Dissertações em Neurociências e Biologia Celular (Mestrado) - PPGNBC/ICB
URI Permanente para esta coleçãohttps://repositorio.ufpa.br/handle/2011/2375
O Mestrado Acadêmico pertence ao Programa de Pós-Graduação em Neurociências e Biologia Celular (PPGNBC) do Instituto de Ciências Biológicas (ICB) da Universidade Federal do Pará (UFPA).
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Navegando Dissertações em Neurociências e Biologia Celular (Mestrado) - PPGNBC/ICB por Assunto "Ácido glutâmico"
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Item Acesso aberto (Open Access) Avaliação dos níveis extracelulares de GABA e glutamato no sistema nervoso central de camundongos infectados com Plasmodium berghuei ANKA(Universidade Federal do Pará, 2024-11) LIMA, Renato Mateus Santos de; OLIVEIRA, Karen Renata Herculano Matos; http://lattes.cnpq.br/3032008039259369Cerebral malaria (CM) caused by Plasmodium falciparum results in high mortality, especially in children under 5, with up to 25% of survivors experiencing neurological sequelae such as cognitive impairment and seizures. The neurochemical mechanisms behind these impairments are not well understood. This study aimed to characterize changes in the levels of the neurotransmitters glutamate (GLU) and γ-Aminobutyric acid (GABA) in the central nervous system (CNS) during experimental cerebral malaria (ECM). ECM was induced in Swiss mice with Plasmodium berghei ANKA (PbA), and the animals were monitored for parasitemia, survival, and neurological impairments using the Rapid Murine Coma and Behavior Scale (RMCBS). On the 7th day post-infection (d.p.i), blood-brain barrier (BBB) disruption was assessed using Evans Blue dye, and glial cell evaluation was performed by immunofluorescence. Results showed that PbA-infected mice began to succumb to CM by the 6th d.p.i, with 100% mortality by the 10th d.p.i. Behavioral impairments were observed from the early stages of infection. Significant BBB permeability changes and increased expression of glial activation markers were noted in infected mice. There was a marked increase in GLU levels in the brain and cerebellum on days 3, 5, and 7 post-infection. GABA levels increased on days 3 and 5, returning to control levels by day 7. These findings indicate significant neurochemical alterations in GABAergic and glutamatergic neurotransmission, accompanied by neurological and vascular impairments, suggesting their involvement in the development of neurological symptoms in CM.Item Acesso aberto (Open Access) Efeito modulador da glutationa na liberação de gaba induzida por glutamato em retinas de embrião de galinha(Universidade Federal do Pará, 2012-06-06) PEREIRA, Tiago de Lima; SILVA, Anderson Manoel Herculano Oliveira da; http://lattes.cnpq.br/8407177208423247The γ-aminobutyric acid (GABA) and glutamate are, respectively, major inhibitory and excitatory neurotransmitters in the central nervous system (CNS) and are essential to the visual processing. Studies show that glutamate induces the release of GABA in the retina, but the mechanisms involved in this release are not well elucidated. Previous work also showed that thiols compounds regulate GABA release, but are not well defined the effects of compounds containing sulfhydryl (-SH) on endogenous levels of this neurotransmitter in the retina. In this context, glutathione (GSH) besides being the most important thiols compounds, have demonstrated perform a neuromodulatory role in the release of neurotransmitters. Thus, the objective of this study was to evaluate a possible modulatory effect of GSH on the release of GABA mediated by glutamate in the retina of chick embryo. For this study, we used as experimental model, retinal tissue intact chick embryo, with seven or eight days of development. In tests of release of GABA, the retinas were treated with GSH (100 and 500 μM), glutamate (50 and 500 μM) and Buthionine Sulfoximine (BSO), an inhibitor of glutathione synthesis, (50 μM) per 15 minutes, and GABA levels released into the extracellular medium were quantified by High Performance Liquid Chromatography (HPLC). For release experiments of thiols compounds, the retinas were incubated with glutamate 100 μM (with or without Na +) per 15 minutes, and their extracellular levels were determined by reaction with DTNB and quantified by spectrophotometry (412 nm). The results show that glutamate, as well as GSH, release GABA. Our data also show that BSO attenuates the release of GABA promoted by glutamate. Furthermore, we demonstrate that glutamate induces release of thiol compounds regardless of sodium. Therefore, it is known that glutamate is able to release thiols and GABA, among them, GSH is most abundant and responsible for also release GABA. It is also known that once inhibited GSH synthesis by BSO, the release of GABA induced by glutamate is attenuated. Then, it is suggested a possible modulation of GSH in the release of GABA induced by glutamate in retina intact chicken embryo.Item Acesso aberto (Open Access) Efeitos do fator de crescimento do nervo sobre os níveis extracelulares de glutamato e compostos tióis na retina embrionária de galinha(Universidade Federal do Pará, 2011-04-20) GARCIA, Tarcyane Barata; SILVA, Anderson Manoel Herculano Oliveira da; http://lattes.cnpq.br/8407177208423247Nerve growth factor (NGF) belongs to the neurotrophin family and induces its effects through activation of two distinct receptor types. NGF was first described by Rita Levi-Montalcini and collaborators as an important factor involved in nerve differentiation and survival. Another role for NGF has been established in neurotransmitter release in the hippocampus, developing visual cortex and cerebellar neuron. However, this phenomenon has not been demonstrated in retina to date. We therefore investigated whether NGF can modulate the glutamate release in the retinal tissue at its peak of the neurotrophic activity (E10-E12). In addition this, we aimed to study the mechanisms of this effect about its dependence on extracellular Ca2+ and participation of Na+-dependent and Na+-independent glutamate transporters. Since high levels of glutamate signalization have been implicated in the oxidative stress, we also investigated the effects of NGF on the thiols compounds. We used intact retinal tissue from chicken embryos (E11) incubated with NGF (10, 50, 100 ng/ml) for different periods (15, 30, 45, 60, 120 min). Extracellular glutamate and thiols content was measured by HPLC methods and colorimetric assay, respectively. We found that NGF rapidly enhances the release of basal glutamate and it can induce thiol release in a more prolonged time of incubation, as well. Interestingly, the NGF-induced increase in the extracellular levels of glutamate was blocked by Ca2+-free medium only in retina treated for 15 min. Retina incubated for 30 min showed a non-vesicular NGF-induced glutamate release. Since glutamate and thiol release was not blocked by Zn2+, we suggested the possible involvement of system Xc- in both processes.NGF-induced increase in the extracellular thiol could be an important protective mechanism enabling retinal neurons to maintain their redox status during development.