Large Calcium-Activated Potassium Channels Contribute to Neuronal Abnormal Firing in the Medial Vestibular Nucleus Following Hypoxia
10.3969/j.issn.1006-7299.2017.01.011
- VernacularTitle:大电导钙激活钾通道参与缺氧致前庭内侧核神经元兴奋性异常
- Author:
Shuhui WU
;
Dan LIU
;
Yong YAN
;
Guangming SHI
- Keywords:
Calcium-activated potassium channels;
Hypoxia;
Whole-cell recording;
Medial vestibu-lar nucleus
- From:
Journal of Audiology and Speech Pathology
2017;25(1):44-48
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of BKCa channel on electrophysiology excitatory regulation in MVN neuron following hypoxia and to reveal its molecular mechanism.Methods C57BL/6 mices were performed MVNs hypoxia mice model,and randomly allowed to normal oxgen group and hypoxia group.The hypoxia group, according to the application of NS1 6 1 9 ,was further divided into the no NS1 6 1 9 pretreatment group and NS1 6 1 9 pre-treatment group.Using the patch clamp experiment technology,we recorded the effects of the MVN abnormal neu-ronal firing and the change of the BKCa currents.Using immunohistochemical technique,the changes of BKCa in the hypoxic MVNs detected were.Results Acute hypoxia increased neuronal activities.NS1619 pretreatment de-creased hypoxia-induced firing rate,and increased and postponed the maximum increase by hypoxia(P<0.05),al-so alleviated 10-min-hypoxia-induced depolarization(P<0.05).Perfusion with hypoxic significantly reduced the BKCa positive neurons(P<0.05).Conclusion These findings suggest that acute hypoxia increases neuronal activi-ties.The decreased MVN BKCa channels contribute to hypoxia-induced abnormal neuronal activities.
