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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pilocarpine (PC), a muscarinic receptor agonist, is used for the induction of experimental models of status epilepticus (SE) for studying the type of seizure-induced brain injury and other neuropathophysiological mechanisms of related disorder. PC was administered to day-old Taiwan Native Breeder chicks and induced severe prolonged seizures (PC+PS) and repeated seizures (PC+RS) during 4h behavioral observations. Results showed that PC+PS group had excessive levels of reactive oxygen species (ROS) and malondialdehyde (MDA) production and lower activities of superoxide dismutase (SOD) and catalase (CAT) compared to the PC+RS group (p<0.05). Neuronal death and single strand DNA were significantly increased in dissociated brain cells of PC+PS group compared to that in the PC+RS group (p<0.01). Furthermore, a decrease in mitochondrial membrane potential (MMP) was observed in PC+PS group as compared with that in PC+RS group indicating neuronal mitochondrial dysfunction in PS group not in RS group. ROS, mitochondrial dysfunction and DNA damage played important roles in pathophysiology of the immature brain to prolonged-seizure-induced damage. A manifest result of depleted enzymatic antioxidants (SOD and CAT) was also contributed for the vulnerability of the neonatal brain to prolonged-seizure-induced oxidative damage. The replenishment of SOD and CAT activities might be useful in protecting brain against prolonged-seizure-induced neuronal death.
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PMID:The effects of pilocarpine-induced status epilepticus on oxidative stress/damage in developing animals. 1934 87

It has been suggested that pilocarpine-induced seizures is mediated by increases in oxidative stress. Current researches have suggested that antioxidant compounds may afford some level of neuroprotection against the neurotoxicity of seizures in cellular level. The objective of the present study was to evaluate the neuroprotective effects of lipoic acid (LA) in rats, against the observed oxidative stress during seizures induced by pilocarpine. Wistar rats were treated with 0.9% saline (i.p., control group), LA (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 of administration of LA (LA plus pilocarpine group). After the treatments all groups were observed for 6h. The enzyme activities as well as the lipid peroxidation and nitrite concentrations were measured using spectrophotometric methods and the results compared to values obtained from saline and pilocarpine-treated animals. Protective effects of LA were also evaluated on the same parameters. In pilocarpine group there was a significant increase in lipid peroxidation and nitrite level. However, no alteration was observed in superoxide dismutase and catalase activities. Antioxidant treatment significantly reduced the lipid peroxidation level and nitrite content as well as increased the superoxide dismutase and catalase activities in hippocampus of rats after seizures induced by pilocarpine. Our findings strongly support the hypothesis that oxidative stress in hippocampus occurs during seizures induced by pilocarpine, proving that brain damage induced by the oxidative process plays a crucial role in seizures pathogenic consequences, and also imply that strong protective effect could be achieved using lipoic acid as an antioxidant.
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PMID:The evaluation of effects of lipoic acid on the lipid peroxidation, nitrite formation and antioxidant enzymes in the hippocampus of rats after pilocarpine-induced seizures. 1936 63

Although physical activity and creatine supplementation have been a documented beneficial effect on neurological disorders, its implications for epilepsy are still controversial. Thus, we decided to investigate the effects of 6 weeks swimming training, creatine supplementation (300 mg/kg; p.o.) or its combination seizures and neurochemical alterations induced by pentylenetetrazol (PTZ). We found that 6 weeks of physical training or creatine supplementation decreased the duration of PTZ-induced seizures in adult male Wistar rats, as measured by cortical and hippocampal electroencephalography and behavioral analysis. Importantly, the combination between physical training and creatine supplementation had additive anticonvulsant effects, since it increased the onset latency for PTZ-induced seizures and was more effective in decrease seizure duration than physical training and creatine supplementation individually. Analysis of selected parameters of oxidative stress and antioxidant defenses in the hippocampus revealed that physical training, creatine supplementation or its combination abrogated the PTZ-elicited increase in levels of thiobarbituric acid-reactive substances (TBARS) and protein carbonylation, as well as decrease in non-protein-thiols content, catalase (CAT) and SOD activities. In addition, this protocol of physical training and creatine supplementation prevented the PTZ-induced decrease in hippocampal Na+,K+-ATPase activity. Altogether, these results suggest that protection elicited physical training and creatine supplementation of selected targets for reactive species-mediated damage decrease of neuronal excitability and consequent oxidative damage elicited by PTZ. In conclusion, the present study shows that physical training, creatine supplementation or its combination attenuated PTZ-induced seizures and oxidative damage in vivo, and provide evidence that combination between creatine supplementation and physical exercise may be a useful strategy in the treatment of convulsive disorders.
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PMID:Additive anticonvulsant effects of creatine supplementation and physical exercise against pentylenetetrazol-induced seizures. 1939 74

This study investigated the anticonvulsant effect of 3-alkynyl selenophene (3-ASP) on pilocarpine (PC)-, pentylenetetrazole (PTZ)- and kainic acid (KA)-induced seizures and mortality in 21-day-old rats. Rats were pretreated by oral route (p.o.) with 3-ASP (10, 25 and 50mg/kg) before intraperitoneal (i.p.) administration of PC (400mg/kg), PTZ (80 mg/kg) or KA (45 mg/kg). 3-ASP increased the latency to the seizure onset on PTZ and KA models. At the dose of 50mg/kg, 3-ASP avoided the death caused by PTZ and KA. 3-ASP (50mg/kg) abolished seizures and death induced by PC in rats. To investigate the antioxidant effect of 3-ASP on rats exposed to PC, the activity of glutathione peroxidase (GPx), glutathione-S-transferase (GST), acetylcholinesterase (AChE), Na(+)K(+)ATPase, superoxide dismutase (SOD) and catalase (CAT) as well as the levels of reactive species (RS) and ascorbic acid (AA) were determined in brains of rats. 3-ASP protected against the increase in RS levels and CAT activity induced by PC in brains of rats. The decrease in the levels of AA and inhibition of Na(+)K(+)ATPase, SOD and AChE activities caused by PC were protected by 3-ASP. Subeffective doses of 3-ASP plus diazepam, 5S,10R-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) or 6,7-dinitroquinoxaline-2,3-dione (DNQX) increased the latency to the seizure onset induced by PC, suggesting the involvement of ionotropic glutamatergic and GABAergic receptors in anticonvulsant action of 3-ASP. The anticonvulsant and antioxidant effects of 3-ASP in 21-day-old rats on PC model were demonstrated.
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PMID:Anticonvulsant and antioxidant effects of 3-alkynyl selenophene in 21-day-old rats on pilocarpine model of seizures. 1948 Sep 88

The present study investigated the effects of isopulegol, a monoterpene alcohol, in PTZ-induced convulsions and verified possible involved mechanisms. Saline, isopulegol or diazepam were intraperitonealy injected 30 min before PTZ. The latency for development of convulsions and mortality, as well as the mortality protection percentage was recorded. For investigating the involvement of GABAergic system, flumazenil was utilized. The activity of antioxidant enzyme catalase as well as the levels of reduced glutathione and lipid peroxidation were measured in brain hippocampus. Similarly to diazepam, isopulegol significantly prolonged the latency for convulsions and mortality of mice. All animals were protected against mortality at higher dose of isopulegol. Flumazenil pretreatment decreased the prolongation of seizure latency induced by both diazepam and isopulegol, although it was not able to reverse the latency and protection percent for mortality. Isopulegol also significantly prevented PTZ-induced increase in lipid peroxidation, preserved catalase activity in normal levels, and prevented the PTZ-induced loss of GSH in hippocampus of mice. These results suggest that the anticonvulsant and bioprotective effects of isopulegol against PTZ-induced convulsions are possibly related to positive modulation of benzodiazepine-sensitive GABA(A) receptors and to antioxidant properties.
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PMID:Effects of isopulegol on pentylenetetrazol-induced convulsions in mice: possible involvement of GABAergic system and antioxidant activity. 1955 70

The relationship between free radical and scavenger enzymes has been found in the epileptic phenomena and reactive oxygen species have been implicated in seizure-induced neurodegeneration. Using the epilepsy model obtained by systemic administration of pilocarpine in rats, we investigated the lipid peroxidation, nitrite content, superoxide dismutase (SOD) and catalase activities in the hippocampus of rats during chronic period. The enzyme activities as well as the lipid peroxidation and nitrite concentrations were measured using spectrophotometric methods and the results compared to values obtained from saline-treated animals. The superoxide dismutase and catalase activities increased during the chronic phase. In addition, lipid peroxidation and nitrite levels increased in same period in the hippocampus of animals observed during spontaneous recurrent seizures. Previous studies showed that animals presenting seizures and submitted to 24h of status epilepticus showed normal levels of superoxide dismutase and increased in catalase activities as well as an increase in hippocampal lipid peroxidation and nitrite concentrations. These results show a direct evidence of lipid peroxidation and nitrite during seizure activity that could be responsible for neuronal damage in the hippocampus of rats, during the establishment of pilocarpine model of epilepsy.
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PMID:Investigation of oxidative stress involvement in hippocampus in epilepsy model induced by pilocarpine. 1961 71

The relationship between free radical and scavenger enzymes has been found in the epilepsy and reactive oxygen species have been implicated in seizure-induced neurodegeneration. It has been suggested that pilocarpine-induced seizures is mediated by increases in oxidative stress. Current researches have suggested that antioxidant compounds may afford some level of neuroprotection against the neurotoxicity of seizures in cellular level. The objective of the present study was to evaluate the neuroprotective effects of lipoic acid (LA) in rats, against the observed oxidative stress during seizures induced by pilocarpine. Wistar rats were treated with 0.9% saline (i.p., control group), LA (20mg/kg, i.p., LA group), pilocarpine (400mg/kg, i.p., P400 group), and the association of LA (20mg/kg, i.p.) plus pilocarpine (400mg/kg, i.p.), 30 min before of administration of LA (LA plus P400 group). After the treatments all groups were observed for 1h. The enzyme activities as well as the lipid peroxidation and nitrite concentrations were measured using spectrophotometric methods and the results compared to values obtained from saline and pilocarpine-treated animals. Protective effects of LA were also evaluated on the same parameters. In P400 group there was a significant increase in lipid peroxidation, nitrite level and glutathione peroxidase (GPx) activity. However, no alteration was observed in superoxide dismutase (SOD) and catalase activities. Antioxidant treatment significantly reduced the lipid peroxidation level and nitrite content as well as increased the SOD, catalase and GPx activities in rat striatum after seizures. Our findings strongly support the hypothesis that oxidative stress in striatum occurs during seizures induced by pilocarpine, proving that brain damage induced by the oxidative process plays a crucial role in seizures pathogenic consequences, and also imply that strong protective effect could be achieved using LA.
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PMID:Effects of lipoic acid on oxidative stress in rat striatum after pilocarpine-induced seizures. 1971 35

Temporal lobe epilepsy is the most common form of epilepsy in humans. Oxidative stress is a mechanism of cell death induced by seizures. Buspirone presents anxyolitic and antidepressant effects due to their ability to stimulate 5-HT(1A) receptor. We studied the buspirone effects on oxidative stress in rat hippocampus after seizures and status epilepticus (SE) induced by pilocarpine. In pilocarpine group there was a significant increase in lipid peroxidation and nitrite levels. However, no alteration was observed in superoxide dismutase and catalase activities. Buspirone pretreatment produces significantly reduction of the lipid peroxidation level (60%) and nitrite content (44%) as well as increased the superoxide dismutase (47%) and catalase (40%) activities in rat hippocampus after seizures, when compared with the pilocarpine group. The intraperitoneal injection of buspirone prior to pilocarpine suppressed the behavioral seizure occurrence. According to our results, the oxidative stress is present during seizures. Buspirone exerted anticonvulsant effects associated with the inhibition of the development of oxidative stress. These results suggest a therapeutic use potential of buspirone in epilepsy treatment.
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PMID:Oxidative stress in rat hippocampus caused by pilocarpine-induced seizures is reversed by buspirone. 1980 Sep 52

Reactive oxygen species have been implicated in seizure-induced neurodegeneration, and there is a correlation between free radical level and scavenger enzymatic activity in the epilepsy. It has been suggested that pilocarpine-induced seizures is mediated by an increase in oxidative stress. Current research has found that antioxidant may provide, in a certain degree, neuroprotection against the neurotoxicity of seizures at the cellular level. Alpha-tocopherol has numerous nonenzymatic actions and is a powerful liposoluble antioxidant. The objective of the present study was to evaluate the neuroprotective effects of alpha-tocopherol (TP) in rats, against oxidative stress caused by pilocarpine-induced seizures. 30 min prior to behavioral observation, Wistar rats were treated with, 0.9% saline (i.p., control group), TP (200 mg/kg, i.p., TP group), pilocarpine (400 mg/kg, i.p., P400 group), or the combination of TP (200 mg/kg, i.p.) and pilocarpine (400 mg/kg, i.p.). After the treatments all groups were observed for 6 h. The enzymatic activities, lipid peroxidation and nitrite concentrations were measured using speccitrophotometric methods and these data were assayed. In P400 group mice there was a significant increase in lipid peroxidation and nitrite levels. However, no alteration was observed in superoxide dismutase (SOD) and catalase activities. In the TP and pilocarpine co-administered mice, antioxidant treatment significantly reduced the lipid peroxidation level and nitrite content, as well as increased the SOD and catalase activities in rat hippocampus after seizures. Our findings strongly support the hypothesis that oxidative stress occurs in hippocampus during pilocarpine-induced seizures, indicate that brain damage induced by the oxidative process plays a crucial role in seizures pathogenic consequences, and imply that strong protective effect could be achieved using alpha-tocopherol.
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PMID:The effects of alpha-tocopherol on hippocampal oxidative stress prior to in pilocarpine-induced seizures. 1994 Oct 68

The present study assessed the effect of carbamazepine and lamotrigine on cognitive function and oxidative stress in brain during chemically induced epileptogenesis in rats. Epileptogenesis was induced by administration of pentylenetetrazole (30 mg/kg, s.c.) on alternate days (three times/week) for 9-11 weeks or until stage 4 of seizure score was achieved. The neurobehavioural parameters used for cognitive assessment were step-down latency in continuous avoidance apparatus and transfer latency in elevated plus maze test paradigm. Carbamazepine and lamotrigine were administered intraperitoneally in doses of 60 mg/kg and 25 mg/kg, respectively, according to the groups, once a day for 11 weeks. Oxidative stress was assessed in isolated homogenized whole brain samples and estimated for the levels of malondialdehyde, reduced glutathione, catalase and superoxide dismutase. The results showed that lamotrigine did not produce any change in cognitive function, while carbamazepine produced cognitive dysfunction. Cognitive decline seen in the carbamazepine-treated pentylenetetrazole-kindled group was also associated with increased oxidative stress. Lamotrigine treatment had no effect on oxidative stress parameters alone, while it significantly decreased oxidative stress in the pentylenetetrazole-kindled group as compared to the pentylenetetrazole-kindled carbamazepine-treated group.
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PMID:Effect of carbamazepine and lamotrigine on cognitive function and oxidative stress in brain during chemical epileptogenesis in rats. 2000 63


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