Vestibular nerve afferents are divided into regular and irregular groups based on the variability of interspike intervals in their resting discharge. Most afferents receive inputs from bouton terminals that contact type II hair cells as well as from calyx terminals that cover the basolateral walls of type I hair cells. Calyces have an abundance of different subtypes of KCNQ (Kv7) potassium channels and muscarinic acetylcholine receptors (mAChRs) and receive cholinergic efferent inputs from neurons in the brainstem. We investigated whether mAChRs affected membrane properties and firing patterns of calyx terminals through modulation of KCNQ channel activity. Patch clamp recordings were performed from calyx terminals in central regions of the cristae of the horizontal and anterior canals in 13–26 day old Sprague-Dawley rats. KCNQ mediated currents were observed as voltage sensitive currents with slow kinetics (activation and deactivation), resulting in spike frequency adaptation so that calyces at best fired a single action potential at the beginning of a depolarizing step. Activation of mAChRs by application of oxotremorine methiodide or inhibition of KCNQ channels by linopirdine dihydrochloride decreased voltage activated currents by ∼30%, decreased first spike latencies by ∼40%, resulted in action potential generation in response to smaller current injections and at lower (i.e., more hyperpolarized) membrane potentials, and increased the number of spikes fired during depolarizing steps. Interestingly, some of the calyces showed spontaneous discharge in the presence of these drugs. Together, these findings suggest that cholinergic efferents can modulate the response properties and encoding of head movements by afferents.

前庭神经传入根据其静息放电间突间隔的变化而分为规则组和不规则组。大多数传入人从与II型毛细胞接触的bouton终​​端以及覆盖I型毛细胞的基底外侧壁的花萼终端接收输入。花萼具有大量不同类型的KCNQ（Kv7）钾通道和毒蕈碱型乙酰胆碱受体（mAChRs），并从脑干中的神经元接受胆碱能传出的输入。我们调查了mAChRs是否通过调节KCNQ通道活性来影响花萼末端的膜特性和发射模式。在13至26日龄的Sprague-Dawley大鼠中，从水平和前管ista的中央区域的花萼末端进行膜片钳记录。观察到KCNQ介导的电流为动力学敏感的电压敏感电流（激活和去激活），导致尖峰频率适应，因此花萼在去极化步骤开始时充其量只能激发单个动作电位。通过应用氧代苯丁胺甲硫氨酸来激活mAChRs或通过盐酸利尼吡啶抑制KCNQ通道可将电压激活电流降低约30％，将第一尖峰潜伏期降低约40％，从而在较小的电流注入和较低的响应下产生动作电位。 ，更多的超极化）膜电位，并增加了去极化步骤中发射的尖峰数量。有趣的是，在这些药物存在下，某些花萼显示出自发放电。一起，