Evaluation of levetiracetam effects on pilocarpine-induced seizures: Cholinergic muscarinic system involvement

Oliveira, Azauri Albano de; Nogueira, Carlos Renato Alves; Nascimento, Viviane S.; Aguiar, Lissiana Magna Vasconcelos; Freitas, Raquel; Sousa, F.C.F.; Viana, Glauce Socorro Barros; Fonteles, M.M.F.

doi:10.1016/j.neulet.2005.05.048

Cited by 31 publications

(22 citation statements)

References 43 publications

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“…Our results of the observed behavioral alterations were previously shown in Oliveira et al (2005), when we described that all animals treated with P400 presented peripheral cholinergic signs (miosis, piloerection, chromodacriorrhea, diarrhea, masticatory) and stereotyped movements (continuous sniffing, paw licking, and rearing), followed by motor limbic seizures in 100% (40/40) of the tested animals. The convulsive process persisted and built up to a SE in 90% (36/40) of these mice, leading to death of all animals.…”

Section: Animals and Experimental Protocolsupporting

confidence: 84%

Effects of Levetiracetam in Lipid Peroxidation Level, Nitrite–Nitrate Formation and Antioxidant Enzymatic Activity in Mice Brain After Pilocarpine-Induced Seizures

et al. 2007

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: Oxidative stress has been implicated in a large number of human degenerative diseases, including epilepsy. Levetiracetam (LEV) is a new antiepileptic agent with broad-spectrum effects on seizures and animal models of epilepsy. Recently, it was demonstrated that the mechanism of LEV differs from that of conventional antiepileptic drugs. Objectifying to investigate if LEV mechanism of action involves antioxidant properties, lipid peroxidation levels, nitrite-nitrate formation, catalase activity, and glutathione (GSH) content were measured in adult mice brain. The neurochemical analyses were carried out in hippocampus of animals pretreated with LEV (200 mg/kg, i.p.) 60 min before pilocarpine-induced seizures (400 mg/kg, s.c.). The administration of alone pilocarpine, 400 mg/kg, s.c. (P400) produced a significant increase of lipid peroxidation level in hippocampus. LEV pretreatment was able to counteract this increase, preserving the lipid peroxidation level in normal value. P400 administration also produced increase in the nitrite-nitrate formation and catalase activity in hippocampus, beyond a decrease in GSH levels. LEV administration before P400 prevented the P400-induced alteration in nitrite-nitrate levels and preserved normal values of catalase activity in hippocampus. Moreover, LEV administration prevented the P400-induced loss of GSH in this cerebral area. The present data suggest that the protective effects of LEV against pilocarpine-induced seizures can be mediated, at least in part, by reduction of lipid peroxidation and hippocampal oxidative stress.

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Section: Animals and Experimental Protocolsupporting

confidence: 84%

Effects of Levetiracetam in Lipid Peroxidation Level, Nitrite–Nitrate Formation and Antioxidant Enzymatic Activity in Mice Brain After Pilocarpine-Induced Seizures

et al. 2007

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“…Several reports have demonstrated that antioxidant compounds displayed an anticonvulsant effect in different animal models (Wilhelm et al, 2009;Oliveira et al, 2005). In this study, ISO revealed an anticonvulsant effect on the pilocarpine model in rats.…”

Section: Discussionsupporting

confidence: 51%

Antioxidant mechanisms of iso-6-cassine in suppressing seizures induced by pilocarpine

Freitas¹,

Silva²,

Silva³

et al. 2011

Rev. bras. farmacogn.

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Abstract:The aim of this study was to evaluate the in vitro antioxidant effects of 12-[(2R,5R,6R)-5-hydroxy-6-methylpiperidin-2-yl]dodecan-2-one (iso-6-cassine; ISO) and the anticonvulsant effects of ISO on pilocarpine-induced seizures in rats. Wistar rats were treated with 0.9% saline (i.p., control group), pilocarpine (400 mg/kg, i.p., pilocarpine group), and the association of ISO (1.0 mg/kg, i.p.) plus pilocarpine (400 mg/kg, i.p.), 30 min after administration of ISO (ISO plus pilocarpine group). After the treatments all groups were observed for 1h. The antioxidant effect of ISO on the pilocarpine model was assessed by determining the activity of glutathione peroxidase (GPx), glutathione-Stransferase (GST) and catalase (CAT) as well as the levels of reactive species (RS) and lipid peroxidation (LP). In vitro, ISO (5 μM) reduced RS and LP. ISO (1.0 mg/kg) and abolished seizures and death induced by pilocarpine in rats. ISO protected against the increase in the RS and LP levels, GST activity as well as the inhibition of GPx activity caused by pilocarpine. In addition, ISO increased the catalase activity in hippocampus of seized rats. In conclusion, the dta suggest that ISO can present anticonvulsant and antioxidant properties in the pilocarpine model of seizures in rats.

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“…As the changes in muscarinic M 1 -like receptors were not correlated with the alterations in AChE activity we can speculate that from the types of muscarinic receptors not only M 1 -like ones are involved in cocaineinduced toxicity in ST and PFC. A recent report (Oliveira et al, 2005) observed a downregulation of M 1 -and M 2 -like receptors after pilocarpine-induced seizures.…”

Section: Discussionmentioning

confidence: 85%

Differential Effects of Cocaine-Induced Seizures and Lethality on M1-Like Muscarinic and Dopaminergic D1- and D2-Like Binding Receptors in Mice Brain

et al. 2006

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This work was designed to study the changes produced by cocaine-induced seizures and lethality on dopaminergic D(1)- and D(2)-like receptors, muscarinic M(1)-like binding sites, as well as acetylcholinesterase activity in mice prefrontal cortex (PFC) and striatum (ST). Binding assays were performed in brain homogenates from the PFC and ST and ligands used were [(3)H]-N-methylscopolamine, [(3)H]-NMS (in the presence of carbachol), [(3)H]-SCH 23390 and [(3)H]-spiroperidol (in presence of mianserin), for muscarinic (M(1)-like), D(1)- and D(2)-like receptors, respectively. Brain acetylcholinesterase (AChE) activity was also determined in these brain areas. Cocaine-induced SE decreased [(3)H]-SCH 23390 binding in both ST and PFC areas. A decrease in [(3)H]-NMS binding and an increase in [(3)H]-spiroperidol binding in PFC was also observed. Cocaine-induced lethality increased [(3)H]-spiroperidol binding in both areas and decreased [(3)H]-NMS binding only in PFC, while no difference was seen in [(3)H]-SCH 23390 binding. Neither SE, nor lethality altered [(3)H]-NMS binding in ST. AChE activity increased after SE in ST while after death the increase occurred in both PFC and ST. In conclusion, cocaine-induced SE and lethality produces differential changes in brain cholinergic and dopaminergic receptors, depending on the brain area studied suggesting an extensive and complex involvement of these with cocaine toxicity in central nervous system.

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Evaluation of levetiracetam effects on pilocarpine-induced seizures: Cholinergic muscarinic system involvement

Cited by 31 publications

References 43 publications

Effects of Levetiracetam in Lipid Peroxidation Level, Nitrite–Nitrate Formation and Antioxidant Enzymatic Activity in Mice Brain After Pilocarpine-Induced Seizures

Effects of Levetiracetam in Lipid Peroxidation Level, Nitrite–Nitrate Formation and Antioxidant Enzymatic Activity in Mice Brain After Pilocarpine-Induced Seizures

Antioxidant mechanisms of iso-6-cassine in suppressing seizures induced by pilocarpine

Differential Effects of Cocaine-Induced Seizures and Lethality on M1-Like Muscarinic and Dopaminergic D1- and D2-Like Binding Receptors in Mice Brain

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