Nicotine alpha 4 beta 2 receptor-mediated free calcium in an animal model of facial nucleus injury  

作　　者：Dawei Sun Wenhai Sun Yanqing Wang Fugao Zhu Rui Zhou Yanjun Wang Banghua Liu Xiuming Wan Huamin Liu 

机构地区：[1]Department of Otolaryngology Head and Neck Surgery, Affiliated Hospital of Qingdao University Medical College, Qingdao 266003, Shandong Province, China [2]Department of Science and Education, Affiliated Hospital of Qingdao University Medical College, Qingdao 266003, Shandong Province, China [3]School of Public Health, Shandong University, Jinan 250012, Shandong Province, China [4]Department of Otolaryngology Head and Neck Surgery, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, Hubei Province, China [5]Department of Oncology, Affiliated Hospital of Qingdao University Medical College, Qingdao 266003, Shandong Province, China

出　　处：《Neural Regeneration Research》2010年第19期1500-1504,共5页中国神经再生研究（英文版）

基　　金：Youth Research Fund of Qingdao University (2007)

摘　　要：Previous studies have demonstrated that the cholinergic system, via nicotinic receptors, regulates intracellular free calcium levels in the facial nucleus under normal physiological conditions. However, the regulation of nicotinic receptors on free calcium levels following facial nerve injury remains unclear. In the present study, an animal model of facial nerve injury was established, and changes in nicotinic receptor expression following facial nerve injury in rats were detected using reverse transcription polymerase chain reaction. Nicotinic receptor-mediated changes of free calcium levels following facial nucleus injury were determined by laser confocal microscopy. Results showed no significant difference in nicotinic receptor expression between the normal group and the affected facial nerve nucleus. The nicotinic receptor a4132 subtype increased free calcium levels following facial nerve injury by promoting calcium transmembrane influx, and L-type voltage-gated calcium channel-mediated influx of calcium ions played an important role in promoting calcium transmembrane influx. The nicotinic receptor-mediated increase of free calcium levels following facial nerve injury provides an important mechanism for the repair of facial nerve injury.Previous studies have demonstrated that the cholinergic system, via nicotinic receptors, regulates intracellular free calcium levels in the facial nucleus under normal physiological conditions. However, the regulation of nicotinic receptors on free calcium levels following facial nerve injury remains unclear. In the present study, an animal model of facial nerve injury was established, and changes in nicotinic receptor expression following facial nerve injury in rats were detected using reverse transcription polymerase chain reaction. Nicotinic receptor-mediated changes of free calcium levels following facial nucleus injury were determined by laser confocal microscopy. Results showed no significant difference in nicotinic receptor expression between the normal group and the affected facial nerve nucleus. The nicotinic receptor a4132 subtype increased free calcium levels following facial nerve injury by promoting calcium transmembrane influx, and L-type voltage-gated calcium channel-mediated influx of calcium ions played an important role in promoting calcium transmembrane influx. The nicotinic receptor-mediated increase of free calcium levels following facial nerve injury provides an important mechanism for the repair of facial nerve injury.

关 键 词：facial nerve injury nicotinic receptor CHOLINE CALCIUM peripheral nerve injury 

分 类 号：Q523[生物学—生物化学] S852.2[农业科学—基础兽医学]