双侧前庭张力的成熟与协调是维护前庭功能的基础；而前庭代偿是指一侧前庭外周损毁后、中枢恢复平衡的现象。前庭内侧核(MVN)含有A、B两型内在膜特性相异的神经元，两型占比以及基于此的中枢响应模式的转变是实现前庭发育与代偿的共同特征。前庭发育时MVN神经元从普遍A型转变为两型各半，而代偿时损毁侧及健侧分别转变为A型及B型为主，但转变机制不明。我们的预实验发现，活动依赖的HCN通道电流是B型神经元内在膜特性区别于A型的关键，并进而决定神经元响应模式。为此我们提出以下假说：1）在发育期前庭传入刺激下，双侧HCN通道表达增多，改变MVN神经元内在膜特性，促成A型向B型转变；2）在代偿时仅有健侧前庭传入刺激，健侧与毁损侧MVN分别上调和下调HCN通道表达，A、B型分侧逆向转变。申报项目将采用C57及HCN基因缺陷小鼠，证实HCN通道对MVN神经元内在膜特性的调控作用，从探索自然发育着手揭示前庭代偿机制。

The function of vestibular system is crucial for animal’s advanced features, while vestibular compensation refers to the phenomena of central vestibular recovery from unilateral destruction of peripheral vestibular organs, but the mechanisms is far from clear. Medial vestibular nucleus(MVN) consists of A and B type neurons with significantly identical intrinsic membrane properties. The constitution rate of two type neurons and the changes of response pattern become both of the common pathway and marks of vestibular development and vestibular compensation. In developed animals, MVN neurons initial mainly consisting of A type convert from A to B type which are half to half; whileas, in the compensation course, the constitution of MVN neurons convert to predominant A type neurons in ipsilesional side and predominant B type neurons in contralesional side, but the mechanism that promotes the above-mentioned shifts is unclear now. We have discovered in our preliminary experiments and demonstrated that the key to differentiate B type from A type neuron lies in its activity-dependant HCN channel currents (Ih). Thus, we propose hypothesis that: 1) at the developmental stages, expression of HCN channels increases following the vestibular afflux of stimulus, and promoting the shift from A to B type; 2) in terms of vestibular compensation, MVN neurons respectively up- or down-regulates the expression of HCN channels on ipsilesional and contralesional sides based on modifications of afflux of stimulus resulting from unilateral vestibular destruction and prompting the reversely transition of A/B type neurons, therefore, leading to the rebalance of central response. This projection plans to adopt both normal and HCN gene defected mice, and aims at investigating the relationship between Ih and intrinsic membrane properties and revealing pivotal role of HCN channels playing in vestibular development and compensation.