Navegando por Assunto "Glutamato"

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Acesso aberto (Open Access)
Adenosina modula os níveis extracelulares de glutamato induzido por hiperosmolaridade em cultura de astrócitos hipotalâmicos
(Universidade Federal do Pará, 2016-04-29) BRAGA, Danielle Valente; DINIZ, Domingos Luiz Wanderley Picanço; http://lattes.cnpq.br/9601463988942971; SILVA, Anderson Manoel Herculano Oliveira da; http://lattes.cnpq.br/8407177208423247
Recent studies have shown that glutamate release by hypothalamic glial cells is an important physiological response to hyperosmolarity. Furthermore, previous studies point out an accentuated increase of the adenosine levels in renal interstitial fluid after the intake sodium increases. This study aims to evaluate the possible relationship between the adenosine and glutamate releases in primary cultures of astrocytes exposed to hyperosmolarity conditions. Hypothalamic astrocytes cultures of Wistar rats at the first two days after birth were exposed to hypertonic sodium solution (340mOsm/L) in different times (3, 5, 10 e 15 min). After this stimulus, the incubation medium was harvested and the extracellular levels of glutamate and adenosine were determined by High Performance Liquid Chromatography. In order to evaluate the relationship between these compounds in hyperosmotic conditions, we have used treatment of the cultures with adenosine, with R-PIA (an agonist of the A1 receptor), as well as with glutamate (an agonist of the NMDA receptor). Our results showed a significant increase of the extracellular levels of glutamate after the hyperosmotic stimulus with a peak at 5 min. Similarly, we have seen an increase of the adenosine levels in the incubation medium after 10 and 15 min. The treatment with glutamate induced an increase in extracellular levels of adenosine after 15 and 20 minutes in isosmotic medium. The exposure to the NMDA receptor did not induce the release of adenosine in none of the concentrations utilized. The pretreatment with adenosine and R-PIA A1 agonist blocked the release of glutamate induced by hyperosmolarity. Our results also showed that the effect of the stimulus on the release of glutamate and adenosine is sodium-dependent and presents a specific response for hypothalamic astrocytes, which can be modulated by the adenosine A1 receptor activation.
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/8407177208423247
Nerve 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.
Acesso aberto (Open Access)
Estressores agudos distintos produzem diferentes magnitudes do comportamento tipo de ansiedade e liberação diferencial de glutamato no cérebro de zebrafish
(Universidade Federal do Pará, 2024-08) MARTINS, Milena Letícia; SILVA, Anderson Manoel Herculano Oliveira da; http://lattes.cnpq.br/8407177208423247; https://orcid.org/0000-0003-4022-8096
Anxiety disorder is one of the most well characterized behavioral disorder in individuals submitted to acute or chronic stress. However, few studies have demonstrated how different types of stressors can modulate the neurochemical alterations involved in generation of anxiety. In the present study, we hypothesize that subjects exposed to different aversive stimuli (mechanical, chemical and spatial restriction) present varied intensity of anxiety-like behavior response associated with distinct pattern of GABA and Glutamate release in the brain. Sixty adult Danio rerio animals were randomly divided into four experimental groups: Control (CTRL), Acute Restraint Stress (ARS), Conspecific Alarm Substance (CAS) and Chasing with Net (CN). After applying the stress protocols, the animals were individually transferred to the Novel Tank Diving Test for behavioral analysis. Subsequently, their brains were collected and subjected to GABA and Glutamate release assay for quantification by HPLC. Our behavioral results showed that all aversive stimuli were capable of inducing anxiety-like behavior. However, the impact of anxiogenic behavior was more prominent in the CN and CAS groups when compared to ARS. This phenomenon was evident in all analyzed behavioral parameters (time on top, freezing, mean speed, maximum speed and erratic swimming). Our data also have shown that all aversive stimuli induced significant decrease in GABA release when compared to the control group. On the other side, only animals exposed to CN and CAS presented increase in extracellular glutamate levels. Different acute stressors induce different intensity of Anxiety-like behavior in zebrafish as well as they provoke specific alterations on the GABAerigic and Glutamatergic release in the brain. These results demonstrate the complexity of anxiety disorders, highlighting that both behavioral and neurochemical responses are highly context-dependent, supporting our initial hypothesis.
Acesso aberto (Open Access)
GABA and glutamate transporters: new events and function in the vertebrate retina
(2013) NASCIMENTO, José Luiz Martins do; SAWADA, Luis Armando; OLIVEIRA, Karen Renata Matos; CRESPO LÓPEZ, Maria Elena; SILVA, Anderson Manoel Herculano Oliveira da; HAMOY, Moisés; SILVA, Consuelo Yumiko Yoshioka e; BASTOS, Gilmara de Nazareth Tavares; PANTOJA, Wendell Mauro Soeiro
The neural retina is a highly complex tissue composed of excitatory and inhibitory neurons and glial cells. Glutamate, the main excitatory neurotransmitter, mediates information transfer from photoreceptors, bipolar cells, and ganglion cells, whereas interneurons, mainly amacrine and horizontal cells, use γ-aminobutyric acid (GABA), the main inhibitory neurotransmitter. In this review we place an emphasis on glutamate and GABA transporters as highly regulated molecules that play fundamental roles in neurotransmitter clearance, neurotransmitter release, and oxidative stress. We pharmacologically characterized glutamate transporters in chicken retina cells and identified two glutamate transporters: one Na+-dependent transporter and one Na+-independent transporter. The Na+-dependent uptake system presented characteristics related to the high-affinity xAG- system (EAAT1), and the Na+-independent uptake system presented characteristics related to the xCG- system, which highly contributes to glutamate transport in the retina. Glutamate shares the xCG- system with another amino acid, L-cysteine, suggesting the possible involvement of glutathione. Both transporter proteins are present mainly in Müller glial cells. GABA transporters (GATs) mediate high-affinity GABA uptake from the extracellular space and terminate the synaptic action of GABA in the central nervous system. GABA transporters can be modulated by molecules that act on specific sites to promote transporter phosphorylation and dephosphorylation. In addition to a role in the clearance of GABA, GATs may also release GABA through a reverse transport mechanism. In the chicken retina, a GAT-1 blocker, but not GAT2/3 blocker, was shown to inhibit GABA uptake, suggesting that GABA release from retina cells is mainly mediated by a GAT-1-like transporter.