Na+,K+-ATPase activity impairment after experimental traumatic brain injury: Relationship to spatial learning deficits and oxidative stress

Lima, Frederico Diniz; Souza, Mauren Assis; Furian, Ana Flávia; Rambo, Leonardo Magno; Ribeiro, Leandro Rodrigo; Martignoni, F; Hoffmann, Maurício Scopel; Fighera, Michele Rechia; Royes, Luiz Fernando Freire; Oliveira, Mauro Schneider; Mello, Carlos Fernando

doi:10.1016/j.bbr.2008.05.013

Cited by 67 publications

(42 citation statements)

References 33 publications

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“…The data reported here are in discordance with those demonstrated in previous studies (Cammack et al 1992) in which hypoxia, spreading depression, and seizure activity change brain ascorbic acid levels. Considering that alterations in the redox state of regulatory sulfhydryl groups in selected targets such as Na?,K?-ATPase (Lima et al 2008), and d-ALA-D activities (Ahamed et al 2008) increase cellular excitability and can facilitate the appearance or propagation of seizures induced by pilocarpine, we decided to investigate how those enzymes act, which have not been studied using the pilocarpine model yet, as well as evaluate the effects of LA pretreatment on the same enzymes. The results presented in this report showed that the appearance of seizure episodes induced by pilocarpine occurred in association with inhibition of d-ALA-D activity, suggesting that seizures, oxidative stress, and d-ALA-D activity are linked events.…”

Section: Discussionmentioning

confidence: 99%

Lipoic Acid Alters δ-Aminolevulinic Dehydratase, Glutathione Peroxidase and Na+,K+-ATPase Activities and Glutathione-Reduced Levels in Rat Hippocampus After Pilocarpine-Induced Seizures

Freitas

2009

Cell Mol Neurobiol

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In the present study, we investigated the effects of lipoic acid (LA) in the brain oxidative stress caused by pilocarpine-induced seizures in adult rats. Wistar rats were treated with 0.9% saline (i.p., control group), lipoic acid (10 mg/kg, i.p., LA group), pilocarpine (400 mg/kg, i.p., pilocarpine group), and the association of LA (10 mg/kg, i.p.) plus pilocarpine (400 mg/kg, i.p.), 30 min before the administration of LA (LA plus pilocarpine group). After the treatments, all groups were observed for 1 h. The enzyme activities [delta-aminolevulinic dehydratase (delta-ALA-D), glutathione peroxidase (GPx), glutathione reductase (GR), and Na+,K+-ATPase] as well as the glutathione-reduced (GSH) and ascorbic acid (AA) concentrations were measured using spectrophotometric methods, and the results were compared to values obtained from saline and pilocarpine-treated animals. Protective effects of LA were also evaluated on the same parameters. In pilocarpine group, no changes were observed in GPx and GR activities and AA content. Moreover, in the same group, decrease in GSH levels as well as a reduction in delta-ALA-D and Na+,K+-ATPase activities after seizures was observed. In turn, in LA plus pilocarpine group, the appearance of seizures was abolished, and the decreases in delta-ALA-D and Na+,K+-ATPase activities produced by seizures as well as increases in GSH levels and GPx activity were reversed, when compared to the pilocarpine seizing group. The results of the present study demonstrated that preadministration of LA abolished seizure episodes induced by pilocarpine in rat, probably by reducing oxidative stress in rat hippocampus caused by seizures.

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Section: Discussionmentioning

confidence: 99%

Lipoic Acid Alters δ-Aminolevulinic Dehydratase, Glutathione Peroxidase and Na+,K+-ATPase Activities and Glutathione-Reduced Levels in Rat Hippocampus After Pilocarpine-Induced Seizures

Freitas

2009

Cell Mol Neurobiol

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“…74,75 It is well established that ion gradients that drive glutamate uptake and the enzymes, such as the Na + -K + -ATPase, that maintain these ion gradients, are compromised in the traumatically-injured brain. 76,77 Importantly, massive increases in extracellular potassium and the indiscriminate release of glutamate has been reported following concussive brain injury. 78 Nonetheless, because we assessed accumulation of radiolabeled glutamate into synaptosomes ex vivo, it is not possible to determine if the lower V max is a result of reversal of transport.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of the Glutamate Transporter Activator (R)-(−)-5-methyl-1-nicotinoyl-2-pyrazoline (MS-153) following Traumatic Brain Injury in the Adult Rat

Fontana

Fox

Zoubroulis

et al. 2016

Journal of Neurotrauma

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Traumatic brain injury (TBI) in humans and in animals leads to an acute and sustained increase in tissue glutamate concentrations within the brain, triggering glutamate-mediated excitotoxicity. Excitatory amino acid transporters (EAATs) are responsible for maintaining extracellular central nervous system glutamate concentrations below neurotoxic levels. Our results demonstrate that as early as 5 min and up to 2 h following brain trauma in brain-injured rats, the activity (V max ) of EAAT2 in the cortex and the hippocampus was significantly decreased, compared with sham-injured animals. The affinity for glutamate (K M ) and the expression of glutamate transporter 1 (GLT-1) and glutamate aspartate transporter (GLAST) were not altered by the injury. Administration of (R)-(-)-5-methyl-1-nicotinoyl-2-pyrazoline (MS-153), a GLT-1 activator, beginning immediately after injury and continuing for 24 h, significantly decreased neurodegeneration, loss of microtubule-associated protein 2 and NeuN (+) immunoreactivities, and attenuated calpain activation in both the cortex and the hippocampus at 24 h after the injury; the reduction in neurodegeneration remained evident up to 14 days post-injury. In synaptosomal uptake assays, MS-153 up-regulated GLT-1 activity in the naïve rat brain but did not reverse the reduced activity of GLT-1 in traumatically-injured brains. This study demonstrates that administration of MS-153 in the acute post-traumatic period provides acute and long-term neuroprotection for TBI and suggests that the neuroprotective effects of MS-153 are related to mechanisms other than GLT-1 activation, such as the inhibition of voltage-gated calcium channels.

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“…In spite of mentioned facts, there have only been a few experimental studies concerning the markers of oxidative stress in the LFPI model in rats. To our knowledge, only some products of oxidative lipid and protein damage in the injured cortex or hippocampus at different time points following LFPI were studied [7,12,26,27].…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress Parameters in Different Brain Structures Following Lateral Fluid Percussion Injury in the Rat

et al. 2011

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Free radicals mediated damage of phospholipids, proteins and nucleic acids results in subsequent neuronal degeneration and cell loss. Aim of this study was to evaluate the existence of lipid and protein oxidative damage and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in various rat brain structures 24 h after lateral fluid percussion brain injury (LFPI). Parietal cortex, hippocampus, thalamus, entorhinal cortex, and cerebellum from the ipsilateral hemisphere were processed for analyses of the thiobarbituric acid reactive substances (TBARS) and oxidized protein levels as well as for the SOD and GSH-Px activities. Immunohistochemical detection of oxidized proteins was also performed. Results of our study showed that LFPI caused significant oxidative stress in the parietal cortex and hippocampus while other brain regions tested in this study were not oxidatively altered by LFPI. GSH-Px activities were significantly increased in the parietal cortex and hippocampus, while the SOD activities remained unchanged following LFPI in all regions investigated.

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Na+,K+-ATPase activity impairment after experimental traumatic brain injury: Relationship to spatial learning deficits and oxidative stress

Cited by 67 publications

References 33 publications

Lipoic Acid Alters δ-Aminolevulinic Dehydratase, Glutathione Peroxidase and Na+,K+-ATPase Activities and Glutathione-Reduced Levels in Rat Hippocampus After Pilocarpine-Induced Seizures

Lipoic Acid Alters δ-Aminolevulinic Dehydratase, Glutathione Peroxidase and Na+,K+-ATPase Activities and Glutathione-Reduced Levels in Rat Hippocampus After Pilocarpine-Induced Seizures

Neuroprotective Effects of the Glutamate Transporter Activator (R)-(−)-5-methyl-1-nicotinoyl-2-pyrazoline (MS-153) following Traumatic Brain Injury in the Adult Rat

Oxidative Stress Parameters in Different Brain Structures Following Lateral Fluid Percussion Injury in the Rat

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