Related Experiment Video
Updated: Jun 27, 2025

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Assessment of Memory Function in Pilocarpine-induced Epileptic Mice
Published on: June 4, 2020
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Effects of L-Type Voltage-Gated Calcium Channel (LTCC) Inhibition on Hippocampal Neuronal Death after
Chang-Jun Lee1, Song-Hee Lee1, Beom-Seok Kang1
1Department of Physiology, Hallym University College of Medicine, Chuncheon 24252, Republic of Korea.
Antioxidants (Basel, Switzerland)
|April 27, 2024
Summary
Amlodipine, an L-type calcium channel blocker, reduces zinc accumulation and neuronal death in epilepsy models. This suggests amlodipine
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Epilepsy involves excessive neuronal activity linked to L-type voltage-gated calcium channels (LTCCs).
- LTCCs mediate calcium and zinc influx, leading to oxidative stress and neuronal death via NADPH oxidase activation.
- Amlodipine (AML) inhibits LTCCs and is used for cardiovascular conditions.
Purpose of the Study:
- To investigate if amlodipine can prevent zinc translocation and accumulation in neurons.
- To evaluate amlodipine's potential to protect against seizure-induced hippocampal neuronal death.
Main Methods:
- An epilepsy model was established in rats using pilocarpine.
- Rats received amlodipine (10 mg/kg daily) after epilepsy onset.
- Cognitive function, zinc accumulation, oxidative stress, and neuronal death were assessed.
Main Results:
- Amlodipine significantly decreased excessive zinc accumulation in neurons.
- Amlodipine reduced reactive oxygen species (ROS) production.
- Amlodipine mitigated seizure-induced hippocampal neuronal death.
Conclusions:
- LTCC inhibition by amlodipine lessens neuronal zinc overload and oxidative stress.
- Amlodipine shows potential as a therapeutic agent for managing epilepsy and its damaging effects.
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