Ontogenetic profile of glutamate uptake in brain structures slices from rats: sensitivity to guanosine

Thomazi, Ana Paula

doi:10.1016/j.mad.2004.04.005

Cited by 66 publications

(27 citation statements)

References 58 publications

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“…This suggests that the effect of guanosine on the uptake of glutamate by astrocytes depends on an imbalance in the extracellular levels of this neurotransmitter, reinforcing the notion that guanosine may have a neuroprotective role in response to CNS injuries [63]. In addition, preliminary in vitro evidence suggests that the ability of guanosine to stimulate astrocytic glutamate uptake is agedependent [64,65]. Future studies are warranted to confirm this hypothesis.…”

Section: The Role Of Guanosine On Glutamatergic Transmissionmentioning

confidence: 60%

Guanosine and its role in neuropathologies

Bettio

Gil-Mohapel

Rodrigues

2016

Purinergic Signalling

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Guanosine is a purine nucleoside thought to have neuroprotective properties. It is released in the brain under physiological conditions and even more during pathological events, reducing neuroinflammation, oxidative stress, and excitotoxicity, as well as exerting trophic effects in neuronal and glial cells. In agreement, guanosine was shown to be protective in several in vitro and/or in vivo experimental models of central nervous system (CNS) diseases including ischemic stroke, Alzheimer's disease, Parkinson's disease, spinal cord injury, nociception, and depression. The mechanisms underlying the neurobiological properties of guanosine seem to involve the activation of several intracellular signaling pathways and a close interaction with the adenosinergic system, with a consequent stimulation of neuroprotective and regenerative processes in the CNS. Within this context, the present review will provide an overview of the current literature on the effects of guanosine in the CNS. The elucidation of the complex signaling events underlying the biochemical and cellular effects of this nucleoside may further establish guanosine as a potential therapeutic target for the treatment of several neuropathologies.

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Section: The Role Of Guanosine On Glutamatergic Transmissionmentioning

confidence: 60%

Guanosine and its role in neuropathologies

Bettio

Gil-Mohapel

Rodrigues

2016

Purinergic Signalling

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“…Despite the existing data regarding the concentrations and involvement of glucose metabolism, MG and AGE molecules in diabetes and neurodegenerative diseases, little is known of the effect of these compounds on brain cell functions, particularly in brain slices where neuroglial circuitry is partially preserved (Thomazi et al 2004;Buyukuysal 2005;Sajikumar and Navakkode 2005). Clarification of these mechanisms is important to establish the possible alterations in each one of these compounds and to design therapeutic approaches with targets of clinical relevance.…”

Section: Introductionmentioning

confidence: 99%

Methylglyoxal and carboxyethyllysine reduce glutamate uptake and S100B secretion in the hippocampus independently of RAGE activation

et al. 2015

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Diabetes is a metabolic disease characterized by high fasting-glucose levels. Diabetic complications have been associated with hyperglycemia and high levels of reactive compounds, such as methylglyoxal (MG) and advanced glycation endproducts (AGEs) formation derived from glucose. Diabetic patients have a higher risk of developing neurodegenerative diseases, such as Alzheimer's disease or Parkinson's disease. Herein, we examined the effect of high glucose, MG and carboxyethyllysine (CEL), a MG-derived AGE of lysine, on oxidative, metabolic and astrocyte-specific parameters in acute hippocampal slices, and investigated some of the mechanisms that could mediate these effects. Glucose, MG and CEL did not alter reactive oxygen species (ROS) formation, glucose uptake or glutamine synthetase activity. However, glutamate uptake and S100B secretion were decreased after MG and CEL exposure. RAGE activation and glycation reactions, examined by aminoguanidine and L-lysine co-incubation, did not mediate these changes. Acute MG and CEL exposure, but not glucose, were able to induce similar effects on hippocampal slices, suggesting that conditions of high glucose concentrations are primarily toxic by elevating the rates of these glycation compounds, such as MG, and by generation of protein cross-links. Alterations in the secretion of S100B and the glutamatergic activity mediated by MG and AGEs can contribute to the brain dysfunction observed in diabetic patients.

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“…The GMP effects were evaluated on brain cortical preparations based on previous studies indicating that this brain structure is responsive to guanine-based purines (GBPs) [37,38].…”

Section: Slice and Tissue Preparationmentioning

confidence: 99%

“…The cortical coronal slices (0.4 mm) from the right parietal area were obtained using a Mcllwain tissue chopper as previously described [38]. The slices were used for glutamate uptake or OGD assays.…”

Section: Slice and Tissue Preparationmentioning

confidence: 99%

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Effects of 3 weeks GMP oral administration on glutamatergic parameters in mice neocortex

Ganzella

Moreira

Almeida

et al. 2011

Purinergic Signalling

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Overstimulation of the glutamatergic system (excitotoxicity) is involved in various acute and chronic brain diseases. Several studies support the hypothesis that guanosine-5′-monophosphate (GMP) can modulate glutamatergic neurotransmission. The aim of this study was to evaluate the effects of chronically administered GMP on brain cortical glutamatergic parameters in mice. Additionally, we investigated the neuroprotective potential of the GMP treatment submitting cortical brain slices to oxygen and glucose deprivation (OGD). Moreover, measurements of the cerebrospinal fluid (CSF) purine levels were performed after the treatment. Mice received an oral administration of saline or GMP during 3 weeks. GMP significantly decreases the cortical brain glutamate binding and uptake. Accordingly, GMP reduced the immunocontent of the glutamate receptors subunits, NR2A/B and GluR1 (NMDA and AMPA receptors, respectively) and glutamate transporters EAAC1 and GLT1. GMP treatment significantly reduced the immunocontent of PSD-95 while did not affect the content of Snap 25, GLAST and GFAP. Moreover, GMP treatment increased the resistance of neocortex to OGD insult. The chronic GMP administration increased the CSF levels of GMP and its metabolites. Altogether, these findings suggest a potential modulatory role of GMP on neocortex glutamatergic system by promoting functional and plastic changes associated to more resistance of mice neocortex against an in vitro excitotoxicity event.Keywords GMP . Guanine-based purines . Glutamatergic system . Excitotoxicity . Oxygen and glucose deprivation . Neuroprotection

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Ontogenetic profile of glutamate uptake in brain structures slices from rats: sensitivity to guanosine

Cited by 66 publications

References 58 publications

Guanosine and its role in neuropathologies

Guanosine and its role in neuropathologies

Methylglyoxal and carboxyethyllysine reduce glutamate uptake and S100B secretion in the hippocampus independently of RAGE activation

Effects of 3 weeks GMP oral administration on glutamatergic parameters in mice neocortex

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