different neural systems, especially the endocannabinoid system, in the mechanisms involved in the chronicity and maintenance of pain. The aim of this review is to bring an update on published data that demonstrate the interaction between glial cells and the endocannabinoid system in the pathophysiology of chronic pain and its treatment. CONTENTS: A narrative review was performed based on a research in the Medline database, using the Keywords "endocannabinoid", "glial cells", "microglial", "astrocytes", "neuroinflammation". CONCLUSION: Deepening the knowledge about the function of glial cells in the endocannabinoid system will open the possibility of acting on the pathophysiological origin of the pain chronification process, attenuating the mechanisms involved in central sensitization.
RESUMO JUSTIFICATIVA E OBJETIVOS: A evidência científica tem ressaltado um papel da ativação das células da glia e de sua interação com diversos sistemas neurais, com destaque para o sistema endocanabinoide e mecanismos envolvidos na cronificação e manutenção da dor. O objetivo deste estudo foi atualizar os dados publicados que mostrem a interação entre as células da glia com o sistema endocanabinoide na fisiopatologia da dor crônica e seu tratamento. CONTEÚDO: Foi realizada uma revisão narrativa baseada em pesquisa na base de dados Medline, com uso dos unitermos "endocannabinoid", "glial cells", "microglial", "astrocytes", "neuroinflammation". CONCLUSÃO: O aprofundamento do conhecimento acerca da função das células da glia no sistema endocanabinoide abrirá a possibilidade de atuação sobre a origem fisiopatológica do processo de cronificação de dor, atenuando os mecanismos envolvidos na sensibilização central.
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ABSTRACT BACKGROUND AND OBJECTIVES: Half of neuropathic pain patients still end up failing clinical treatments. Electrical stimulation of the posterior insular cortex (ESI) modulates sensory and nociceptive circuits. This study evaluated the effects of a range of frequencies of ESI proposed to improve neuropathic pain. METHODS: Male Sprague Dawley rats, 280-340 g, submitted to the chronic constriction of the right sciatic nerve were tested for mechanical sensitivity using the paw pressure and von Frey flaments tests, and for thermal sensitivity using the hot plate test. The rats were submitted to ESI 10, 60 or 100 Hz (one, five or seven ESI, 15 min, 210 µs, 1V), applied to the posterior insular cortex, and were evaluated in the tests before and after ESI, or in follow-up of 48, 72 and 168h. The open field evaluated general activity after ESI 5. The involvment of opioid and cannabinoid testes were evaluated through treatment with naloxone and SR1416A - antagonist and inverse agonist/antagonist of the receptors, respectively, after ESI 5, while activation of astrocytes, marked by glial fibrillary acid protein (GFAP), and of microglia, marked by IBA-1 (glial marker), in the spinal cord evaluated by immunohistochemistry. RESULTS: Data demonstrate that 10, 60, and 100 Hz ESIs modulate mechanical and thermal sensitivity. ESI 5 increased immunoreactivity of GFAP in the spinal cord, without altering IBA-1 (glial marker). Naloxone and SR141716A reversed the antinociception of 60 Hz ESI 5. 60 Hz ESI 7 induced antinociception up to 72h. CONCLUSION: 60 Hz ESI induces opioid and cannabinoid-dependent antinociception and regulates glia. HIGHLIGHTS 60 Hz-delivered ESI was the best analgesic protocol for the insular stimulation. Data showed a prolonged analgesic effect up to 72h after repetitive ESI. ESI regulates glia activation in pain modulatory system.
RESUMO JUSTIFICATIVA E OBJETIVOS: Metade dos pacientes com dor neuropática são refratários aos tratamentos. A estimulação elétrica do córtex insular (EECI) posterior modula circuitos sensoriais e nociceptivos. Assim, este estudo avaliou os efeitos de uma faixa de frequências de EECI como tratamento em modelo animal de dor neuropática. MÉTODOS: Ratos machos, Sprague Dawley, 280-340 g, submetidos a cirurgia para indução de constrição crônica (ICC) do nervo isquiático direito, foram avaliados em relação à sensibilidade mecânica com a utilização do teste de pressão de pata e de flamentos de von Frey, e sensibilidade térmica usando o teste de placa quente. Os ratos foram submetidos a EECI de 10, 60 ou 100 Hz (uma, cinco ou sete EECI, 15 min, 210 µs, 1V), aplicada ao córtex insular posterior esquerdo, e avaliados nos testes antes e após EECI, ou em follow up de 48, 72 e 168 horas. Por meio do teste de campo aberto, avaliou-se a atividade geral após a EECI5. O envolvimento de receptores opioides e canabinoides foi avaliado por meio da administração de naloxona e SR141716A - antagonista e agonista/antagonista inverso dos receptores, respectivamente - após a EECI 5, enquanto a ativação de astrócitos - marcada por proteína ácida fibrilar glial (GFAP), e de micróglia - marcada por IBA-1 - na medula espinal foi avaliada por imuno-histoquímica. RESULTADOS: Os dados mostraram que EECI em 10, 60 e 100 Hz modulam a sensibilidade mecânica e térmica dos animais. A EECI 5 aumentou a imunorreatividade de GFAP na medula espinhal, sem alterar IBA-1 (marcador glial). Naloxona e SR141716A reverteram a antinocicepção produzida por EECI 5 de 60 Hz. EECI 7 de 60 Hz induziu antinocicepção por até 72 horas. CONCLUSÃO: A EECI 60 Hz produz antinocicepção dependente de opioides e canabinoides e regula a glia. DESTAQUES A EECI de 60 Hz foi o melhor protocolo analgésico para nossa estimulação insular. Os dados mostram um efeito analgésico prolongado de até 72h após repetidas EECI. A EECI regula a ativação da glia no sistema modulatório da dor.
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Introdução: o tabagismo é uma das principais causas evitáveis de mortes no mundo representando um problema de saúde pública. Objetivo: investigar a relação da exposição passiva à fumaça principal do cigarro e as possíveis alterações histomorfométricas das células gliais, arteríolas e da matriz extracelular do nervo olfatório de ratas. Metodologia: trata-se de um estudo experimental, analítico e quantitativo. Vinte ratas randomizadas divididas em dois grupos, controle e tabaco, foram expostas à inalação da fumaça principal do cigarro por 60 dias utilizando dispositivo validado na literatura. Resultados: a exposição à inalação da fumaça principal do cigarro resultou em alterações significativas no grupo tabaco, tais como, elevação nos níveis de cotinina no plasma sanguíneo, aumento na espessura da parede dos vasos sanguíneos, aumento na porcentagem do colágeno total do tecido, diminuição no número total de astrócitos e aumento no número total de micróglias. Conclusão: a exposição à fumaça principal do cigarro resulta em alterações histomorfométricas que poderiam causar alterações funcionais no nervo olfatório como perda sensorial olfativa. Os achados constatados são fortes o suficiente para servir como alerta a toda a população e às autoridades de saúde, no que se refere às leis antifumo, principalmente em ambientes fechados.
Introduction: smoking is one of the main preventable causes of death in the world and represents a worldwide public health problem. Objective: to investigate the relationship of second hand tobacco smoke and possible histomorphometric changes of glial cells, arterioles and extracellular matrix of the olfactory nerve in rats. Methodology: experimental, analytical and quantitative study, twenty wistar animals randomized into two control and tobacco groups, were exposed to inhalation of main cigarette smoke for 60 days using a device validated in the literature. Results: exposure to inhalation of main cigarette smoke resulted in changes in the tobacco group, such as increased levels of cotinine in the blood plasma, increased thickness of the blood vessel wall, increased percentage of total tissue collagen, decreased in the total number of astrocytes and increase in the total number of microglia. Conclusion: exposure to main cigarette smoke results in histomorphometric changes that can cause changes in the olfactory nerve such as sensory olfactory loss. Our findings are strong enough to serve as a warning to the entire population and to health authorities in relation to smokefree laws especially in closed environments.
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Animais , Masculino , Feminino , Nervo Olfatório , Ratos , Tabagismo , Neuroglia , Colágeno , Produtos do Tabaco , Anatomia , Métodos de Análise Laboratorial e de CampoRESUMO
RESUMEN: El trastorno del espectro autista (TEA) se caracteriza por presentar déficits persistentes en la comunicación y en la interacción social. Además, patrones de comportamiento, intereses o actividades de tipo restrictivo o repetitivo. Su etiología es compleja y heterogenia, y los mecanismos neurobiológicos que dan lugar al fenotipo clínico aún no se conocen por completo. Las investigaciones apuntan a factores genéticos y ambientales que afectan el cerebro en desarrollo. Estos avances coinciden con un aumento en la comprensión de las funciones fisiológicas y el potencial patológico de la neuroglia en el sistema nervioso central (SNC) que llevó a la noción de la contribución fundamental de estas células en el TEA. Así, el objetivo de este artículo fue revisar brevemente los factores de riesgo clave asociados al TEA y luego, explorar la contribución de la neuroglia en este trastorno. Se destaca el rol de los astrocitos, los microglocitos y los oligodendrocitos en el control homeostático del SNC, en la regulación inmunitaria del cerebro y en la mielinización axonal, así como el mal funcionamiento y las alteraciones morfológicas de estas células en los cerebros autistas.
SUMMARY: Autism spectrum disorder (ASD) is characterized by persistent deficits in communication and social interaction, as well as restrictive or repetitive activities or interests. Its etiology is complex and heterogeneous, and the neurobiological mechanisms that give rise to the clinical phenotype are not yet fully understood. Research points to genetic and environmental factors that affect the developing brain. These advances are consistent with an enhanced understanding of the physiological functions and pathological potential of neuroglia in the central nervous system (CNS) which supports the conclusion of the contribution of these cells in ASD. Therefore, the objective of this article was to briefly review the key risk factors associated with ASD and then explore the contribution of glia in this disorder. The role of astrocytes, microgliocytes and oligodendrocytes in the homeostatic control of the CNS in the immune regulation of the brain and in axonal myelination, as well as malfunction and morphological alterations of these cells in autistic brains are emphasized.
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Humanos , Neuroglia/patologia , Transtorno do Espectro Autista/fisiopatologia , Transtorno do Espectro Autista/patologia , Oligodendroglia/patologia , Astrócitos/patologia , Microglia/patologia , Transtorno do Espectro Autista/etiologia , HomeostaseRESUMO
RESUMEN: Desde su descubrimiento, las células no neuronales del sistema nervioso recibieron el nombre de glia, palabra de origen griego que significa unión o pegamento, porque se creía que su función era formar una especie de masilla en la que se encuentran inmersas las neuronas. Desde entonces, mediante nuevas técnicas de tinción, se descubrieron otros tipos celulares que fueron catalogados también como glía, que hasta la fecha siguen siendo consideradas como las células de unión o pegamento del tejido nervioso. El objetivo de este artículo es cuestionar el uso inadecuado del término glía y proponer un nuevo término para designar a las células no neuronales. A pesar del enorme conocimiento que actualmente se tiene de estas células y de la gran variedad de funciones que realizan para mantener el correcto funcionamiento de las neuronas y los circuitos nerviosos, aún se les conserva el nombre de glía, un término errado que desdibuja el verdadero papel que cumplen y su importancia para el sistema nervioso. Por lo anterior, se propone el término "sinneuronas", del prefijo griego syn que significa con o junto con, lo que daría a entender que son células que presentan cercanía estructural y funcional con las neuronas.
SUMMARY: Since their discovery, the non-neuronal cells of the nervous system have been called glia, a word of Greek origin that means union or glue, because it was believed that their function was to form a kind of putty, in which neurons are immersed. Thereafter, new cell types discovered by new staining techniques, were also classified as glia, which to this day are still considered as binding cells or glue of nerve tissue. The objective of this paper is to question the inappropriate use of the term glia and to propose a new term to designate non-neuronal cells. Despite the enormous knowledge that is currently available of these cells and the great variety of functions they perform to maintain the proper functioning of neurons and nerve circuits, they still retain the name of glia, an inappropriate name that blurs the true role they play. Therefore, the term "synneuronas" is proposed, from the Greek prefix syn which means with or together with, what would suggest that they are cells that present structural and functional proximity with to neurons.
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Humanos , Sistema Nervoso Autônomo/anatomia & histologia , Neuroglia , Terminologia como AssuntoRESUMO
The serotonergic and immunological hypothesis of depression proposes that certain types of excessive stress distort the relationship between the activities of the innate immune and central nervous systems, so that the stress caused by an infection, or excessive psychological stress, activate toll-like receptors such as the TLR-4, the transcription factor NF-kB, the inflammasome NLRP3, as well as the secretion of interleukin-1 beta (IL-1ß), interleukin-6 (IL-6) and other factors of the innate immune response, causing first, the general symptoms of the disease which appear with any infection, but also those characteristic of depressive illness such as dysphoria and anhedonia. The evidence indicates that, if the stimulus persists or recurs within 24 hours, the indole-2, 3-dioxygenase enzyme (IDO) of the kynurenine metabolic pathway, which increases the synthesis of quinolinic acid, is activated with an associated reduction of serotonin synthesis. Quinolinic acid activates NMDA receptors in the central nervous system and stimulates the secretion of interleukins IL-6 and 1L-1ß, among others, promoting hyper-activity of the HPA axis and reinforcing a bias of the tryptophan metabolism to produce quinolinic acid, and interleukins by the innate immune system, further reducing the synthesis of serotonin and consolidating the depressive process. We discuss the evidence showing that this process can be initiated by either interleukin stimulated by an infection or some vaccines or excessive psychological stress that activates the HPA axis together with said innate immune response, causing a process of aseptic inflammation in the central nervous system.
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Depressão/fisiopatologia , Sistema Hipotálamo-Hipofisário/fisiopatologia , Cinurenina/metabolismo , Modelos Neurológicos , Modelos Psicológicos , Sistema Hipófise-Suprarrenal/fisiopatologia , Serotonina/metabolismo , Animais , Infecções Bacterianas/imunologia , Infecções Bacterianas/fisiopatologia , Encéfalo/fisiopatologia , Citocinas/fisiologia , Depressão/imunologia , Humanos , Sistema Hipotálamo-Hipofisário/imunologia , Comportamento de Doença/fisiologia , Imunidade Inata , Indolamina-Pirrol 2,3,-Dioxigenase/fisiologia , Inflamação/imunologia , Inflamação/fisiopatologia , Interleucinas/fisiologia , Neuroglia/fisiologia , Sistema Nervoso Periférico/imunologia , Sistema Nervoso Periférico/fisiopatologia , Sistema Hipófise-Suprarrenal/imunologia , Ácido Quinolínico/fisiologia , Receptores de N-Metil-D-Aspartato/fisiologia , Serotonina/deficiência , Isolamento Social , Estresse Psicológico/imunologia , Estresse Psicológico/fisiopatologia , Receptor 4 Toll-Like/fisiologia , Triptofano/metabolismo , Vacinas/efeitos adversosRESUMO
La hipótesis sobre las causas de la depresión basada en la acción de la serotonina y del sistema inmunológico, propone que ciertos tipos de estrés distorsionan la relación entre la actividad del sistema inmunitario innato y la del sistema nervioso central. El estrés causado por una infección o el estrés psicológico excesivo activan receptores de tipo toll, como el TLR-4, el factor de transcripción NF-kB, el inflamasoma NLRP3, así como la secreción de interleucina 1 beta (IL-1ß) e interleucina 6 (IL-6); esto causa, en primer lugar, los síntomas generales de enfermedad que aparecen con cualquier infección, pero también los síntomas característicos de la depresión como disforia y anhedonia. Las evidencias indican que, si el estímulo persiste o se repite en las siguientes 24 horas, se activa la enzima indolamina 2,3-dioxigenasa (IDO) de la vía metabólica de la quinurenina, lo cual incrementa la síntesis del ácido quinolínico y reduce la síntesis de serotonina. El ácido quinolínico activa los receptores de N-metil-D-aspartato (NMDA) en el sistema nervioso central y estimula la secreción de, entre otras, las interleucinas IL-6 e 1L-1ß, las cuales promueven la hiperactividad del eje hipotálamohipófiso-suprarrenal y refuerzan la desviación del metabolismo del triptófano hacia la producción de ácido quinolínico, así como de las interleucinas de la inmunidad innata, con lo cual se reduce más la síntesis de serotonina y se consolida el proceso depresivo. Este proceso puede ser iniciado por las interleucinas estimuladas por una infección, así como por algunas vacunas o por un estrés psicológico excesivo que active el eje hipotálamo-hipófiso-suprarrenal simultáneamente con la respuesta inmunológica innata, con lo que se provocaría un proceso de inflamación estéril en el sistema nervioso central.
The serotonergic and immunological hypothesis of depression proposes that certain types of excessive stress distort the relationship between the activities of the innate immune and central nervous systems, so that the stress caused by an infection, or excessive psychological stress, activate toll-like receptors such as the TLR-4, the transcription factor NF-kB, the inflammasome NLRP3, as well as the secretion of interleukin-1 beta (IL-1ß), interleukin-6 (IL-6) and other factors of the innate immune response, causing first, the general symptoms of the disease which appear with any infection, but also those characteristic of depressive illness such as dysphoria and anhedonia. The evidence indicates that, if the stimulus persists or recurs within 24 hours, the indole-2, 3-dioxygenase enzyme (IDO) of the kynurenine metabolic pathway, which increases the synthesis of quinolinic acid, is activated with an associated reduction of serotonin synthesis. Quinolinic acid activates NMDA receptors in the central nervous system and stimulates the secretion of interleukins IL-6 and 1L-1ß, among others, promoting hyper-activity of the HPA axis and reinforcing a bias of the tryptophan metabolism to produce quinolinic acid, and interleukins by the innate immune system, further reducing the synthesis of serotonin and consolidating the depressive process. We discuss the evidence showing that this process can be initiated by either interleukin stimulated by an infection or some vaccines or excessive psychological stress that activates the HPA axis together with said innate immune response, causing a process of aseptic inflammation in the central nervous system.
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Depressão , Sistema Hipófise-Suprarrenal , Serotonina , Neuroglia , Interleucina-6 , Interferon gama , Interleucina-10 , Interleucina-1beta , Sistema Imunitário , Imunidade Inata , Sistema NervosoRESUMO
Glial cells (also known as glia or neuroglia) are structures which are found in large numbers throughout the nervous system, fulfilling multiple functions, such as regulating the synapses, providing structure, support and nutrition, contributing towards the immune response and tissue oxygenation. Knowledge regarding glial cells has increased during the last few years, since Virchow defined them as supporting connective tissue, followed by Ramón y Cajal who described them as tissue in themselves, until today when a first order physiological role has been recognised for them and a leading role in the appearance and progression of various pathological processes, primarily in the group of Neurodegenerative Diseases (ND). The ND represents a group of pathologies which gradually cause the degeneration of nervous tissue, have a broad spectrum regarding their appearance and, in some cases, are the direct consequence of genetic alterations leading to physiological changes in the nervous system. The present article has thus been aimed at describing glial cells' genetic interaction with ND through a systemic review of the pertinent literature. The mechanisms through which the different classes of glial cells become involved in the appearance of ND are poorly understood; however, evidence indicates that their role could be a critical factor in these pathologies' appearance, regulation and chronicity, these being largely determined by different types of cellular interactions and interaction with the microenvironment. This review shows that ND genetics regarding glial cells' cellular, molecular and genetic functioning represents a complex and understudied process; studying these factors could be a key step for ascertaining the origin of these pathologies, thereby leading to more effective therapies being developed.
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Doenças Neurodegenerativas/patologia , Neuroglia/patologia , Animais , Humanos , Doenças Neurodegenerativas/genética , Neuroglia/metabolismoRESUMO
The effects of physical exercise on cerebral function have been reported in various research studies, thereby leading to better understanding of the brain's cellular mechanisms related to adaptations concerning physical exercise and the different cell responses which become compromised regarding chronic mechanisms. Relearning patterns of movement may thus be an alternative clinical approach affecting cognition and brain plasticity. Recent evidence has shown that neurogenesis can become increased by exercise; nevertheless, moderation mechanisms and the times involved in this process are not at all clear. This review thus provides an update for understanding physical exercise-induced neurogenesis, covering mediating mechanisms and maturation. This is important as glial cell mechanisms are signals activating the neurons and synaptically influencing them, as well as their development, transmission and plasticity via a series of secreted signals depending on contact in human beings. Neurogenesis thus represents a natural model for understanding how new neurons become regenerated and incorporated into brain circuits, thus representing therapeutic potential regarding delay or repair of brain damage caused by injury or disease.
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Exercício Físico , Neurogênese , Neuroglia/metabolismo , Condicionamento Físico Animal , Animais , HumanosRESUMO
ABSTRACT Introduction: Peripheral nerve adaptation is critical for strength gains. However, information about intensity effects on nerve morphology is scarce. Objective: To compare the effects of different intensities of resistance training on radial nerve structures. Methods: Rats were divided into three groups: control (GC), training with 50% (GF1) and training 75% (GF2) of the animal’s body weight. The morphological analysis of the nerve was done by light and transmission electron microscopy. One-way ANOVA and the Tukey’s post hoc test were applied and the significance level was set at p≤0.05. Results: Training groups had an increase of strength compared to GC (p≤0.05). All measured nerve components (mean area and diameter of myelin fibers and axons, mean area and thickness of the myelin sheath, and of neurofilaments and microtubules) were higher in GF2 compared to the other (p≤0.05). Conclusion: Results demonstrated greater morphological changes on radial nerve after heavier loads. This can be important for rehabilitation therapies, training, and progression.
RESUMO Introdução: A adaptação dos nervos periféricos é fundamental para ganhos de força. No entanto, as informações relativas aos efeitos da intensidade sobre a morfologia do nervo são escassas. Objetivo: Comparar os efeitos de diferentes intensidades de treinamento de resistência sobre estruturas do nervo radial. Métodos: Os ratos foram divididos em três grupos: controle (GC) e treinamento com 50% (GF1) e 75% (GF2) do peso corporal do animal. A análise morfológica do nervo foi feita com microscopia óptica e eletrônica de transmissão. A one-way ANOVA e o teste post hoc de Tukey foram aplicados e o nível de significância foi estabelecido em p ≤ 0,05. Resultados: Os grupos treinamento tiveram aumento de força com relação ao GC (p ≤ 0,05). Todos os componentes medidos do nervo (área média e diâmetro de fibras de mielina e axônios, área média e espessura da bainha de mielina, neurofilamentos e microtúbulos) foram maiores no GF2 em comparação com os demais (p ≤ 0,05). Conclusão: Os resultados demonstraram maiores alterações morfológicas no nervo radial depois de cargas mais pesadas. Isso pode ser importante para terapias de reabilitação, treinamento e progressão.
RESUMEN Introducción: La adaptación de los nervios periféricos es fundamental para el aumento de fuerza. Sin embargo, la información sobre el efecto de la intensidad sobre la morfología del nervio es escasa. Objetivo: Comparar el efecto de diferentes intensidades de entrenamiento de resistencia en las estructuras del nervio radial. Métodos: Las ratas se dividieron en tres grupos: control (GC) y entrenamiento con 50% (GF1) y con 75% (GF2) del peso corporal del animal. El análisis morfológico del nervio se hizo con microscopía óptica y electrónica de transmisión. Se aplicaron la prueba ANOVA de una vía y la prueba post hoc de Tukey y el nivel de significación se fijó en p ≤ 0,05. Resultados: Los grupos de entrenamiento tuvieron aumento de la fuerza con respecto al grupo control (p ≤ 0,05). Todos los componentes medidos del nervio (área media y diámetro de las fibras de mielina y axones, área media y espesor de la vaina de mielina, neurofilamentos y microtúbulos) fueron mayores en GF2 en comparación con los otros grupos (p ≤ 0,05). Conclusión: Los resultados mostraron mayores cambios morfológicos en el nervio radial después de las cargas más pesadas. Esto puede ser importante para terapias de rehabilitación, entrenamiento y progresión.
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A avulsão de raízes motoras, na interface do sistema nervoso central e periférico, já bem descrito na literatura, promove uma significativa perda sináptica com degeneração de cerca de 80% dos motoneurônios afetados. Não existem estratégias eficazes que propiciem uma reversão ou amenização deste quadro, mas alguns estudos já mostram que o passo fundamental é preservar os motoneurônios afetados. Pesquisas em diferentes áreas com células-tronco (CT) adultas estão sendo realizadas nos últimos anos e apresentam resultados promissores para a medicina regenerativa. Investigações recentes têm apontado para diferentes fontes de CT em tecidos adultos tais como de medula óssea, de sangue de cordão umbilical, tecido muscular, tecido nervoso, líquido amniótico entre outras. De modo geral, estas células apresentam como características principais a capacidade de proliferação e a diferenciação para outros tipos celulares. Entretanto, os principais problemas para o uso clínico das CT adultas são: i) pequena quantidade de células multipotentes, ii) o controle da diferenciação, iii) insuficiência no número de células viáveis e iiii) difícil obtenção. Como alternativa às dificuldades anteriormente citadas, o tecido adiposo tem sido foco de intensos estudos, pois este tecido possui rica fonte de células pluripotentes, além de apresentarem características positivas como fácil acesso ao tecido adiposo subcutâneo, obtenção em quantidade abundante e processo de isolamento celular relativamente simples. Apesar deste tecido apresentar organização complexa, é na fração celular do estroma vascular que se encontra uma rica população de células pluripotentes. Dados de literatura demonstram que as células mesenquimais derivadas de tecido adiposo (AT-MSC - Células mesenquimais de tecido adiposo), mediante incubação com meios de cultura variados, diferenciam-se em adipócitos, osteócitos, mioblastos, hepatócitos, células vasculares entre outras.
It is well described in the literature that avulsion motor at the interface of the central and peripheral nervous system, promotes a significant loss of synaptic degeneration and 80% of motor neurons death. There is no effective strategies that favor a reversal or mitigation of this framework, but some studies have shown that the key step is to preserve motor neurons affected. Researches in different areas with stem cell (CT) adults are being undertaken in recent years and show promising results for regenerative medicine. Recent investigations have pointed to different sources of CT in adult tissues such as bone marrow, umbilical cord blood, brain, muscle tissue, amniotic fluid, among others. Generally, these cells have as main characteristics capacity for proliferation and differentiation to other cell types. However, the main problems for the clinical use of adult SC are: i) small amount of multipotent cells, ii) differentiation control, iii) low number of viable cells and iiii) difficulty to obtain. As an alternative to the difficulties mentioned above, adipose tissue has been the focus of intense study, because this tissue has a rich source of stem cells, in addition to having positive characteristics such as easy access to subcutaneous adipose tissue, obtained in abundant quantities and isolation process relatively simple. Despite the complex tissue organization, the stromal vascular fraction is rich of pluripotent population cells. Literature data show that stromal cells derived from adipose tissue (AT-MSC-adipose tissue mesenchymal stem cells) can differentiate by incubation with various culture media into adipocytes, osteocytes, myoblasts, hepatocytes, vascular cells, among others. The AT-MSC differentiation into neuronal cells is still subject of discussion and criticism in literature, since no established protocol has induced differentiation into function neuronal cells.
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Ratos , Células-Tronco , Transplante Heterólogo , Neuroglia , Neuroimunomodulação , Raízes Nervosas Espinhais , Nervos EspinhaisRESUMO
INTRODUCTION: The pathophysiology of cerebral ischemia is essential for early diagnosis, neurologic recovery, the early onset of drug treatment and the prognosis of ischemic events. Experimental models of cerebral ischemia can be used to evaluate the cellular response phenomena and possible neurological protection by drugs. OBJECTIVE: To characterize the cellular changes in the neuronal population and astrocytic response by the effect of Dimethyl Sulfoxide (DMSO) on a model of ischemia caused by cerebral embolism. METHODS: Twenty Wistar rats were divided into four groups (n= 5). The infarct was induced with α-bovine thrombin (40 NIH/Unit.). The treated group received 90 mg (100 µL) of DMSO in saline (1:1 v/v) intraperitoneally for 5 days; ischemic controls received only NaCl (placebo) and two non-ischemic groups (simulated) received NaCl and DMSO respectively. We evaluated the neuronal (anti-NeuN) and astrocytic immune-reactivity (anti-GFAP). The results were analyzed by densitometry (NIH Image J-Fiji 1.45 software) and analysis of variance (ANOVA) with the Graph pad software (Prism 5). RESULTS: Cerebral embolism induced reproducible and reliable lesions in the cortex and hippocampus (CA1)., similar to those of focal models. DMSO did not reverse the loss of post-ischemia neuronal immune-reactivity, but prevented the morphological damage of neurons, and significantly reduced astrocytic hyperactivity in the somato-sensory cortex and CA1 (p <0.001). CONCLUSIONS: The regulatory effect of DMSO on astrocyte hyperreactivity and neuronal-astroglial cytoarchitecture , gives it potential neuroprotective properties for the treatment of thromboembolic cerebral ischemia in the acute phase.
INTRODUCCIÓN: La fisiopatolog ía de la isquemia cerebral es fundamental para el diagnóstico oportuno, la recuperación neurológica, la instauración temprana del tratamiento y el pronóstico del evento isquémico. Los modelos experimentales de isquemia cerebral, permiten evaluar los fenómenos de respuesta celular y la posible neuroprotección por fármacos. OBJETIVO: caracterizar los cambios celulares en la población neuronal y la respuesta astrocitaria por efecto del dimetilsulfóxido (DMSO) en un modelo de isquemia por embolia cerebral. Métodos: Se utilizaron 20 ratas Wistar distribuidas en cuatro grupos (n =5). Se indujo embolia cerebral con α- trombina bovina (40 NIH/Unit.) y el grupo tratado recibió 90 mg (100 µL) de DMSO en NaCl (1:1 v/v) intraperitoneal por 5 días; el control isquémico, recibió solamente NaCl (placebo) y los dos grupos no isqu émicos (simulados) recibieron NaCl y DMSO respectivamente. Se evaluó la inmunoreactividad neuronal (anti-NeuN) y astrocitaria (anti-GFAP). Los resultados fueron analizados por densitometría (Fiji-Image J NIH 1.45 software) y análisis de varianza (ANOVA) con el programa Graph pad Prism 5. RESULTADOS: La embolia cerebral produjo lesiones reproducibles y confiables en corteza e hipocampo (CA1), similares a las de los modelos focales. El DMSO no revirtió la pérdida de la inmunoreactividad neuronal postisquemia, pero previno el daño morfológico neuronal y redujo significativamente la hiperreactividad astrocitaria en CA1 y corteza somatosensoria (p <0.001). CONCLUSIONES: El efecto regulatorio del DMSO sobre la hiperreactividad astrocitaria y la citoarquitectura neuronal - astroglial, le confiere características potencialmente neuroprotectivas para el tratamiento de la isquemia cerebral tromboembólica en fase aguda.
RESUMO
Neurodegenerative diseases are pathological conditions that have an insidious onset and chronic progression. Different models have been established to study these diseases in order to understand their underlying mechanisms and to investigate new therapeutic strategies. Although various in vivo models are currently in use, in vitro models might provide important insights about the pathogenesis of these disorders and represent an interesting approach for the screening of potential pharmacological agents. In the present review, we discuss various in vitro and ex vivo models of neurodegenerative disorders in mammalian cells and tissues.
Assuntos
Animais , Camundongos , Ratos , Doença de Alzheimer/patologia , Esclerose Lateral Amiotrófica/patologia , Técnicas de Cultura/métodos , Doença de Huntington/patologia , Doença de Parkinson/patologia , Doença de Alzheimer/etiologia , Esclerose Lateral Amiotrófica/etiologia , Astrócitos , Células Cultivadas , Modelos Animais de Doenças , Doença de Huntington/etiologia , Microglia , Doenças Neurodegenerativas/etiologia , Doenças Neurodegenerativas/patologia , Doença de Parkinson/etiologiaRESUMO
CONTEXT: Neuroglial ectopia has been defined as a mass composed of differentiated neuroectodermal tissue isolated from the spinal canal or cranial cavity and remains rare. This lesion has to be considered in the differential diagnosis among newborn infants with classical symptoms of respiratory distress, neck mass and feeding difficulties. We present a rare case of extensive parapharyngeal and skull base neuroglial ectopia in 6-month-old girl who presented respiratory and feeding obstruction at birth. CASE REPORT: A six-month-old girl who presented upper respiratory and feeding obstruction at birth and was using tracheostomy and gastrostomy tubes was referred to our institution. Complete surgical excision of the mass consisted of a transcervical-transparotid approach with extension to the infratemporal fossa by means of a lateral transzygomatic incision, allowing preservation of all vital neurovascular structures. The anatomopathological examination showed a solid mass with nests of neural tissue, with some neurons embedded in poorly encapsulated fibrovascular stroma, without mitotic areas, and with presence of functioning choroid plexus in the immunohistochemistry assay. Neurovascular function was preserved, thus allowing postoperative decannulation and oral feeding. Despite the large size of the mass, the child has completed one year and six months of follow-up without complications or recurrence. Neuroglial ectopia needs to be considered in diagnosing airway obstruction among newborns. Surgical treatment is the best choice and should be performed on clinically stable patients. An algorithm to guide the differential diagnosis and improve the treatment was proposed.
CONTEXTO: Tecido neuroglial ectópico é definido como uma massa composta de tecido neuroectodermal diferenciado, isolado do canal espinhal ou da cavidade craniana e permanece raro. Esta lesão tem de fazer parte do diagnóstico diferencial em neonatos com os clássicos sintomas de obstrução respiratória, massa cervical e dificuldade para alimentação. Descreve-se um raro caso de tecido neuroglial ectópico extensor em parafaringe e base de crânio em uma menina de seis meses de idade que apresentou os sintomas de obstrução respiratória e alimentar ao nascimento. RELATO DE CASO: Menina de seis meses de idade que apresentou obstrução respiratória alta e alimentar ao nascimento, usando traqueostomia e gastrostomia, foi encaminha à instituição. A ressecção cirúrgica completa da massa utilizou um acesso transcervical-transparotídeo com extensão para fossa infratemporal pela incisão lateral transzigomática, permitindo identificação e preservação das estruturas neurovasculares vitais. O exame anatomopatológico evidenciou uma massa sólida com ninhos de tecido neuronal com alguns neurônios imersos em estroma fibrovascular, de pouca cápsula, sem áreas de mitoses e presença de plexo coroide funcionante ao exame imunoistoquímico. As funções neurovasculares foram preservadas na cirurgia, permitindo a decanulação e alimentação via oral no pós-operatório. Apesar do grande tamanho da massa, a criança completou um ano e meio de acompanhamento sem quaisquer complicações ou recorrência. O tecido neuroglial ectópico deve ser considerado no diagnóstico de obstruções de vias aéreas no neonato. O tratamento cirúrgico é o melhor e deve ser feito no paciente clinicamente estável. Um algoritmo para orientar o diagnóstico diferencial e melhorar o tratamento foi proposto.
Assuntos
Feminino , Humanos , Lactente , Coristoma/diagnóstico , Neuroglia , Doenças Faríngeas/diagnóstico , Faringe , Base do Crânio , Algoritmos , Coristoma/congênito , Diagnóstico Diferencial , Doenças Faríngeas/congênitoRESUMO
Una de las más importantes pero la menos común de las manifestaciones de enfermedad autoinmune la constituye la vasculitis, la cual modifica la historia de la enfermedad, dependiendo del órgano afectado. Esta revisión incluye las más importantes manifestaciones y complicaciones de los sistemas nerviosos central y periférico que se desarrollan por vasculitis en las enfermedades reumáticas, ya sea como una primera manifestación de enfermedad o como acompañante de enfermedad sistémica. También hacemos una revisión de la inmunopatogénesis, los principales hallazgos radiológicos, hallazgos en las biopsias de tejido cerebral o de nervio periférico, en las biopsias de músculo, con los posibles diagnósticos diferenciales conocidos.
The vasculitis is one of the most common manifestations of autoimmune diseases, it will change the medical evolution depending on the affected organ. This review includes the most important manifestations and complications in the central and peripheral nervous system, due to vasculitis developed in the setting of rheumatic diseases, as a primary manifestation or as a part of other symptoms, as well. Also, an up date in immunopathogenesis, radiology, peripheral and central nervous biopsy, muscle biopsy findings, and differential diagnosis is made.