Navegando por Assunto "Transporte de glutamato"

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Acesso aberto (Open Access)
Alterações neuroquímicas no tecido retiniano murino em modelo de malária cerebral induzida pela infecção por Plasmodium berghei (ANKA)
(Universidade Federal do Pará, 2011-07-21) OLIVEIRA, Karen Renata Matos; NASCIMENTO, José Luiz Martins do; http://lattes.cnpq.br/7216249286784978
Cerebral Malaria (CM) is a severe complication resulting from Plasmodium falciparum infection. This condition has usually been associated with cognitive, behavioral and motor dysfunctions, being the retinopathy the most serious consequence resulting from the disease. The pathophysiologymechanisms underlying the complications of CM remain incompletely understood. Several experimental models of CM have already been developed in order to clarify those mechanisms related to this syndrome. In this context, the present work has been performed to investigate which possible neurochemistry alteration could be involved in the CM pathology. Male and female susceptible C57Bl/6 mice (6-8 week old) infected with ≈106 parasitized red blood cells (PbA), showed a low parasitaemia (15-20%), with evident clinical signs as: respiratory failure, ataxia, hemiplegia, and coma followed by animal death. In parallel to the clinical characterization of CM, retinal analysis demonstrated that the disease led to a decrease in the glutathione levels with 2 days post inoculation. However, this decrease was not so evident with the course of the infection (4º and 6º days post- infection). We further demonstrated that the increase in the glutathione levels during the infection is followed by the increase in the 3H-glutamate uptake rate (4º and 6º days post-infection), suggesting that CM condition causes an up-regulation of the transporters systems. Immunofluorescence data demonstrated that besides the activity increases, CM condition also stimulated the increase of the xCG- system expression in the retinal tissue. Furthermore, our findings also highlighted that in the retina the neurochemistries alterations occurs in a manner independent on the establishment of an inflammatory response, once TNF-α levels and NOS-2 expression were altered only in the cerebral tissue.
Acesso aberto (Open Access)
O transportador XCG- medeia a captação de glutamato independente de sódio em cultura primária de células gliais da cóclea de camundongos neonatos
(Universidade Federal do Pará, 2022-10-20) MARTINS, Luana Carvalho; OLIVEIRA, Karen Renata Herculano Matos; http://lattes.cnpq.br/3032008039259369
The cochlea is a sensory organ of the auditory system whose excitatory synapses are mediated by L-Glutamate. Since glutamate has physiological and pathological repercussions on the cochlea, the crucial role of glutamate transport mechanisms capable of regulating the extracellular concentration of this neurotransmitter in order to maintain auditory function is highlighted. Within this context, in this study we sought to investigate the activity and expression of glutamate transport systems in an in vitro model of primary cultures of cochlear glial cells obtained from newborn mice of the Balb/C lineage. For this, we determined the sodium dependent and independent glutamate transport by means of glutamate uptake and release assays whose extracellular concentrations were quantified using High Performance Liquid Chromatography coupled to a fluorescence detector. Finally, the cells were subjected to immunofluorescence assay for XCG sodium-independent glutamate transporter labeling. In our results, we demonstrate that cochlear glial cells have a glutamate transport system mediated by the XCG- transporter. Such data suggest a possible role of this transporter in the control of extracellular concentrations of glutamate and regulation of the redox state, which may help to preserve auditory function.