Change of intracellular Caconcentration and related signaling pathway in hippocampal cells after high-intensity sound exposure / 生理学报

ABSTRACT

High-intensity sound often leads to the dysfunction and impairment of central nervous system (CNS), but the underlying mechanism is unclear. The present study was aimed to investigate the related mechanisms of CNS lesions in Bama miniature pig model treated with high-intensity sound. The pigs with normal hearing were divided into control and high-intensity sound (900 Hz-142 dB SPL, 15 min) groups. After the treatment, hippocampi were collected immediately. Fluo-4 was used to indicate intracellular Caconcentration ([Ca]) change. Real-time PCR and Western blot were used to detect mRNA and protein expressions of calcium-sensing receptor, L-Cachannel α2/δ1 subunit, PKC and PI3K, respectively. DAPI staining was used to identify nuclear features. The result showed that high-intensity sound exposure resulted in significantly swollen cell nucleus and increased [Ca]in hippocampal cells. Compared with control group, high-intensity sound group showed increased levels of PI3K, PKC and L-Cachannel α2/δ1 subunit mRNA expressions, as well as up-regulated PKC and calcium-sensing receptor protein expressions. These results suggest that the high-intensity sound activates PKC signaling pathway and induces calcium overload, eventually leads to hippocampal injury, which would supply a novel strategy to prevent nervous system from high-intensity sound-induced injury.