ABSTRACT
Abstract Prolonged overexposure to catecholamines causes toxicity, usually credited to continuous adrenoceptor stimulation, autoxidation, and the formation of reactive pro-oxidant species. Non-differentiated SH-SY5Y cells were used to study the possible contribution of oxidative stress in adrenaline (ADR)-induced neurotoxicity, as a model to predict the toxicity of this catecholamine to peripheral nerves. Cells were exposed to several concentrations of ADR (0.1, 0.25, 0.5 and 1mM) and two cytotoxicity assays [lactate dehydrogenase (LDH) release and 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl tetrazolium bromide (MTT) reduction] were performed at several time-points (24, 48, and 96h). The cytotoxicity of ADR was concentration- and time-dependent in both assays, since the lowest concentration tested (0.1mM) also caused significant cytotoxicity at 96h. N-acetyl-cysteine (1mM), a precursor of glutathione synthesis, prevented ADR-induced toxicity elicited by 0.5mM and 0.25mM ADR following a 96-h exposure, while the antioxidant Tiron (100µM) was non-protective. In conclusion, ADR led to mitochondrial distress and ultimately cell death in non-differentiated SH-SY5Y cells, possibly because of ADR oxidation products. The involvement of such processes in the catecholamine-induced peripheral neuropathy requires further analysis.
Subject(s)
Epinephrine/agonists , Peripheral Nervous System Diseases/classification , Toxicity , Neurons/classification , Peripheral Nerves/abnormalities , Bromides/antagonists & inhibitors , Oxidative Stress/drug effects , Antioxidants/pharmacologyABSTRACT
O objetivo deste trabalho de revisão foi dissertar sobre a regulação hormonal da ingestão alimentar e do peso corporal. A ingestão de macronutrientes, o gasto energético e o balanço entre a síntese de hormônios que aumentam a atividade dos neurônios orexígenos e anorexígenos são fatores determinantes na regulação da ingestão alimentar e no controle do peso corporal. Os hormônios leptina, insulina e opeptídeo YY são grandes potenciadores da atividade dos neurônios anorexígenos POMC/CART. Por outro lado, a ação da grelina aumenta a atividade dos neurônios orexígenos NPY/AgRP. Estes hormônios sintetizados perifericamente atravessam a barreira-hemato-encefálica e se ligam aos seus receptores no núcleo arqueado hipotalâmico com o objetivo de regular a ingestão alimentar e controlar o balanço energético. Estes mecanismos revelam a complexidade do controle do balanço energético e todos os centros envolvidos na busca pela homeostase energética.
The purpose of a literature review was to explain about the hormonal regulation and neural control of thefood intake and body weight. The ingestion of macronutrients, the energy cost of food and hormonesynthesis that increases the activity of the orexygenic and anorexygenic neurons are determinative factors in the regulation of the food intake and body weight. The leptin, insulin and peptide YY increaseactivity of the anorexygenic neurons POMC/CART. However, the ghrelin increases activity of the orexygenicneurons NPY/AgRP. These hormones crossing the barrier hematoencephalic and binds to specificsreceptors in the hypothalamic arcuate nucleus. These mechanisms show to the complexity of the foodintake control and all the involved centers in the search for the energy homeostasis.
Subject(s)
Humans , Appetite Depressants , Hormones , Eating , Neurons/classificationABSTRACT
In order to know the effects of caloric stimulation on neuronal firing in medial vestibular nuclei (MVN) by middle ear irrigation, the middle ear was irrigated with ice (4 degrees C), hot (44 degrees C), and warm (37 degrees C) water, and the firing rate of MVN neuron was extracellularly recorded. The results showed that the firing rate of MVN neuron was changed by caloric stimulation, and the majority of MVN neurons showed excitation by irrigation with hot water and inhibition by ice water (type A). The neuronal firing was recovered immediately after the cessation of the stimulation. I It was concluded that the neuronal firing rate in MVN was changed by caloric stimulation in middle ear cavity. The response was different in various neurons.
Subject(s)
Cold Temperature , Ear, Middle , Electrophysiology , Endolymph/physiology , Hot Temperature , Therapeutic Irrigation , Neurons/classification , Neurons/physiology , Rats, Wistar , Vestibular Nerve/physiology , Vestibular Nuclei/physiologyABSTRACT
La apoptosis es un mecanismo de daño celular que ocurre en el normal desarrollo y en la regulación de tejidos y órganos en vertebrados. Neuronas bajo apoptosis dependiente o independiente de p53, dependiendo UPON del estímulo que conduce a fragmentación del DNA. Muchas neuronas en el desarrollo del sistema nervioso sufren apoptosis, siendo la ciclina D1 un esencial mediador del daño celular neural. Otras características de apoptosis son la condensación del núcleo, la fragmentación de la cromatina junto a los sitios de ruptura en los nucleosomas, la rotura de la membrana y la formación de cuerpos apoptóticos. Entre los posibles mecanismos moleculares estan: (a) la activación de proteasas, como ICE (II-1 ß converting enzyme); y una pequeña Ribonucleoproteína U1, siendo sustratos para ICE y sus homólogos (tales como ICH y otras proteínas). El gen p53 codifica un factor de transcripción que contribuye a varias diferentes actividades celulares, incluyendo la opoptosis, la respuesta celular a la radiación, y la actividad de proteínas tales como GADD, Bcl-2 (represor de apoptosis) y Bax. p53 ejecuta un papel como un inhibidor de apoptosis por transactivación de la expresión del gen Bax. El gen supresor de tumores p53 limita la proliferación celular por parada del ciclo celular en G1, o por apoptosis, dependiendo del contexto celular. La proteína p21 es un inhibidor de ciclinas dependientes de kinasas, la cual es transactivada por p53. Durante la apoptosis hay una activación de c-myc, y del factor de transcripción NF-kB (factor nuclear kappa ß), el cual es un importante regulador de la apoptosis. Como un ejemplo de señalización apoptosis nosotros hemos seleccionado el problema relatando el sistema Fas/APO en timocitos
Subject(s)
Humans , Apoptosis/immunology , Cyclins/administration & dosage , Interleukins/adverse effects , Necrosis , Neurons/classification , Proteins/classificationABSTRACT
Se presenta la prevalencia de hipocausia neurosensoriales en 24 familiares ubicados en diferentes poblados del estado Nva. Esparta. De 329 individuos estudiados, 27 (8,9 por ciento) mostraron diferentes grados de transtornos auditivos, 16 de los cuales se asociaron a complejos sindromáticos, siendo el más frecuente la renitis pigmentosa correspondiente clínicamente al síndrome de Usher
Subject(s)
Humans , Male , Female , Hearing/physiology , Deafness/classification , Mitochondria/chemistry , Neurons/classificationABSTRACT
La infección por el virus de la Encefalitis Venezolana produjo un aumento significativo en el número de sitios de fijación del H3-GABA en el cerebelo. La infección también causó una disminución en la afinidad de estos receptores por GABA