Inhibition of delayed induction of p38 mitogen-activated protein kinase attenuates kainic acid-induced neuronal loss in the hippocampus

The activation of p38 mitogen-activated protein kinase (MAPK) has been implicated in the pathological changes accompanying inflammatory and apoptotic processes of various cell types including neurons. In a kainic acid (KA)-induced mouse seizure model, p38 MAPK is induced in reactive astrocytes in th...

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Bibliographic Details
Published in:Brain research 2004-05, Vol.1007 (1), p.188-191
Main Authors: Kim, Seung-Woo, Yu, Young-Mi, Piao, Chun Shu, Kim, Jung-Bin, Lee, Ja-Kyeong
Format: Article
Language:English
Subjects:
Activating Transcription Factor 2
Animals
Astrocyte
Biological and medical sciences
Blotting, Western
Cell Death - drug effects
Cyclic AMP Response Element-Binding Protein - metabolism
Drug Interactions
Enzyme Inhibitors - pharmacology
Excitatory Amino Acid Agonists - toxicity
Gliosis
Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy
Hippocampus - cytology
Imidazoles - pharmacology
Immunohistochemistry - methods
Kainic Acid - toxicity
Male
Medical sciences
Mice
Mice, Inbred BALB C
Mitogen-Activated Protein Kinase 8
Mitogen-Activated Protein Kinases - antagonists & inhibitors
Mitogen-Activated Protein Kinases - metabolism
Nervous system (semeiology, syndromes)
Neurology
Neurons - cytology
Neurons - drug effects
p38 MAPK
p38 Mitogen-Activated Protein Kinases
Protein Isoforms - pharmacology
Pyridines - pharmacology
SB203580
Status epilepticus
Time Factors
Transcription Factors - metabolism
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Summary:The activation of p38 mitogen-activated protein kinase (MAPK) has been implicated in the pathological changes accompanying inflammatory and apoptotic processes of various cell types including neurons. In a kainic acid (KA)-induced mouse seizure model, p38 MAPK is induced in reactive astrocytes in the CA3 region of the hippocampus where severe neuronal loss occurs. Here we report the delayed and protracted activation of p38 MAPK in the CA3 region of the hippocampus of mice treated with KA. In this model, the inhibition of p38 MAPK isoforms by SB203580, a specific inhibitor, attenuated neuronal loss in the CA3 and CA1 regions of the hippocampus, which was accompanied by the suppression of the p38 MAPK activation as well as astrogliosis. Thus, the delayed and sustained induction of p38 MAPK plays a crucial role in the neuronal damage of KA-induced brain seizures.
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2004.02.009