Neuronal intrinsic excitability is the propensity of a neuron to generate action potentials (AP) after beyond-threshold signaling stimuli. Destabilized excitability, a feature of many neurological disorders including but not limited to epilepsy, autism and pain, is hypothesized to be related to defects in homeostatic intrinsic plasticity regulation. In healthy neurons, intrinsic homeostatic plasticity is responsible for stabilizing their excitability when the network activity become chronically abnormal, being either extremely high or low. In another word, after the global activity has been too silent for a long time, a same level of stimulus can now more easily to trigger an AP. However, critical cellular sites and important molecular players participating in this regulatory mechanism remain to be elucidated. Thus, I launched two studies to tackle these un-answered questions.