Effects of Excitotoxic Lesion with Inhaled Anesthetics on Nervous System Cells of Rodents.
| Autor: | Quiroz-Padilla MF; Laboratorio de Bases Biologicas del Comportamiento, Facultad de Psicologia, Universidad de la Sabana, Bogota, Colombia., Guillazo-Blanch G; Departamento de Psicobiologia y Metodologia de las Ciencias de la Salud, Instituto de Neurociencias, Universidad Autonoma de Barcelona, Barcelona, Spain., Sanchez MY; Facultad de Enfermeria y Rehabilitacion, Programa de Fisioterapia, Universidad de la Sabana, Bogota, Colombia.; Fundacion de Neuroregeneracion en Colombia, Grupo de investigacion NeuroRec Bogota, Bogota, Colombia., Dominguez-Sanchez MA; Facultad de Enfermeria y Rehabilitacion, Programa de Fisioterapia, Universidad de la Sabana, Bogota, Colombia., Gomez RM; Fundacion de Neuroregeneracion en Colombia, Grupo de investigacion NeuroRec Bogota, Bogota, Colombia. |
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| Jazyk: | angličtina |
| Zdroj: | Current pharmaceutical design [Curr Pharm Des] 2018; Vol. 24 (1), pp. 4-14. |
| DOI: | 10.2174/1381612823666170817125015 |
| Abstrakt: | Different anesthesia methods can variably influence excitotoxic lesion effects on the brain. The main purpose of this review is to identify potential differences in the toxicity to nervous system cells of two common inhalation anesthesia methods, isoflurane and sevoflurane, used in combination with an excitotoxic lesion procedure in rodents. The use of bioassays in animal models has provided the opportunity to examine the role of specific molecules and cellular interactions that underlie important aspects of neurotoxic effects relating to calcium homeostasis and apoptosis activation. Processes induced by NMDA antagonist drugs involve translocation of Bax protein to mitochondrial membranes, allowing extra-mitochondrial leakage of cytochrome C, followed by sequence of changes that ending in activation of CASP-3. The literature demonstrates that the use of these anesthetics in excitotoxic surgery increases neuroinflammation activity facilitating the effects of apoptosis and necrosis on nervous system cells, depending on the concentration and exposure duration of the anesthetic. High numbers of microglia and astrocytes and high levels of proinflammatory cytokines and caspase activation possibly mediate these inflammatory responses. However, it is necessary to continue studies in rodents to understand the effect of the use of inhaled anesthetics with excitotoxic lesions in different developmental stages, including newborns, juveniles and adults. Understanding the mechanisms of regulation of cell death during development can potentially provide tools to promote neuroprotection and eventually achieve the repair of the nervous system in pathological conditions. (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.) |
| Databáze: | MEDLINE |
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