Kainic Acid Treatment Increases Ca²⁺-mediated Neurotoxicity in the Mouse Hippocampus.
10.11637/kjpa.2016.29.2.71
- Author:
Jung Eun LEE
1
Author Information
1. Department of Thoracic and Cardiovascular Surgery, Gyeongsang National University Hospital, Institute of Health Sciences, Gyeongsang National University School of Medicine, Korea. ilikerem@hanmail.net
- Publication Type:Original Article
- Keywords:
Kainic acid;
Calcium;
Lyn/Btk;
Seizure;
Hippocampus
- MeSH:
Animals;
Blotting, Western;
Calcium;
Cell Death;
Electroencephalography;
Hippocalcin;
Hippocampus*;
Kainic Acid*;
Mice*;
Neurons;
Phosphorylation;
Phosphotransferases;
Proteolysis;
Seizures;
Tyrosine
- From:Korean Journal of Physical Anthropology
2016;29(2):71-79
- CountryRepublic of Korea
- Language:English
-
Abstract:
Kainic acid (KA)-induced neuronal cell death is associated with intracellular Ca²⁺ influx. However, it is unknown whether Lyn/Btk pathway is involved in the Ca²⁺-mediated neurotoxicity and neuronal death induced by KA. In the present study, we investigated the altered expression of Ca²⁺-controlled proteins in KA-treated hippocampus. Mice were sacrificed at 24 h after KA (20 mg/kg) systemic injection. We conducted Electroencephalographic (EEG) recording and examined hippocampal alterations by Western blotting and immunostaining in control mice or KA-treated mice. EEG tests showed that KA-treated mice increased seizure frequency and severity compared with control mice during KA-induced seizures. We found that KA decreases hippocalcin and calpain-mediated proteolysis in the hippocampus. In particular, the phosphorylation of Lyn and Btk was increased in KA-treated hippocampus compared to those of control mice. Our findings identify tyrosine kinases such as Lyn/Btk as a critical regulator of Ca²⁺-mediated neurotoxicity in KA-induced seizures.
