Midkine, heparin-binding growth factor, blocks kainic acid-induced seizure and neuronal cell death in mouse hippocampus

BMC Neuroscience

Research Article

Dongsun Park¹  In J Lim²  Jae K Ryu³  Yun B Kim⁴  Min C Lee⁵  Hong J Lee⁶  Seung U Kim⁶ 

[1] College of Veterinary Medicine, Chungbuk National University, Cheongju, Korea;Department of Physiology, Chung-Ang University College of Medicine, Seoul, Korea;Division of Neurology, Department of Medicine, UBC Hospital, University of British Columbia, Vancouver, Canada;Division of Neurology, Department of Medicine, UBC Hospital, University of British Columbia, Vancouver, Canada;College of Veterinary Medicine, Chungbuk National University, Cheongju, Korea;Division of Neurology, Department of Medicine, UBC Hospital, University of British Columbia, Vancouver, Canada;Department of Pathology, Chonnam National University Medical School, Gwangju, Korea;Division of Neurology, Department of Medicine, UBC Hospital, University of British Columbia, Vancouver, Canada;Medical Research Institute, Chung-Ang University College of Medicine, Seoul, Korea;

关键词: Temporal Lobe Epilepsy;    Kainic Acid;    Granule Cell Layer;    Nissl Staining;    Stratum Pyramidale;   

DOI  :  10.1186/1471-2202-11-42

 received in 2009-08-31, accepted in 2010-03-26,  发布年份 2010

来源: Springer

【 摘 要 】

BackgroundMidkine (MK), a member of the heparin-binding growth factor family, which includes MK and pleiotrophin, is known to possess neurotrophic and neuroprotective properties in the central nervous system. Previous studies have shown that MK is an effective neuroprotective agent in reducing retinal degeneration caused by excessive light and decreasing hippocampal neuronal death in ischemic gerbil brain. The present study was undertaken to investigate whether MK acts as an anticonvulsant in kainic acid (KA)-induced seizure in mouse and blocks KA-mediated neuronal cell death in hippocampus.ResultsIncreased expression of MK was found in hippocampus of mouse following seizures induced by intracerebroventricular injection of KA, and MK expression was found in glial fibrillary acidic protein (GFAP)-positive astrocytes. Concurrent injection of MK and KA attenuated KA-induced seizure activity and cell death of hippocampal neurons including pyramidal cells and glutamic acid decarboxylase 67 (GAD67)-positive GABAergic interneurons in the CA3 and hilar area.ConclusionThe results of the present study indicate that MK functions as an anticonvulsant and neuroprotective agent in hippocampus during KA-induced seizures.

【 授权许可】

CC BY   
© Kim et al; licensee BioMed Central Ltd. 2010