Kainic Acid Treatment Increases Ca2+-mediated Neurotoxicity in the Mouse Hippocampus
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초록
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.
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.
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