NMDA Preconditioning Protects against Seizures and Hippocampal Neurotoxicity Induced by Quinolinic Acid in Mice

Boeck, Carina Rodrigues; Ganzella, Marcelo; Lottermann, Amilcar; Vendite, Deusa

doi:10.1111/j.0013-9580.2004.65203.x

Cited by 56 publications

(64 citation statements)

References 29 publications

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“…Experimental studies have evaluated the neuroprotective effects of preconditioning over seizures and neuronal loss (Kitagawa et al, 1990;Bortolotto et al, 1991;Sasahira et al, 1995;Najm et al, 1998;Andre et al, 2000;Zhang et al, 2002;Boeck et al, 2004;Andre et al, 2007;de Araujo Herculano et al, 2011;Xue et al, 2011). Most preconditioning studies used a subthreshold stimulus, followed by the same stimulus in a status epilepticus (SE)-inducing dosage.…”

Section: Introductionmentioning

confidence: 99%

“…Most preconditioning studies used a subthreshold stimulus, followed by the same stimulus in a status epilepticus (SE)-inducing dosage. Examples of this preconditioning approach include subthreshold kainic acid (KA) injection or a short KA-induced seizure previous to KA-induced SE (Najm et al, 1998;Zhang et al, 2002), nonconvulsive NMDA treatment before quinolinic acid-induced SE (Boeck http et al, 2004;de Araujo et al, 2011) and one episode of bicuculline-induced seizure prior to a later bicucullineinduced seizure episode (Sasahira et al, 1995). Other studies used a preconditioning stimulus different from the SE-inducing stimulus, taking advantage of the cross-tolerance phenomenon, where an insult can induce tolerance from a later insult of different nature (Kirino, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Decreased neuron loss and memory dysfunction in pilocarpine-treated rats pre-exposed to hypoxia

et al. 2016

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Abstract-Preconditioning can induce a cascade of cellular events leading to neuroprotection against subsequent brain insults. In this study, we investigated the chronic effects of hypoxic preconditioning on spontaneous recurrent seizures (SRS), neuronal death, and spatial memory performance in rats subjected to pilocarpine (Pilo)-induced status epilepticus (SE). Rats underwent a short hypoxic episode (7% O 2 + 93% N 2 ; 30 min on two consecutive days) preceding a 4-h SE (HSE group). Control groups were rats submitted to SE only (SE), rats subjected to hypoxia only (H) or normoxia-saline (C). Animals were monitored for the occurrence of SRS, and spatial memory performance was evaluated in the radial-arm maze. Hippocampal sections were analyzed for cell death and mossy fiber sprouting at 1 or 60 days after SE. Compared to SE group, HSE had increased SE latency, reduced number of rats with SRS, reduced mossy fiber sprouting at 60 days, and reduced cell death in the hilus and the CA3 region 1 and 60 days after SE. Additionally, HSE rats had better spatial memory performance than SE rats. Our findings indicated that short hypoxic preconditioning preceding SE promotes long-lasting protective effects on neuron survival and spatial memory. Ó

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Decreased neuron loss and memory dysfunction in pilocarpine-treated rats pre-exposed to hypoxia

et al. 2016

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“…infusion in rats. In addition, Boeck et al (2004) showed that NMDA preconditioning promotes protection against QA-induced seizures and cell death.…”

Section: Introductionmentioning

confidence: 99%

Atorvastatin Prevents Hippocampal Cell Death due to Quinolinic Acid-Induced Seizures in Mice by Increasing Akt Phosphorylation and Glutamate Uptake

et al. 2009

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Statins are cholesterol-lowering agents due to the inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. Recent studies have shown statins possess pleiotropic effects, which appear to be independent from its cholesterol-lowering action. In this study, we investigated whether atorvastatin would have protective effects against hippocampal cell death promoted by quinolinic acid (QA)-induced seizures in mice. Mice were pretreated with Atorvastatin (1 or 10 mg/kg) or vehicle (saline, 0.9%), orally, once a day for 7 days before the intracerebroventricular (i.c.v.) QA infusion (36.8 nmol/site). Atorvastatin treatment with 1 mg/kg/day did not significantly prevent QA-induced seizures (13.34%). However, administration of atorvastatin 10 mg/kg/day prevented the clonic and/or tonic seizures induced by QA in 29.41% of the mice. Additionally, administration of atorvastatin 10 mg/kg/day significantly prevented QA-induced cell death in the hippocampus. Atorvastatin treatment promoted an increased Akt phosphorylation, which was sustained after QA infusion in both convulsed and non-convulsed mice. Moreover, atorvastatin pretreatment prevented the reduction in glutamate uptake into hippocampal slices induced by QA i.c.v. infusion. These results show that atorvastatin attenuated QA-induced hippocampal cellular death involving the Akt pathway and glutamate transport modulation. Therefore, atorvastatin treatment might be a useful strategy in the prevention of brain injury caused by the exacerbation of glutamatergic toxicity in neurological diseases such as epilepsy.

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“…scioncorp.com). The area where PI fluorescence (in pixels) was detectable above the background (damaged area of hippocampal slices) was analyzed using the ''density slice'' option of the Scioncorp software through the division of PI fluorescence by the total area of the slice [43].…”

Section: Preparation Of Hippocampal Slicesmentioning

confidence: 99%

ConBr, a Lectin from Canavalia brasiliensis Seeds, Protects Against Quinolinic Acid-Induced Seizures in Mice

et al. 2011

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Lectins are proteins capable of reversible binding to carbohydrates or glycoconjugates. In the central nervous system of mammals, lectins with affinity for mannose/glucose or galactose can modulate cellular communication. ConBr, a lectin isolated from the seeds of Canavalia brasiliensis, previously showed antidepressant effect in the forced swimming test in mice, with involvement of the monoaminergic system. In this study, we investigated the neuroprotective effects of ConBr against quinolinic acid (QA), a well-known NMDA agonist that produces severe neurotoxicity when administered in vivo. ConBr (10 μg/site) administered via intracerebroventricular (i.c.v.) showed a neuroprotective activity against seizures induced by QA (36.8 nmol/site; i.c.v.) when administered 15 min prior to QA, with a percentage of protection around 50%. ConBr was also able to significantly decrease the severity of the seizures but without changes in the latency of the first convulsion or the duration of the seizures. This effect was dependent on the structural integrity of the ConBr protein and its binding capacity to oligosaccharides residues. ConA, a lectin with high similarity to ConBr, did not reverse the QA-induced seizures. Moreover, ConBr was able to protect against hippocampal cell death caused by QA, which was measured by propidium iodide incorporation. QA caused activation of JNK2 and improved the phosphorylation of Ser831 and 845 on the AMPA receptor GluR1 subunit, and both of these effects were counteracted by ConBr. Our data suggest that the lectin ConBr may exert a modulatory action on NMDA receptors, which inhibits its activity in response to QA.

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NMDA Preconditioning Protects against Seizures and Hippocampal Neurotoxicity Induced by Quinolinic Acid in Mice

Cited by 56 publications

References 29 publications

Decreased neuron loss and memory dysfunction in pilocarpine-treated rats pre-exposed to hypoxia

Decreased neuron loss and memory dysfunction in pilocarpine-treated rats pre-exposed to hypoxia

Atorvastatin Prevents Hippocampal Cell Death due to Quinolinic Acid-Induced Seizures in Mice by Increasing Akt Phosphorylation and Glutamate Uptake

ConBr, a Lectin from Canavalia brasiliensis Seeds, Protects Against Quinolinic Acid-Induced Seizures in Mice

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