Holt Avril Genene, Asako Mikiya, Duncan R Keith, Lomax Catherine A, Juiz Jose M, Altschuler Richard A
Kresge Hearing Research Institute, Department of Otolaryngology, Head and Neck Surgery, University of Michigan, 1301 East Ann Street, Ann Arbor, MI 48109-0506, USA.
Hear Res. 2006 Jun-Jul;216-217:146-53. doi: 10.1016/j.heares.2006.03.009. Epub 2006 May 2.
Two-pore domain potassium channels (K(2PD)+) play an important role in setting resting membrane potential by regulating background leakage of potassium ions, which in turn controls neuronal excitability. To determine whether these channels contribute to activity-dependent plasticity following deafness, we used quantitative real-time PCR to examine the expression of 10 K(2PD)+ subunits in the rat cochlear nucleus at 3 days, 3 weeks and 3 months after bilateral cochlear ablation. There was a large sustained decrease in the expression of TASK-5, a subunit that is predominantly expressed in auditory brain stem neurons, and in the TASK-1 subunit which is highly expressed in several types of cochlear nucleus neurons. TWIK-1 and THIK-2 also showed significant decreases in expression that were maintained across all time points. TWIK-2, TREK-1 and TREK-2 showed no significant change in expression at 3 days but showed large decreases at 3 weeks and 3 months following deafness. TRAAK and TASK-3 subunits showed significant decreases at 3 days and 3 weeks following deafness, but these differences were no longer significant at 3 months. Dramatic changes in expression of K(2PD)+ subunits suggest these channels may play a role in deafness-associated changes in the excitability of cochlear nucleus neurons.
双孔结构域钾通道（K(2PD)+）通过调节钾离子的背景泄漏在设定静息膜电位方面发挥重要作用，而钾离子背景泄漏又控制着神经元的兴奋性。为了确定这些通道是否在耳聋后与活动相关的可塑性中起作用，我们使用定量实时聚合酶链反应检测了双侧耳蜗切除术后3天、3周和3个月大鼠耳蜗核中10种K(2PD)+亚基的表达。主要在听觉脑干神经元中表达的TASK-5亚基以及在几种类型的耳蜗核神经元中高表达的TASK-1亚基的表达持续大幅下降。TWIK-1和THIK-2的表达也在所有时间点均显著下降。TWIK-2、TREK-1和TREK-2在3天时表达无显著变化，但在耳聋后3周和3个月时表达大幅下降。TRAAK和TASK-3亚基在耳聋后3天和3周时表达显著下降，但在3个月时这些差异不再显著。K(2PD)+亚基表达的显著变化表明这些通道可能在与耳聋相关的耳蜗核神经元兴奋性变化中起作用。
