Delayed induction of p38 MAPKs in reactive astrocytes in the brain of mice after KA-induced seizure

Yongzhe Che, Young Mi Yu, Pyung Lim Han, Ja Kyeong Lee

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39 Scopus citations


Activation of p38 mitogen-activated protein kinase (p38 MAPK) has been implicated in pathological changes in inflammatory and apoptotic processes in various cell types including neurons. Here we report the delayed induction of p38 MAPKs in the brain of mice following kainic acid (KA)-induced seizure. The immunoreactivities of p38α and p38β MAPKs were markedly increased in the brain 4 days after KA administration, especially in the areas undergoing selective neuronal loss. In particular, p38β was dramatically increased in reactive astrocytes of CA3 and CA1 regions of hippocampus with its enriched localization in the nucleus of astrocytes. The induction of p38β was sustained for more than 10 days after KA-treatment. Pre-administration of the selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI), which suppressed the delayed neuronal death as well as astrogliosis in hippocampus of seizure-experienced animals, dramatically repressed the delayed induction of p38β MAPK in astrocytes. The repression was reversed by the co-injection with L-arginine (L-arg), a substrate for NOS, which coincided with the aggravation of neuronal death. Together, these data suggested a role of p38 MAPK signal pathway in delayed neuronal death and/or in reactive gliosis in mice with KA-induced seizure.

Original languageEnglish
Pages (from-to)157-165
Number of pages9
JournalMolecular Brain Research
Issue number1-2
StatePublished - 19 Oct 2001

Bibliographical note

Funding Information:
This work was supported by a grant (HMP-00-B-21300-0213) from the Korean Health 21 R&D Project, Ministry of Health and Welfare, Republic of Korea for J-K Lee.


  • Astrocyte
  • Delayed neuronal death
  • Gliosis
  • p38 MAPK
  • Status epilepticus


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