Abstract
Kainic acid (KA)-induced neuronal cell death is associated with intracellular Ca 2+ influx. However, it is unknown whether Lyn/Btk pathway is involved in the Ca 2+ -mediated neurotoxicity and neuronal death induced by KA. In the present study, we investigated the altered expression of Ca 2+ -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 Ca 2+ -mediated neurotoxicity in KA-induced seizures.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
