State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
PLoS One. 2012;7(12):e52148. doi: 10.1371/journal.pone.0052148. Epub 2012 Dec 20.
Whether large conductance Ca(2+)-activated potassium (BK) channels are present in the substantia nigra pars reticulata (SNr) is a matter of debate. Using the patch-clamp technique, we examined the functional expression of BK channels in neurons of the SNr and showed that the channels were activated or inhibited by internal high-energy phosphates (IHEPs) at positive and negative membrane potentials, respectively. SNr neurons showed membrane potential hyperpolarization under glucose-deprivation conditions which was attenuated by paxilline, a specific BK channel blocker. In addition, Fluo-3 fluorescence recording detected an increase in the level of internal free calcium (Ca(2+)) during ischemic hyperpolarization. These results confirm that BK channels are present in SNr neurons and indicate that their unique IHEP sensitivity is requisite in neuronal ischemic responses. Bearing in mind that the K(ATP) channel blocker tolbutamide also attenuated the hyperpolarization, we suggest that BK channels may play a protective role in the basal ganglia by modulating the excitability of SNr neurons along with K(ATP) channels under ischemic stresses.
大电导钙激活钾（BK）通道是否存在于黑质网状部（SNr）存在争议。本研究采用膜片钳技术，观察了 SNr 神经元中 BK 通道的功能表达，并证实通道分别在正膜电位和负膜电位下被内部高能磷酸化合物（IHEPs）激活或抑制。葡萄糖剥夺条件下，SNr 神经元表现出膜电位超极化，该超极化可被特异性 BK 通道阻断剂 paxilline 所减弱。此外，Fluo-3 荧光记录检测到缺血性超极化时细胞内游离钙（[Ca（2+）]（i））水平升高。这些结果证实了 BK 通道存在于 SNr 神经元中，并表明其独特的 IHEP 敏感性是神经元缺血反应所必需的。鉴于 K（ATP）通道阻断剂甲苯磺丁脲也减弱了超极化，我们推测 BK 通道可能通过调节 SNr 神经元的兴奋性，与缺血应激下的 K（ATP）通道一起，在基底神经节中发挥保护作用。
