Related Experiment Video
Updated: Jun 14, 2026
Lipidomics and Transcriptomics in Neurological Diseases
Published on: March 18, 2022
Midkine, heparin-binding growth factor, blocks kainic acid-induced seizure and neuronal cell death in mouse
Yun B Kim1, Jae K Ryu, Hong J Lee
1Division of Neurology, Department of Medicine, UBC Hospital, University of British Columbia, Vancouver, Canada.
Background:
Midkine (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.
Results:
Increased 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.
Conclusion:
The results of the present study indicate that MK functions as an anticonvulsant and neuroprotective agent in hippocampus during KA-induced seizures.
Insights
Midkine (MK) acts as an anticonvulsant and neuroprotective agent. This study shows MK reduces seizures and neuronal death in the hippocampus during kainic acid-induced seizures in mice.
Area of Science:
- Neuroscience
- Molecular Biology
Background:
- Midkine (MK) is a heparin-binding growth factor with known neurotrophic and neuroprotective properties in the central nervous system.
- Previous research demonstrated MK's efficacy in reducing light-induced retinal degeneration and ischemic hippocampal neuronal death.
Purpose of the Study:
- To investigate the anticonvulsant potential of Midkine (MK) in kainic acid (KA)-induced seizures.
- To determine if MK can prevent neuronal cell death in the hippocampus mediated by KA.
Main Methods:
- Induction of seizures in mice using intracerebroventricular injection of kainic acid (KA).
- Assessment of MK expression in the hippocampus post-seizure.
- Administration of MK concurrently with KA to evaluate its effects on seizure activity and neuronal survival.
Main Results:
- Increased MK expression was observed in the mouse hippocampus following KA-induced seizures, localized to GFAP-positive astrocytes.
- Co-administration of MK with KA significantly attenuated seizure activity.
- MK treatment reduced KA-induced death of hippocampal neurons, including pyramidal cells and GAD67-positive interneurons in the CA3 and hilar regions.
Conclusions:
- Midkine (MK) exhibits anticonvulsant properties in the context of KA-induced seizures.
- MK demonstrates significant neuroprotective effects within the hippocampus during seizures.
- These findings highlight MK's therapeutic potential for seizure-related neurological damage.
