The abnormal function of the voltage-gated potassium channel Kv10.2 can induce epilepsy. However, the physiological function of Kv10.2 in the central nervous system remains unclear. In this study, we found that Kv10.2 knockout (KO) increased the complexity of neurons in the CA3 subarea of hippocampus. Kv10.2 KO led to enlarged somata, elongated dendritic length, and increased the number of dendritic tips in cultured rat hippocampus neurons. Kv10.2 KO also increased Synapsin I and PSD95 protein density in cultured rat hippocampal neurons. Whole cell patch-clamp recordings of brain slices in the CA3 subarea of hippocampus revealed that Kv10.2 KO increased the amplitude of spontaneous excitatory postsynaptic currents (sEPSC) and miniature excitatory postsynaptic currents (mEPSC), depolarized the resting membrane potential and increased the action potential firing, reduced the rheobase and increased the input resistance, which results in enhanced neuronal excitability. Furthermore, we made electroencephalogram (EEG) recordings of brain activity in freely moving rats before and after inducing seizures by pentylenetetrazole (PTZ) injection. Kv10.2 KO rats dramatically increased the EEG amplitude during epilepsy. Behavioral observation after seizure induction revealed that Kv10.2 KO rats demonstrated shortened onset latency, prolonged duration, and increased seizure severity when compared with wild type rats. Therefore, this study provides a new link between Kv10.2 and neuronal morphology and higher intrinsic excitability.

电压门控钾通道Kv10.2的异常功能可诱发癫痫病。但是，Kv10.2在中枢神经系统中的生理功能仍不清楚。在这项研究中，我们发现Kv10.2基因敲除（KO）增加了海马CA3子区域神经元的复杂性。在培养的大鼠海马神经元中，Kv10.2 KO导致躯体增大，树突长度延长以及树突尖端数量增加。Kv10.2 KO还增加了培养的大鼠海马神经元中突触蛋白I和PSD95蛋白的密度。海马CA3区域脑切片的全细胞膜片钳记录表明，Kv10.2 KO增加了自发性兴奋性突触后电流（sEPSC）和微型兴奋性突触后电流（mEPSC）的幅度，使静止的膜电位去极化，增加动作电位的放电，减少流变碱并增加输入阻力，从而增强神经元兴奋性。此外，我们制作了脑电图（EEG），记录了戊四氮（PTZ）注射诱发癫痫发作前后自由活动大鼠的大脑活动。Kv10.2 KO大鼠在癫痫发作期间脑电图振幅显着增加。诱发癫痫发作后的行为观察表明，与野生型大鼠相比，Kv10.2 KO大鼠表现出缩短的发作潜伏期，延长的持续时间和发作的严重程度。因此，这项研究为Kv10.2与神经元形态和更高的内在兴奋性之间提供了新的联系。这导致神经元兴奋性增强。此外，我们制作了脑电图（EEG），记录了戊四氮（PTZ）注射诱发癫痫发作前后自由活动大鼠的大脑活动。Kv10.2 KO大鼠在癫痫发作期间脑电图振幅显着增加。诱发癫痫发作后的行为观察表明，与野生型大鼠相比，Kv10.2 KO大鼠表现出缩短的发作潜伏期，延长的持续时间和发作的严重程度。因此，这项研究为Kv10.2与神经元形态和更高的内在兴奋性之间提供了新的联系。这导致神经元兴奋性增强。此外，我们制作了脑电图（EEG），记录了戊四氮（PTZ）注射诱发癫痫发作前后自由活动大鼠的大脑活动。Kv10.2 KO大鼠在癫痫发作期间显着增加了脑电图振幅。诱发癫痫发作后的行为观察表明，与野生型大鼠相比，Kv10.2 KO大鼠表现出缩短的发作潜伏期，延长的持续时间和发作的严重程度。因此，这项研究为Kv10.2与神经元形态和更高的内在兴奋性之间提供了新的联系。2只KO大鼠在癫痫发作期间显着增加了EEG振幅。诱发癫痫发作后的行为观察表明，与野生型大鼠相比，Kv10.2 KO大鼠表现出缩短的发作潜伏期，延长的持续时间和发作的严重程度。因此，这项研究为Kv10.2与神经元形态和更高的内在兴奋性之间提供了新的联系。2只KO大鼠在癫痫发作期间显着增加了EEG振幅。诱发癫痫发作后的行为观察表明，与野生型大鼠相比，Kv10.2 KO大鼠表现出缩短的发作潜伏期，延长的持续时间和发作的严重程度。因此，这项研究为Kv10.2与神经元形态和更高的内在兴奋性之间提供了新的联系。