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1.
Bol. latinoam. Caribe plantas med. aromát ; 18(5): 459-479, sept. 2019. ilus
Artigo em Inglês | LILACS | ID: biblio-1008268

RESUMO

Neuronal cell damage is often caused by prolonged misuse of Methylphenidate (MPH). Topiramate (TPM) carries neuroprotective properties but its assumed mechanism remains unclear. The present study evaluates in vivo role of various doses of TPM and its mechanism against MPH-induced motor activity and related behavior disorder. Thus, we used domoic acid (DOM), bicuculline (BIC), Ketamine (KET), Yohimibine (YOH) and Haloperidole (HAL) as AMPA/kainite, GABAA, NMDA, ɑ2 adrenergic and D2 of dopamine receptor antagonists respectively. Open Field Test (OFT), Elevated Plus Maze (EPM) and Forced Swim Test (FST) were used to study motor activity, anxiety and depression level. TPM (100 and 120 mg/kg) reduced MPH-induced rise and inhibited MPH-induced promotion in motor activity disturbance, anxiety and depression. Pretreatment of animals with KET, HAL, YOH and BIC inhibited TPM- improves anxiety and depression through the interacting with Dopaminergic, GABAA, NMDA and ɑ2-adrenergic receptors.


El daño a las células neuronales a menudo es causado por el uso prolongado de metilfenidato (MPH). El topiramato (TPM) tiene propiedades neuroprotectoras, pero su mecanismo de acción no es claro. El presente estudio evalúa el papel in vivo de varias dosis de TPM y su mecanismo contra la actividad motora inducida por MPH y el trastorno de comportamiento relacionado. Utilizamos ácido domoico (DOM), bicuculina (BIC), ketamina (KET), yohimbina (YOH) y haloperidol (HAL), así como antagonistas AMPA/kainato, GABAA, NMDA, ɑ2-adrenérgico y D2 dopaminérgicos, respectivamente. Se utilizaron las pruebas de campo abierto (OFT), elevación de laberinto (EPM) y natación forzada (FST) para estudiar la actividad motora, la ansiedad y el nivel de depresión. El TPM (100 y 120 mg/kg) redujo el aumento inducido por MPH e inhibió la promoción inducida por MPH en la alteración de la actividad motora, la ansiedad y la depresión. El tratamiento previo de animales con KET, HAL, YOH y BIC inhibió el TPM, mejora la ansiedad y la depresión a través de la interacción con los receptores dopaminérgicos, GABAA, NMDA y ɑ2-adrenérgico.


Assuntos
Animais , Masculino , Ratos , Comportamento Animal/efeitos dos fármacos , Fármacos Neuroprotetores/farmacologia , /farmacologia , Transtornos Mentais/prevenção & controle , Metilfenidato/efeitos adversos , Ratos Wistar , Neurotransmissores/metabolismo , Transtornos Mentais/induzido quimicamente , Atividade Motora/efeitos dos fármacos
3.
Rev. ADM ; 75(4): 187-195, jul.-ago. 2018. ilus
Artigo em Espanhol | LILACS | ID: biblio-914912

RESUMO

El sueño es un requerimiento biológico para la vida, sus alteraciones o su ausencia pueden disminuir la calidad de vida, el estado anímico y funcional, afectando seriamente la salud. Un sueño placentero y reparador implica cursar por facetas de profundidad diversa y actividad neuronal compleja. En este artículo se intentan explicar las generalidades del proceso del sueño y algunos de sus trastornos que lo relacionan con aumento de la actividad de los músculos masticatorios (bruxismo). Son presentados aspectos clínicos y neuronales que inducen a un incremento de microdespertares como alteración del sueño, estimulando bruxismo nocturno y bruxismo asociado a apnea nocturna. Son discutidas las posibles relaciones bidireccionales entre bruxismo diurno y nocturno secundarias a modifi caciones en la cantidad y calidad del proceso del sueño. De la misma manera, son sugeridas algunas consideraciones semiológicas y nosológicas para el mejor manejo y control del bruxismo asociado a las alteraciones del sueño, bajo el diagnóstico, atención y supervisión de equipos de atención multi- e interdisciplinarios (AU)


Sleep is a biological requirement for life, its alterations or privation thereof may reduce a person's quality of life, his or her state of mind and physical functions, which signifi cantly aff ects their health. Pleasant and repairing sleep implies going through variable deepness sleep stages, and a complex neuronal activity. This article intends to explain the generalities of the sleep process and certain disorders, particularly those in connection with the activity of the mastication muscles (bruxism). Clinical and neuronal aspects are presented inducing an increase in micro-awakenings such as sleep alterations stimulating nocturnal and bruxism associated with sleep apnea. Bidirectional connections between diurnal and nocturnal bruxism are argued as secondary to changes in the amount and quality of the sleep process. In the same manner, certain considerations associated to semiology and nosology of the diverse bruxism manifestations are considered for the better handling and control of the bruxism associated with sleep alterations under the diagnosis attention and supervision of multi- and interdisciplinary teams (AU)


Assuntos
Humanos , Transtornos do Despertar do Sono , Bruxismo do Sono , Fases do Sono , Dissonias , Neurotransmissores , Parassonias , Equipe de Assistência ao Paciente , Síndromes da Apneia do Sono , Sono REM , Estresse Psicológico
4.
Rev. ADM ; 75(4): 202-213, jul.-ago. 2018. tab
Artigo em Espanhol | LILACS | ID: biblio-915340

RESUMO

El bruxis mo muestra una fi siopatología compleja, donde se involucran señales aferentes y eferentes reguladas por el SNC a través de la expresión de neurotransmisores que repercute en una hiperactividad muscular disfuncional y eventualmente dañina. Para intentar comprender bruxismo desde sus particularidades neurofi siológicas, fue realizada una revisión bibliográfi ca en las bases de Medline y PubMed con el objetivo de establecer la relación entre neurotransmisores y el sistema neuromasticatorio, señalando las posibles alteraciones en su liberación que desencadenen irregularidades en los movimientos rítmicos de la mandíbula (rhythmic jaw Mmovement [RJM]) durante el sueño, inducidos por desórdenes en el sistema nervioso central, por trastornos psicológicos y psiquiátricos, drogadicción y prescripciones médicas, y en alguna medida a una respuesta reactiva a situaciones locales y cambios adaptativos. El funcionamiento masticatorio depende de la integración del aporte sensorial (aferente) de componentes como lo son el ligamento periodontal, músculos masticatorios, dientes y articulación temporomandibular, que puede ser perturbado; cuando alguna de estas partes sufre alteraciones en su integridad, infl amación o sobrecarga funcional o por alteraciones morfológicas, observándose una variedad de respuestas adaptativas y compensatorias (eferentes). En bruxismo esta información local es de relevancia menor, ya que este se rige por cambios centrales observados durante el sueño o bien alteraciones de infl uencia psicológica durante el bruxismo diurno. Consiguientemente, el bruxismo trae apareados cambios biológicos, emocionales y de conducta que repercuten en músculos mayores, preferentemente localizados en cabeza y cuello, ocasionando de manera secundaria numerosas alteraciones; particularmente en la región estomatognática, se observan diversos deterioros como daño de las mucosas, dolor miofascial y articular y atrición dental. La comprensión de los complejos procesos neurofi siológicos que determinan la aparición y persistencia de bruxismo puede ayudar a establecer estrategias de control y tratamiento (AU)


Bruxism shows a complex pathophysiology, where afferent and aff erent signals regulated by the CNS, through the expression of neurotransmitters with repercussion in dysfunctional and eventually harmful muscular hyperactivity. To try to understand bruxism from its neurophysiological peculiarities, a bibliographic review was carried out on the bases of Medline and PubMed, with the aim of establishing the relationship between neurotransmitters and the neuromasticatory system, pointing out the possible alterations in their release that trigger irregularities in the rhythmic movements of the jaw (rhythmic jaw movement [RJM]) during sleep induced by disorders in the central nervous system, psychological and psychiatric alterations, drug addiction and medical prescriptions, and to some extent, a reactive response to local situations and adaptive changes. The masticatory functioning depends on the integration of the sensory input (aff erent) of components such as the periodontal ligament, masticatory muscles, teeth and temporomandibular joint, which can be disturbed when any of these parts suff er alterations in their integrity, infl ammation, functional overload or morphological alterations, observing a variety of adaptive and compensatory (efferent) responses. In bruxism, this local information is of minor relevance, since it is governed by central changes observed during sleep or changes in psychological infl uence during daytime bruxism. Consequently, bruxism brings with it biological, emotional and behavioral changes that aff ect major muscles, preferably located in the head and neck, causing in a secondary way many other alterations. Particularly in the stomatognathic region, several deteriorations are observed, such as mucosal damage, myofascial and joint pain and dental attrition. The understanding of the complex neurophysiological processes that determine the appearance and persistence of bruxism can help to establish control and treatment strategies (AU)


Assuntos
Humanos , Transtornos de Ansiedade , Bruxismo , Geradores de Padrão Central , Neurofisiologia , Neurotransmissores , Estresse Psicológico , Dor Facial , Mandíbula/fisiologia , Sistema Estomatognático
5.
Rev. chil. enferm. respir ; 33(3): 186-189, set. 2017.
Artigo em Espanhol | LILACS | ID: biblio-899675

RESUMO

Resumen El tabaquismo es factor de riesgo y a la vez una adicción compleja con componentes físicos, psicológicos y sociales. Adicción es la necesidad compulsiva de volver a consumir una droga para experimentar sus efectos, en el caso la nicotina, estimulación, euforia, placer, aumento de la atención concentración y memoria, además de disminución de la ansiedad, estrés y apetito. El Manual Diagnóstico y Estadístico de los Trastornos Mentales (DSM V) cataloga el tabaquismo como una adicción, la nicotina es una de las drogas más adictivas que existen, junto con la cocaína y la heroína, además demora 10 segundos en llegar al cerebro cuando se fuma. La nicotina se relaciona con distintos sistemas de neurotransmisión en el sistema nervioso central, es agonista de los receptores α4β2 de acetilcolina, siendo la unión receptor- neurotransmisor de alta sensibilidad. Las vías neurofisiológicas más importes implicadas en la dependencia por la nicotina son dopaminérgica (la más importante), noradrenérgica, GABA-érgica, glutamatérgica y endocanabinoide. El síndrome de abstinencia es una característica básica de la adicción, y es un conjunto de síntomas y signos, físicos y psíquicos que aparecen como consecuencia de la interrupción, reducción o abandono del tabaco. El síndrome de abstinencia se produce como consecuencia de varios factores: disminución de los niveles de cortisol plasmáticos, disminución de los niveles de noradrenalina en el Locus Coeruleous (LC) y principalmente disminución de los niveles de dopamina en el Núcleo Accumbens.


Smoking is a risk factor and at the same time a complex addiction with physical, psychological and social components. Addiction is the compulsive need to re-consume a drug to experience its effects, in the case of nicotine, stimulation, euphoria, pleasure, increased attention concentration and memory, plus decreased anxiety, stress and appetite. The Diagnostic and Statistical Manual of Mental Disorders (DSM V) lists smoking as an addiction, nicotine is one of the most addictive existing drugs, along with cocaine and heroin, and it takes 10 seconds to reach the brain when people smokes. Nicotine is related to different neurotransmission systems in the central nervous system, it is an agonist of acetylcholine α4β2 receptors, being the receptor-neurotransmitter junction of high sensitivity. The most important neurophysiological pathways involved in nicotine dependence are dopaminergic (most important), noradrenergic, GABA-ergic, glutamatergic and endocannabinoid. Abstinence syndrome is a basic characteristic of addiction, and is a set of physical and psychological symptoms and signs that appear because of interruption, reduction, or smoking cessation. Abstinence syndrome occurs as a consequence of several factors: decreased plasma cortisol levels, decreased levels of noradrenaline in the Locus Coeruleous and mainly decreased dopamine levels in Nucleous Accumbens.


Assuntos
Humanos , Síndrome de Abstinência a Substâncias , Tabagismo/epidemiologia , Tabagismo/fisiopatologia , Comportamento Aditivo , Neurotransmissores
6.
Braz. j. med. biol. res ; 50(12): e6432, 2017. tab, graf
Artigo em Inglês | LILACS | ID: biblio-888964

RESUMO

Brain serotonin and dopamine are neurotransmitters related to fatigue, a feeling that leads to reduced intensity or interruption of physical exercises, thereby regulating performance. The present review aims to present advances on the understanding of fatigue, which has recently been proposed as a defense mechanism instead of a "physiological failure" in the context of prolonged (aerobic) exercises. We also present recent advances on the association between serotonin, dopamine and fatigue. Experiments with rodents, which allow direct manipulation of brain serotonin and dopamine during exercise, clearly indicate that increased serotoninergic activity reduces performance, while increased dopaminergic activity is associated with increased performance. Nevertheless, experiments with humans, particularly those involving nutritional supplementation or pharmacological manipulations, have yielded conflicting results on the relationship between serotonin, dopamine and fatigue. The only clear and reproducible effect observed in humans is increased performance in hot environments after treatment with inhibitors of dopamine reuptake. Because the serotonergic and dopaminergic systems interact with each other, the serotonin-to-dopamine ratio seems to be more relevant for determining fatigue than analyzing or manipulating only one of the two transmitters. Finally, physical training protocols induce neuroplasticity, thus modulating the action of these neurotransmitters in order to improve physical performance.


Assuntos
Humanos , Animais , Exercício Físico/fisiologia , Dopamina/fisiologia , Serotonina/fisiologia , Fadiga/etiologia , Fadiga/metabolismo , Fatores de Tempo , Encéfalo/metabolismo , Neurotransmissores/metabolismo , Desempenho Atlético/fisiologia
7.
São Paulo; s.n; s.n; 2016. 188 p. tab, graf, ilus.
Tese em Português | LILACS | ID: biblio-846610

RESUMO

O metabolismo do triptofano (Trp) se dá pela via das quinureninas (QUIN), pela via serotoninérgica (SER) e pela via das aminas traço. A primeira gera QUIN e uma variedade de outros metabólitos secundários. Quando conduzida pela enzima indolamina 2,3 dioxigenase (IDO) contribui para os fenômenos de tolerância e imune escape de células tumorais; e quando conduzida pela triptofano 2,3 dioxigenase (TDO) no fígado, participa na síntese da niacina e NAD. A via SER leva à formação do neurotransmissor serotonina (SER), que pode gerar o hormônio melatonina (MEL), respectivamente e outros metabólitos biologicamente ativos. Outra via menos estudada, a via das aminas traço, produz produtos neuroativos. Dada a abrangência e importância das rotas metabólicas do Trp, nós desenvolvemos e validamos uma metodologia bioanalítica robusta, seletiva e sensível por cromatografia líquida de alta eficiência (HPLC), acoplado espectrometria de massas (MS) para a determinação simultânea do Trp e seus 15 metabólitos. Para tanto, escolhemos para a avaliação das três vias, linhagens de glioma humano. A escolha por este tipo celular deveu-se ao grande interesse de estudos de metabolismo de Trp em células tumorais, no qual células de glioma tem sido modelo. Nos ensaios com as células de glioma acompanhamos os efeitos de um indutor e inibidores da primeira etapa de metabolização do Trp pela via das quinureninas, ou seja, IFN-γ (indutor da IDO), 1-metiltriptofano (1-MT; inibidor competitivo da IDO) e 680C91 (inibidor seletivo da TDO). Pudemos observar o impacto que a indução ou a inibição do primeiro passo teve sobre os metabólitos subsequentes e as diferenças no metabolismo das duas linhagens estudadas, A172 e T98G. A linhagem T98G só tem atividade de IDO, enquanto que a A172 tem tanto atividade IDO quanto TDO. A indução por IFN-γ mostrou que essa citocina não só atua na formação da via QUIN, mas possui um impacto modesto nas demais rotas. Observamos também que a inibição do 1-MT mostrou seu impacto nos metabólitos invdividualmente, do que a simples relação Trp-QUIN. Contudo, nosso resultados nos permitiu mostrar pela primeira vez a descrição completa dessas vias, em especial nessas linhagens celulares, podendo supor estratégias terapêuticas nessas rotas que estão relacionadas a progressão ou não tumoral


The tryptophan metabolism (Trp) takes place by means of kynurenine (QUIN), by the serotonin pathway (SER) and by the pathway of trace amines synthesis. The first generates QUIN and a variety of other secondary metabolites. When driven by the enzyme indoleamine 2,3 dioxygenase (IDO) contributes to the phenomena of tolerance and immune escape of tumor cells; and when conducted by tryptophan 2,3 -dioxygenase (TDO) in the liver, participates in the niacin synthesis NAD. The SER pathway leads to the serotonin neurotransmitter (SER) formation, which can generate the hormone melatonin (MEL), respectively and other biologically active metabolites. Another less studied amines trace synthesis pathway produces neuroactive products. Given the scope and importance of Trp metabolic pathways,we developed and validated a robust, sensitive and selective bioanalytical method by high performance liquid chromatography (HPLC) coupled mass spectrometry (MS) for simultaneous determination of TRP and its 16 metabolites. Therefore, we chose to evaluate the three routes, glioma cell lines. The initial choice of this type of cell was due to the great interest in Trp metabolism studies in tumor cells, which glioma cells has been a model. In assays with glioma cells, we followed the effects of an inductor and inhibitors of the first stage of Trp metabolism, via the kynurenine pathway, or IFN -γ (IDO inducer) 1- methyltryptophane (1- MT; competitive IDO inhibitor) and 680C91 (selective TDO inhibitor). We could observe the first step induction or inhibition impact had over the further metabolites and the metabolism differences between the two studied strains, A172 and T98G. The T98G glioma cell has only IDO activity, while the A172 has both IDO and TDO activity as well. The IFN-γ indution showed that this cytokine not only acts in the formation of QUIN route, but has a modest impact on the others routes. Inhibition of IDO showed that the competitive inhibitor has activity in itself than a simple Trp-QUIN relationship. However, our results allow us to show the first time the complete description of these pathways, in particular, in these cell lines that can assume therapeutic strategies in these routes that are related or not with tumor progression


Assuntos
Métodos de Análise/análise , Linhagem Celular , Glioma/complicações , Doenças Metabólicas/prevenção & controle , Triptofano , Cromatografia Líquida de Alta Pressão/métodos , Indolamina-Pirrol 2,3,-Dioxigenase , Melatonina , Neurotransmissores , Neurônios Serotoninérgicos , Proteínas da Membrana Plasmática de Transporte de Serotonina , Triptofano
8.
Int. j. morphol ; 33(1): 213-221, Mar. 2015. ilus
Artigo em Inglês | LILACS | ID: lil-743788

RESUMO

All organs of the immune system are innervated and almost all neurotransmitter receptors are present on immune cells. We studied the effects of sympathetic innervation in the development of amebic liver abscess (ALA) in rats. Our results showed that lack of sympathetic innervation promote a decrease in size of ALA. We found scarce amoebas, increased the number of neutrophils and a few collagen fibers surrounding the abscess, meanwhile in control group, we observed abscesses areas with typical necrosis including trophozoites and neutrophils. Macrophages were differentially distributed surrounding abscess area in control and vehicle groups, but equally located in and outside of the abscesses in sympathectomized rat. No significant differences were observed on NK cells in analysed groups. In cytokines quantification studies, we observed down-expression of IFN-g and TNF-a, moreover, we found overexpression of IL-10 in sympathectomized and ALA group. In conclusion, our results suggest that elimination of sympathetic nerve fibers in a model rat of amebic liver abscess induces reduction of the innate immune response and presence of amebas through the liver at seven days post-inoculation.


Todos los órganos del sistema inmune están inervados y casi todos los receptores para neurotransmisores están presentes en las células de la respuesta inmune. Nosotros estudiamos el efecto de la inervación simpática en el desarrollo del Absceso Hepático Amebiano (AHA) en ratas. Nuestros resultados muestran que la inervación simpática promueve una disminución en el tamaño del AHA. Nosotros encontramos áreas fibróticas bien definidas con algunas amibas, mayor número de neutrófilos y pocas fibras de colágena rodeando el área de daño, mientras que en el grupo control, nosotros observamos áreas con necrosis, trofozoítos y pocos neutrófilos en el área fibrótica. Los macrófagos se observaron distribuidos en el área fibrótica en los animales simpatectomizados, mientras que en los controles encontramos a los macrófagos distribuidos en la periferia del absceso. No se encontró diferencia significativa en la distribución y cantidad de células NK. En el estudio de citocinas nosotros observamos una disminución de IFN-g y TNF-a y un incremento de IL-10 en animales simpatectomizados. En conclusión, nuestros resultados sugieren que la eliminación de las fibras del sistema nervioso simpático en el modelo de AHA en rata, reduce la respuesta inmune innata y persisten amebas en el tejido dañados a los 7 días post-inoculación.


Assuntos
Animais , Masculino , Ratos , Abscesso Hepático Amebiano/imunologia , Sistema Nervoso Simpático/imunologia , Sistema Nervoso Simpático/metabolismo , Entamoeba histolytica , Imunidade Inata , Imuno-Histoquímica , Abscesso Hepático Amebiano/metabolismo , Microscopia Eletrônica de Transmissão , Neurotransmissores/imunologia , Ratos Wistar , Simpatectomia Química
9.
Rev. chil. neuropsicol. (En línea) ; 9(1/2): 30-35, jul.-dic.2014. tab
Artigo em Espanhol | LILACS | ID: lil-783429

RESUMO

La enfermedad de Parkinson (EP), se identifica como una enfermedad neurodegenerativa, que tiende a atacar al Sistema Nervioso Central, dañando severamente regiones neuronales de la sustancia negra. A nivel mundial la EP ocupa la segunda posición como la enfermedad de degeneración neuronal con mayor prevalencia. Los orígenes de la EP resultan multifactoriales, pues al presente se desconoce una única causa biológica o genética que explique su etiología de forma plena y satisfactoria. Se reconocen en la actualidad una variedad de siete tipos de Parkinsonismo, que producen afectaciones en sus distintas etapas, tanto a nivel de los sistemas de serotonina, noradrenalina como acetilcolina. Los drásticos efectos que provoca la EP sobre la Calidad de Vida (CV) de los pacientes, puede ser evaluada científica y cuantitativamente, desde las múltiples pruebas y evaluaciones que han surgido dentro del campo de las ciencias de la salud. Los cuatro síntomas más comunes para el reconocimiento del Parkinsonismo, son la inestabilidad postural, la rigidez corporal, la bradicinesia y los temblores. La EP continúa siendo poco intervenida en sus etapas tempranas de aparición, especialmente en naciones en vías de desarrollo, por lo que se requiere mayor unidad entre disciplinas científicas y sistemas públicos de salud, para mejorar la CV de estas poblaciones...


Parkinson's disease (PD), is identified as a neurodegenerative disease, tending to attack the Central Nervous System, severely damaging neural regions of substantia nigra. Globally PD ranks second as the most prevalent neuronal degeneration disease. The origins of PD are multifactorial, because nowadays a unique biological or genetic cause to explain the etiology of full and satisfactory way is unknown. They now recognize a variety of seven types of Parkinsonism, producing affectations in its various stages, both at the serotonin, norepinephrine and acetylcholine systems. The drastic effects caused by PD on Quality of Life (QoL) of patients, can be evaluated quantitatively and scientifically and from the multiple tests and evaluations that have emerged within the field of health sciences. The four most common symptoms of Parkinsonism recognition are postural instability, body rigidity, bradykinesia and tremors. PD is still little intervened in the early stages of emergence, especially in developing nations, so that greater unity between scientific disciplines and public health systems are required to improve the QoL’s populations...


Assuntos
Humanos , Degeneração Neural/fisiopatologia , Doença de Parkinson/fisiopatologia , Doença de Parkinson/psicologia , Neurotransmissores/fisiologia , Qualidade de Vida
10.
Clinics ; 69(10): 699-705, 10/2014. tab, graf
Artigo em Inglês | LILACS | ID: lil-730463

RESUMO

A ketogenic diet is an important therapy used in the control of drug-refractory seizures. Many studies have shown that children and adolescents following ketogenic diets exhibit an over 50% reduction in seizure frequency, which is considered to be clinically relevant. These benefits are based on a diet containing high fat (approximately 90% fat) for 24 months. This dietary model was proposed in the 1920s and has produced variable clinical responses. Previous studies have shown that the mechanisms underlying seizure control involve ketone bodies, which are produced by fatty acid oxidation. Although the pathways involved in the ketogenic diet are not entirely clear, the main effects of the production of ketone bodies appear to be neurotransmitter modulation and antioxidant effects on the brain. This review highlights the impacts of the ketogenic diet on the modulation of neurotransmitters, levels of biogenic monoamines and protective antioxidant mechanisms of neurons. In addition, future perspectives are proposed. .


Assuntos
Adolescente , Criança , Humanos , Epilepsia/dietoterapia , Dieta Cetogênica/métodos , Monoaminas Biogênicas/metabolismo , Epilepsia/metabolismo , Corpos Cetônicos/metabolismo , Ilustração Médica , Fármacos Neuroprotetores/metabolismo , Neurotransmissores/metabolismo
11.
Braz. dent. j ; 25(6): 561-564, Nov-Dec/2014. tab
Artigo em Inglês | LILACS | ID: lil-732249

RESUMO

The incidence of facial trauma is high. This study has the primary objective of documenting and cataloging maxillofacial fractures in polytrauma patients. From a total of 1229 multiple trauma cases treated at the Emergency Room of the Santo Antonio Hospital - Oporto Hospital Center, Portugal, between August 2001 and December 2007, 251 patients had facial wounds and 209 had maxillofacial fractures. Aged ranged form 13 to 86 years. The applied selective method was based on the presence of facial wound with Abbreviated Injury Scale ≥1. Men had a higher incidence of maxillofacial fractures among multiple trauma patients (86.6%) and road traffic accidents were the primary cause of injuries (69.38%). Nasoorbitoethmoid complex was the most affected region (67.46%) followed by the maxilla (57.42%). The pattern and presentation of maxillofacial fractures had been studied in many parts of the world with varying results. Severe multiple trauma patients had different patterns of maxillofacial injuries. The number of maxillofacial trauma is on the rise worldwide as well as the incidence of associated sequelae. Maxillofacial fractures on multiple trauma patients were more frequent among males and in road traffic crashes. Knowing such data is elementary. The society should have a key role in the awareness of individuals and in prevention of road traffic accidents.


É alta a incidência de traumas na face. Este estudo teve por objetivo documentar e catalogar as fraturas maxilofaciais em pacientes com politraumatismos. De um total de 1229 casos de politraumatizados tratados na Sala de Emergência do Hospital de Santo António - Centro Hospitalar do Porto, Portugal, entre Agosto de 2001 e Dezembro de 2007, 251 pacientes tiveram ferimentos na face e 209 apresentaram fraturas maxilofaciais. As idades variaram de 13 a 86 anos. O método de seleção baseou-se na presença de ferimentos na face com Abreviated Injury Scale ≥1. Os homens apresentaram maior incidência de fraturas maxilofaciais (86,6%) entre os pacientes com múltiplos traumatismos na face e os acidentes de trânsito foram a causa principal dos traumatismos (69,38%). A região mais afetada foi o complexo naso-órbito-etmoidal (67,46%), seguido pela maxila (57,42%). O padrão e a apresentação das fraturas maxilofaciais tem sido estudado em muitas regiões do mundo com resultados variados. Pacientes com politraumatizados graves apresentaram padrões diferentes de traumatismos maxilofaciais. O número de traumatismos maxilofaciais tem aumentado à escala mundial, assim como a incidência das sequelas associadas. Entre os pacientes com traumatismos múltiplos, a maioria pertencia ao sexo masculino, assim como a causa mais frequente foram os acidentes automobilísticos. É elementar o conhecimento destes dados. A sociedade tem um papel primordial nos cuidados individuais e na prevenção dos acidentes de trânsito.


Assuntos
Animais , Masculino , Camundongos , Ratos , Reativadores da Colinesterase , Colina/análogos & derivados , Diazinon/antagonistas & inibidores , Neurotransmissores/farmacologia , Fisostigmina/antagonistas & inibidores , Pirrolidinas/antagonistas & inibidores , Colina/metabolismo , Colina/farmacologia , Inibidores da Colinesterase/toxicidade , Diazinon/toxicidade , Camundongos Endogâmicos ICR , Fisostigmina/toxicidade , Pirrolidinas/toxicidade , Ratos Endogâmicos , Receptores Colinérgicos/efeitos dos fármacos , Receptores Colinérgicos/metabolismo
12.
Braz. j. pharm. sci ; 50(4): 757-764, Oct-Dec/2014. tab, graf
Artigo em Inglês | LILACS | ID: lil-741362

RESUMO

Chronic antidepressant administration increases neurotrophin levels in the central and peripheral nervous system, leading to an increase of neuronal sprouting, reestablishment of neural networks and neurotransmitter levels. Injured peripheral nerves regenerate at very slow rates. However, the recovery of the hypogastric nerve in rodents after injury is significantly improved with neurotrophin administration. Accordingly, our goal was to determine whether treatment with the antidepressant fluoxetine affects catecholamine levels and neuronal function, after surgical denervation of the rat vas deferens. Noradrenaline levels in the denervated vas deferens were higher in fluoxetine-treated animals than in the vehicle-treated group, as measured by high performance liquid chromatography. In functional studies of smooth muscle contraction, the responses induced by phenylephrine or ATP, as well as pre-synaptic α2-adrenoceptor reactivity, were not modified by chronic treatment with the antidepressant. However, the contraction mediated by neuronal release of noradrenaline induced by tyramine was increased on days 7 and 21 after denervation in rats treated with fluoxetine. These data indicate that fluoxetine can improve functional recovery after rat vas deferens denervation.


A administração crônica de antidepressivos aumenta os níveis de neurotrofinas no sistema nervoso central, levando a um aumento da arborização neuronal, restabelecendo a rede neural e os níveis de neurotransmissores. Lesões do sistema nervoso periférico mostram uma regeneração muito lenta. Entretanto, a recuperação após a lesão do nervo hipogástrico em roedores é significativamente melhorada após a administração de neurotrofinas. Nesse sentido, nosso objetivo foi verificar se o tratamento com o antidepressivo, fluoxetina, interfere nos níveis de catecolaminas e na função neuronal, após a desnervação cirúrgica do ducto deferente de rato. Nos vasos deferentes desnervados, os níveis de catecolaminas nos grupos tratados com fluoxetina foram maiores que no grupo veículo, quantificados em cromatografia líquida de alta eficiência (CLAE). Nos estudos funcionais, a contração da musculatura lisa induzida pela fenilefrina ou pelo ATP, assim como a reatividade pré-sináptica α2-adrenérgica, não foram modificadas com o tratamento crônico de fluoxetina. Contudo, nas contrações mediadas pela liberação neuronal de norepinefrina induzida por tiramina, observou-se aumento da contração nos dias 7 e 21 após a desnevação em ratos tratados com fluoxetina. Esses dados indicam que a fluoxetina pode melhorar a recuperação funcional do vaso deferente de rato após a desnervação.


Assuntos
Ratos , Antidepressivos/efeitos adversos , Fluoxetina/efeitos adversos , Neurotransmissores , Sistema Nervoso Central/anormalidades , Norepinefrina/farmacocinética
13.
Rev. bras. educ. fís. esp ; 28(4): 535-544, 12/2014. tab
Artigo em Português | LILACS | ID: lil-731194

RESUMO

O envelhecimento provoca uma diminuição na concentração de serotonina, que por sua vez, pode produzir anormalidades de comportamento como: agressividade, insônia, comportamento suicida ou criminal e perda do desejo sexual. Entretanto, estudos demonstram que o exercício aeróbio parece aumentar agudamente as concentrações de triptofano e serotonina. Por outro lado, não há relatos na literatura de estudos que tenham investigado os efeitos de diferentes intensidades e volumes de exercício aeróbio sobre as concentrações de triptofano e serotonina em mulheres idosas. O objetivo do presente estudo foi verificar os efeitos agudos de diferentes intensidades e volumes de exercício aeróbio sobre as concentrações de triptofano e serotonina em mulheres idosas fisicamente ativas. Para tanto, 49 mulheres idosas (idade entre 60 e 75 anos), fisicamente ativas, foram distribuídas em seis grupos: controle (GC; n = 8) e cinco experimentais: 1) exercício aeróbio realizado a 90% do limiar ventilatório (LV90; n = 8); 2) exercício realizado em intensidade de limiar ventilatório (LV; n = 8), 3) exercício realizado em intensidade relativa a 90% do ponto de compensação respiratório (PCR90; n = 8), todos com duração de 20 min; 4) teste de esforço máximo (Gmáx; n = 8); e 5) exercício realizado em intensidade de limiar ventilatório com duração de 60 min (LV60min; n = 9). Antes e após a realização das sessões de exercícios foram realizadas coletas de sangue venoso para quantificação das concentrações de triptofano e serotonina. Não foram identificadas diferenças significativas (p > 0,05) entre (GC, LV90, LV, PCR90, Gmáx e LV60min) e intragrupos (pré e pós) nas concentrações de serotonina e triptofano. Em conclusão, sessões agudas de exercício aeróbio realizado em diferentes intensidades e volumes não resultaram em alterações significativas nas concentrações de serotonina e tripotofano em mulheres idosas


Aging causes a decrease in the concentration of serotonin, which in turn, can produce abnormalities of behavior as aggression, insomnia, suicidal or criminal behavior and loss of sexual desire. However, studies show that aerobic exercise seems to increase acutely the concentrations of tryptophan and serotonin. Furthermore, there are no reports of studies that have investigated the effects of different intensities and volumes of aerobic exercise on the concentrations of tryptophan and serotonin in older women physically active. The aim of this study was to determine the acute effects of different intensities and volumes of aerobic exercise on the levels of tryptophan and serotonin in older women. For this, 49 older women (aged 60 to 75 years) physically active were divided into six groups: being a control group (CG, n = 8) and five experimental groups: 1) aerobic exercise performed at 90% of ventilatory threshold (VT90, n = 8); 2) intensity exercise performed at ventilatory threshold (VT, n = 8); 3) intensity exercise performed on 90% of the respiratory compensation point (RCP90, n = 8), each with lasting 20 min; 4) maximal incremental test (MIT, n = 8); and 5) exercise held in ventilatory threshold intensity with lasting 60 min (VT60min, n = 9). Before and after completion of the exercise sessions, venous blood samples were collected to quantify the levels of tryptophan and serotonin. There were no differences (p > 0.05) between and within groups in the concentrations of serotonin and tryptophan. In conclusion, acute bouts of aerobic exercise performed at different intensities and volumes did not result in significant changes in the concentrations of serotonin and tryptophan in older women


Assuntos
Humanos , Feminino , Idoso , Triptofano , Envelhecimento , Exercício Físico , Serotonina , Saúde do Idoso , Neurotransmissores
14.
Salud pública Méx ; 56(4): 379-385, jul.-ago. 2014. ilus, tab
Artigo em Inglês | LILACS | ID: lil-733303

RESUMO

This commentary addresses some of the diverse questions of current interest with regard to the health effects of air pollution, including exposure-response relationships, toxicity of inhaled particles and risks to health, multipollutant mixtures, traffic-related pollution, accountability research, and issues with susceptibility and vulnerability. It considers the challenges posed to researchers as they attempt to provide useful evidence for policy-makers relevant to these issues. This commentary accompanies papers giving the results from the ESCALA project, a multi-city study in Latin America that has an overall goal of providing policy-relevant results. While progress has been made in improving air quality, driven by epidemiological evidence that air pollution is adversely affecting public health, the research questions have become more subtle and challenging as levels of air pollution dropped. More research is still needed, but also novel methods and approaches to address these new questions.


Este comentario aborda algunos de los temas de interés actual en relación con los efectos de la contaminación del aire sobre la salud, tales como las relaciones exposición-respuesta, la toxicidad y riesgos para la salud de las partículas inhaladas, las mezclas de contaminantes múltiples, la contaminación relacionada con el tráfico, la investigación sobre responsabilidad, y los problemas de susceptibilidad y vulnerabilidad. Considera los retos que se presentan a los investigadores que intentan proporcionar evidencia para los responsables políticos en estas cuestiones. Este texto acompaña otros trabajos con resultados del proyecto ESCALA, un estudio en varias ciudades de América Latina que tiene como objetivo general proporcionar resultados relevantes para la política pública. Aunque ha habido avances para mejorar la calidad del aire, gracias a la evidencia epidemiológica de que la contaminación aérea está afectando negativamente a la salud pública, las preguntas de investigación se han vuelto más sutiles y difíciles a medida que los niveles de contaminación se reducen. Se necesita más investigación, pero también nuevos métodos y enfoques capaces de enfrentar estas preguntas.


Assuntos
Animais , Camundongos , Colina/análogos & derivados , Junção Neuromuscular/metabolismo , Neurotransmissores/metabolismo , Pró-Fármacos/metabolismo , Colina/metabolismo , Inibidores da Colinesterase/farmacologia , Estimulação Elétrica , Edrofônio/farmacologia , /farmacologia , Camundongos Endogâmicos , Metilaminas/farmacologia , Neostigmina/farmacologia , Fármacos Neuromusculares Despolarizantes/farmacologia , Inibidores da Captação de Neurotransmissores/farmacologia , Piperidinas/farmacologia , Rana pipiens
15.
Rev. neuropsiquiatr ; 77(1): 3-18, ene.-mar. 2014. tab
Artigo em Inglês | LILACS, LIPECS | ID: lil-723476

RESUMO

Approximately one million people worldwide die from suicide every year. High risk populations include active military, adolescents, the elderly and the chronically mentally and physically ill. More than 90% of suicides are in individuals with a diagnosable psychiatric disorder. Practically all of the major psychiatric disorders are associated with an increased risk for suicide, but depression accounts for more than half of the cases. Clinical observation, epidemiological studies, psychological autopsies, genetics, neurochemistry and brain imaging have yielded important findings that have contributed to our increased understanding of suicide. The strongest biological factor associated with suicide is decreased serotonergic neurotransmission, particularly in the ventral prefrontal cortex. Deficits in ventromedial prefrontal cortex function are associated with impulsivity and impaired decision making. Additionally, a burgeoning body of evidence supports a central role of other biogenic amines and the hypothalamic-pituitary-adrenal (HPA) axis in suicide diathesis. Cognitive and psychological factors for high suicide risk include hopelessness, psychological or mental pain, impulsivity, poor problem solving skills, perfectionism, and self-dislike. Strong protective factors against suicide include access and utilization of healthcare resources, connectedness to family and community, and culture and religious beliefs that discourage suicide. Despite this plethora of research, we still lack reliable predictors of suicide risk and must rely heavily upon self-report and clinical judgment. Thus, it remains singularly difficult to predict who is going to commit suicide. Therefore, there is an urgent unmet need to develop effective early detection methods and treatments, particularly for high-risk populations.


Aproximadamente un millón de personas mueren cada año debido a suicidio. Poblaciones de alto riesgo de suicidio incluyen militares, adolescentes, ancianos, y pacientes con enfermedades crónicas mentales o médicas. Más de 90% de suicidios ocurren en personas que sufren de alguna enfermedad psiquiátrica. Prácticamente todas las enfermedades psiquiátricas aumentan el riesgo de suicidio, sin embargo la depresión está asociada a más de la mitad de los casos de suicidio. Hallazgos clínicos, epidemiológicos, autopsias psicológicas, en genética, neuroquímica, y neuroimágenes han incrementado significativamente nuestro conocimiento sobre el suicidio. El factor biológico más consistentemente asociado a suicidio es la disminución en la neurotransmisión serotoninérgica, particularmente en la zona ventral de la corteza prefrontal. Déficits en la función de la zona ventral de la corteza prefrontal están asociadas a impulsividad y a subóptima toma de decisiones. Las otras aminas biogénicas y el eje hipotalámico-pituitaria-adrenal (HPA) también parecen estar involucrados en la proclividad al suicidio. Los factores cognitivos y psicológicos involucrados en suicidio incluyen desesperanza, dolor psicológico o mental, impulsividad, pobre habilidad para solucionar problemas, perfeccionismo y pobre autoestima. Los factores de protección contra el suicidio más estudiados son: acceso y utilización de servicios de salud, conexión significativa con familia y la comunidad, y creencias religiosas y culturales que se oponen al suicidio. A pesar de la abundancia de estudios realizados, aun carecemos de factores fidedignos de predicción de riesgo de suicidio y debemos basarnos en el reporte del individuo y emplear el juicio clínico. Por eso continúa siendo tremendamente difícil predecir quién morirá por suicidio...


Assuntos
Humanos , Depressão , Fatores de Risco , Neurotransmissores/uso terapêutico , Suicídio , Transtornos Mentais
16.
Rev. Investig. Salud. Univ. Boyacá ; 1(1): 45-62, 2014. ilus, tab
Artigo em Espanhol | LILACS, COLNAL | ID: biblio-908723

RESUMO

Introducción. Si bien lo ideal es llevar a cabo la preservación de los tejidos en el menor tiempo posible luego de la muerte de un animal objeto de un estudio neurohistoquímico, con frecuencia es inevitable trabajar con tejido nervioso obtenido varias horas post mórtem. Objetivo, Estudiar el efecto de la degradación post mórtem sobre la inmunorreacción de di-ferentes antígenos en el cerebro de ratón. Métodos. Se inocularon ratones con virus de la rabia y se extrajeron los cerebros luego de fijar los animales con paraformaldehído me-diante perfusión. En otro grupo de animales la extracción de los encéfalos se hizo para fi-jarlos por inmersión con el mismo fijador y en diferentes horas post mórtem. En un vibráto-mo se obtuvieron cortes coronales de los ce-rebros, y estos se procesaron para inmunode-tección de rabia y de otros cuatro antígenos. Resultados. Cuatro de los antígenos evalua-dos, calbindina, parvoalbúmina, glutamato y ácido gamma-aminobutírico (GABA), presen-taron pérdida de inmunorreacción cuando el tejido cerebral se había tratado previamente mediante fijación por inmersión. Este efecto fue más acentuado cuando aumentó el tiempo post mórtem antes de la fijación. Por el con-trario, la inmunorreacción al virus de la rabia se incrementó cuando transcurrieron más de seis horas post mórtem antes de la fijación. Conclusiones. La fijación por perfusión es ideal para estudios de inmunohistoquími-ca de diferentes antígenos. La degradación tisular post mórtem generalmente provoca disminución de la inmunorreacción. No obs-tante, los antígenos del virus de la rabia in-crementan su inmunorreacción a medida que transcurre el tiempo post mórtem antes de la fijación.


Introduction: It is advisable to carry out the preservation of tissues in the shortest time after the death of an animal subject of neu-rochemical study but it is often unavoidable to work with nervous tissue obtained several hours postmortem. Objective: To study the effect of postmor-tem degradation on immunoreactivity of di-fferent antigens in the mouse brain. Methods: Mice were inoculated with rabies virus and the brains were removed after the animals were fixed by perfusion with parafor-maldehyde. In another group of animals the brain extraction was performed and they were fixed by immersion in the same fixative solu-tion at different hours postmortem. Coronal sections of the brains were obtained in a vibra-tome and they were processed for immunode-tection of rabies, and other four antigens. Results: Four of the antigens studied, cal-bindin, parvalbumin, glutamate and GABA, showed loss of immunoreactivity when brain tissue was pretreated by immersion fixa-tion. This effect was more noticeable when postmortem time increase before the fixing. Conversely immunoreactivity to rabies virus was increased over six hours postmortem before fixation. Conclusions: Fixation by perfusion is ideal for immunohistochemical studies of diffe-rent antigens. Postmortem tissue degrada-tion usually causes decreased immunoreac-tivity. However, rabies virus antigens show increased immunoreactivity when elapses more postmortem time before fixation.


Assuntos
Animais , Vírus da Raiva , Imuno-Histoquímica , Neurotransmissores , Mudanças Depois da Morte
17.
Rev. Inst. Nac. Hig ; 44(2): 56-64, dic. 2013. tab, graf
Artigo em Espanhol | LILACS, LIVECS | ID: lil-746327

RESUMO

El objetivo de esta investigación fue evaluar los efectos fisiológicos y neuroquímicos en 60 ratones machos cepas Naval Medical Research Institute (NMRI) en edad adulto-joven con pesos promedios de 25,45 ± 3,05 g, sometidos durante seis semanas a dosis del principio psicoactivo de la marihuana el Δ-9-tetrahidrocannabinol en concentraciones entre 4 - 20%. Se realizaron tomas de sangre retroorbital para evaluar parámetros hematológicos y bioquímicos antes, durante y post experiencia. Se monitorearon medidas tales como: peso, ingesta de agua, alimentos, actividad locomotora horizontal y vertical, entre otros. Al final de la experiencia se realizo autopsia y toma de muestras de regiones cerebrales, para medir niveles de neurotransmisores aminoacidicos y dopamina. Estos resultados permiten concluir que altas concentraciones del principio psicoactivo de la marihuana hacen más dependiente al consumidor con los consecuentes daños fisiológicos y neurológicos. Esto lleva a que cada vez se necesite más droga para producir el mismo efecto.


The objective of this research was to evaluate the physiological and neurochemical effects in 60 (Naval Medical Research Institute) NMRI male mice strains in young adult - age average weight 25.45 ± 3.05 g, underwent six weeks at doses of the psychoactive ingredient in marijuana the Δ -9-tetrahydrocannabinol in concentrations between 4-20 %. Retroorbital blood shots were conducted to evaluate hematological and biochemical parameters before, during and post experience. Weight, water intake, food, horizontal and vertical locomotors activity include: measures such as monitored. At the end of the experience autopsy was conducted and sampling of brain regions to measure levels of amino acid neurotransmitters and dopamine. These results suggest that high concentrations of the psychoactive ingredient in marijuana consumers become more dependent with consequent physiological and neurological damage. This leads to more and more drugs is needed to produce the same effect.


Assuntos
Humanos , Masculino , Feminino , Adulto , Camundongos , Bioquímica/classificação , Cannabis/efeitos dos fármacos , Dopamina/fisiologia , Neurotransmissores , Dronabinol/análise , Saúde Pública , Pesquisa Científica e Desenvolvimento Tecnológico , Hematologia , Camundongos/anormalidades
18.
Rev. otorrinolaringol. cir. cabeza cuello ; 73(2): 174-188, ago. 2013. ilus, graf
Artigo em Espanhol | LILACS | ID: lil-690564

RESUMO

El sistema eferente auditivo está constituido por el sistema olivococlear y por vías descendentes que provienen de la corteza auditiva y se dirigen a la cóclea. El sistema olivococlear se divide en una porción medial y una lateral, con neuronas que inervan a las células ciliadas externas y a fibras del nervio auditivo respectivamente. El principal neurotransmisor de las sinapsis olivococleares es acetilcolina, y tanto las células ciliadas externas como las fibras del nervio auditivo poseen receptores para esta molécula. El sistema eferente córtico-coclear se origina en la capa V y VI de la corteza auditiva y proyecta a los colículos inferiores y complejo olivar superior, donde a través del sistema olivococlear se conecta con el órgano receptor auditivo. En este artículo se revisan importantes hallazgos obtenidos en los últimos años que involucran (i) nuevos neurotransmisores y receptores del sistema eferente auditivo; (ii) vías descendentes de la corteza auditiva y su rol fisiológico sobre las respuestas cocleares y (iii) rol del sistema eferente auditivo en patologías audiológicas y neuropsiquiátricas.


The auditory efferent system is composed by the olivocochlear fibers and descending projections that originate in the auditory cortex and end in the cochlea. The olivocochlear system is divided into a medial and lateral division, with fibers directed to the outer hair cells and to the auditory nerve fibers respectively. It is known that acetylcholine is the main neurotransmitter of the olivocochlear synapses and that outer hair cells and auditory nerve fibers have receptors to this molecule. The cortico-cochlear efferent system originates in layers V and VI of the auditory cortex. These descending projections are directed to the inferior colliculus and superior olivary complex, a site in which the olivocochlear fibers emerge and connect the brain with the cochlear receptor. In this article recent discoveries obtained in the last years are reviewed: (i) new neurotransmitters and receptors of the olivocochlear system; (ii) anatomy and physiology of descending pathways from the auditory cortex to the cochlea and, (iii) clinical role of auditory efferents in audiological and neuropsychiatric pathologies.


Assuntos
Humanos , Córtex Auditivo/fisiologia , Vias Auditivas/fisiologia , Cóclea/fisiologia , Neurotransmissores/fisiologia , Vias Eferentes/fisiologia , Neurônios Eferentes/fisiologia , Córtex Auditivo/fisiopatologia , Vias Auditivas/fisiopatologia , Cóclea/citologia , Vias Eferentes/fisiopatologia
19.
Braz. j. med. biol. res ; 46(4): 327-338, 05/abr. 2013.
Artigo em Inglês | LILACS | ID: lil-671387

RESUMO

Several forebrain and brainstem neurochemical circuitries interact with peripheral neural and humoral signals to collaboratively maintain both the volume and osmolality of extracellular fluids. Although much progress has been made over the past decades in the understanding of complex mechanisms underlying neuroendocrine control of hydromineral homeostasis, several issues still remain to be clarified. The use of techniques such as molecular biology, neuronal tracing, electrophysiology, immunohistochemistry, and microinfusions has significantly improved our ability to identify neuronal phenotypes and their signals, including those related to neuron-glia interactions. Accordingly, neurons have been shown to produce and release a large number of chemical mediators (neurotransmitters, neurohormones and neuromodulators) into the interstitial space, which include not only classic neurotransmitters, such as acetylcholine, amines (noradrenaline, serotonin) and amino acids (glutamate, GABA), but also gaseous (nitric oxide, carbon monoxide and hydrogen sulfide) and lipid-derived (endocannabinoids) mediators. This efferent response, initiated within the neuronal environment, recruits several peripheral effectors, such as hormones (glucocorticoids, angiotensin II, estrogen), which in turn modulate central nervous system responsiveness to systemic challenges. Therefore, in this review, we shall evaluate in an integrated manner the physiological control of body fluid homeostasis from the molecular aspects to the systemic and integrated responses.


Assuntos
Animais , Humanos , Líquidos Corporais/fisiologia , Homeostase/fisiologia , Vias Neurais/fisiologia , Neurossecreção/fisiologia , Neurotransmissores/fisiologia , Transdução de Sinais/fisiologia , Mapeamento Encefálico , Concentração Osmolar
20.
Invest. clín ; 54(1): 74-89, mar. 2013. ilus, tab
Artigo em Espanhol | LILACS | ID: lil-740338

RESUMO

La estimulación magnética transcraneal ha llamado la atención de neurocientíficos y público en general por la posibilidad de estimular y “controlar” el sistema nervioso de forma no invasiva, realizar diagnósticos más exactos, y aplicar tratamientos y programas de rehabilitación más efectivos en múltiples enfermedades que afectan el sistema nervioso. Así mismo, esta novedosa herramienta ha ayudado a develar la complejidad del comportamiento neural, sus conexiones y su modulación plástica. La estimulación magnética aplicada de manera simple o pareada, se ha convertido en una alternativa útil en el diagnóstico de enfermedades como esclerosis múltiple, enfermedad de Parkinson, epilepsia, distonía, esclerosis lateral amiotrófica, enfermedad cerebro vascular, así como el sueño y sus trastornos, entre otras alteraciones. A nivel terapéutico, se ha sugerido el uso de la estimulación magnética repetitiva con diferentes niveles de evidencia en depresión refractaria a tratamiento farmacológico convencional, tinitus, afonía psicógena, enfermedad de Alzheimer, autismo, enfermedad de Parkinson, distonías, accidente cerebro vascular, epilepsia, trastornos de ansiedad generalizada, estrés post-traumático, alucinaciones auditivas, dolor crónico, afasias, trastorno obsesivo compulsivo, disquinesias inducidas por L-Dopa, manía y síndrome de Rasmussen, entre otros trastornos. Su beneficio en neurorehabilitación es una realidad inocultable, en cuyo caso se ha podido usar con efectividad y, prácticamente, sin efectos secundarios.


Magnetic stimulation has called the attention of neuroscientists and the public due to the possibility to stimulate and “control” the nervous system in a non-invasive way. It has helped to make more accurate diagnosis, and apply more effective treatments and rehabilitation protocols in several diseases that affect the nervous system. Likewise, this novel tool has increased our knowledge about complex neural behavior, its connections as well as its plastic modulation. Magnetic stimulation applied in simple or paired-pulse protocols is a useful alternative in the diagnosis of diseases such as multiple sclerosis, Parkinson disease, epilepsy, dystonia, amyotrophic lateral sclerosis, cerebrovascular disease, and sleep disorders. From the therapeutic perspective, magnetic stimulation applied repetitively has been found useful, with different degrees of efficacy, in treating resistant depression, tinnitus, psychogenic dysphonia, Alzheimer disease, autism, Parkinson disease, dystonia, stroke, epilepsy, generalized anxiety as well as post traumatic stress disorder, auditory hallucinations, chronic pain, aphasias, obsessive-compulsive disorders, L-dopa induced dyskynesia, mania and Rasmussen syndrome, among others. The potential of magnetic stimulation in neurorehabilitation is outstanding, with excellent range of safety and, in practical terms, without side effects.


Assuntos
Humanos , Doenças do Sistema Nervoso/diagnóstico , Doenças do Sistema Nervoso/terapia , Estimulação Magnética Transcraniana/tendências , Encefalopatias/diagnóstico , Encefalopatias/metabolismo , Encefalopatias/terapia , Transtornos Mentais/metabolismo , Transtornos Mentais/terapia , Doenças do Sistema Nervoso/metabolismo , Doenças do Sistema Nervoso/reabilitação , Neurotransmissores/sangue , Neurotransmissores/líquido cefalorraquidiano , Segurança do Paciente , Seleção de Pacientes , Inquéritos e Questionários , Estimulação Magnética Transcraniana/efeitos adversos , Estimulação Magnética Transcraniana/métodos
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