Toshiaki Yokoi, Daisuke Tokuhara, Mika Saito, Hiroyuki Ichiba, Tsunekazu Yamano
{"title":"幼鼠癫痫持续状态后海马BDNF和TrkB的表达。","authors":"Toshiaki Yokoi, Daisuke Tokuhara, Mika Saito, Hiroyuki Ichiba, Tsunekazu Yamano","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>The immature brain is more susceptible to seizures than mature brains but less vulnerable to seizure-induced neuronal loss. We studied age-related susceptibility and vulnerability to kainic acid-induced status epilepticus (KASE) in rats in terms of hippocampal expression of brain-derived neurotrophic factor (BDNF) and tyrosine kinase B receptor (TrkB).</p><p><strong>Methods: </strong>Immunohistochemical and Western analysis were performed after kainic acid (KA)-induced status epilepticus (SE).</p><p><strong>Results: </strong>KA doses required to induce SE increased from 1.5 mg/kg in 1-week-old rats to 10 mg/kg at 4 weeks of older. After SE the older rats showed spontaneous seizures and hippocampal pyramidal neuronal loss-unlike rats under 4 weeks old. Hippocampal BDNF protein expression had increased fivefold in 1-week-old rats and threefold in 8-week-old rats 1 day after SE, returning to baseline 2 days after SE. TrkB expression showed little effect from KASE at either age.</p><p><strong>Conclusions: </strong>These results indicated that the critical period as for vulnerability to SE was the age of 4-week-old and older in the rat. Since the response patterns of BDNF and TrkB to SE were similar between neonatal and the adult rats, our study revealed that the observed transient upregulation of BDNF did not contribute to cause epilepsy in neonatal rats.</p>","PeriodicalId":19613,"journal":{"name":"Osaka city medical journal","volume":"53 2","pages":"63-71"},"PeriodicalIF":0.0000,"publicationDate":"2007-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Hippocampal BDNF and TrkB expression in young rats after status epilepticus.\",\"authors\":\"Toshiaki Yokoi, Daisuke Tokuhara, Mika Saito, Hiroyuki Ichiba, Tsunekazu Yamano\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>The immature brain is more susceptible to seizures than mature brains but less vulnerable to seizure-induced neuronal loss. We studied age-related susceptibility and vulnerability to kainic acid-induced status epilepticus (KASE) in rats in terms of hippocampal expression of brain-derived neurotrophic factor (BDNF) and tyrosine kinase B receptor (TrkB).</p><p><strong>Methods: </strong>Immunohistochemical and Western analysis were performed after kainic acid (KA)-induced status epilepticus (SE).</p><p><strong>Results: </strong>KA doses required to induce SE increased from 1.5 mg/kg in 1-week-old rats to 10 mg/kg at 4 weeks of older. After SE the older rats showed spontaneous seizures and hippocampal pyramidal neuronal loss-unlike rats under 4 weeks old. Hippocampal BDNF protein expression had increased fivefold in 1-week-old rats and threefold in 8-week-old rats 1 day after SE, returning to baseline 2 days after SE. TrkB expression showed little effect from KASE at either age.</p><p><strong>Conclusions: </strong>These results indicated that the critical period as for vulnerability to SE was the age of 4-week-old and older in the rat. Since the response patterns of BDNF and TrkB to SE were similar between neonatal and the adult rats, our study revealed that the observed transient upregulation of BDNF did not contribute to cause epilepsy in neonatal rats.</p>\",\"PeriodicalId\":19613,\"journal\":{\"name\":\"Osaka city medical journal\",\"volume\":\"53 2\",\"pages\":\"63-71\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2007-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Osaka city medical journal\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Osaka city medical journal","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Hippocampal BDNF and TrkB expression in young rats after status epilepticus.
Background: The immature brain is more susceptible to seizures than mature brains but less vulnerable to seizure-induced neuronal loss. We studied age-related susceptibility and vulnerability to kainic acid-induced status epilepticus (KASE) in rats in terms of hippocampal expression of brain-derived neurotrophic factor (BDNF) and tyrosine kinase B receptor (TrkB).
Methods: Immunohistochemical and Western analysis were performed after kainic acid (KA)-induced status epilepticus (SE).
Results: KA doses required to induce SE increased from 1.5 mg/kg in 1-week-old rats to 10 mg/kg at 4 weeks of older. After SE the older rats showed spontaneous seizures and hippocampal pyramidal neuronal loss-unlike rats under 4 weeks old. Hippocampal BDNF protein expression had increased fivefold in 1-week-old rats and threefold in 8-week-old rats 1 day after SE, returning to baseline 2 days after SE. TrkB expression showed little effect from KASE at either age.
Conclusions: These results indicated that the critical period as for vulnerability to SE was the age of 4-week-old and older in the rat. Since the response patterns of BDNF and TrkB to SE were similar between neonatal and the adult rats, our study revealed that the observed transient upregulation of BDNF did not contribute to cause epilepsy in neonatal rats.