慢性疼痛发病率高，发病机制不清，严重影响患者的身心健康和生活质量，临床防治任重道远。去极化反跳是部分神经元接受超极化刺激后的固有反应，可能与T型钙电流（IT）和超极化激活阳离子电流（Ih）相关，在慢性疼痛的发生发展中具有关键作用。脊髓背角胶状质（SG）神经元是痛觉的传递与整合的“闸门”，SG表达去极化反跳神经元的形态、电生理特性及其突触联系不明。我们的前期研究发现，抑制SG的Ih可降低动作电位发放频率、减弱神经元兴奋性。我们推测，去极化反跳可通过调控SG神经元兴奋性，参与疼痛局部神经回路的调制。本项目拟结合全细胞膜片钳、免疫组织化学、单细胞RT-PCR等方法，揭示大鼠SG去极化反跳神经元及其突触前、后神经元的形态、电生理特性，进一步研究SG神经元去极化反跳的特征与功能，从而完善慢性疼痛的脊髓机制，为慢性疼痛临床治疗提供新靶点及理论依据。

Chronic pain is highly prevalent and our understanding of its underlying mechanisms is incomprehensive. It seriously impacts on patients’ well-being as well as life quality, and its clinical management is still a huge challenge. Rebound depolarization is related to T-type calcium current (IT) and hyperpolarization–activated current (Ih). It is a subsequent response to hyperpolarizing stimulation and plays a critical role in the development and maintenance of chronic pain. Spinal substantia gelatinosa (SG) neurons have been identified as the “central gate” of transmitting and modulating nociceptive information. However, the morphological and electrophysiological features, together with the synaptic connections of neurons exhibiting rebound depolarization remain unclarified. Our preliminary studies found that inhibition of Ih decreases the frequency of action potential and depresses the excitability of SG neurons. Therefore, we hypothesis that rebound depolarization could modulate local pain signaling by altering neuronal excitability in SG. By using combination of whole-cell patch-clamp, immunohistochemistry, and single-cell RT-PCR methods, we will elucidate the morphological and electrophysiological properties as well as physiological function of neurons exhibiting rebound depolarization. We will further illustrate the morphological and electrophysiological properties of neurons which pre- and post- connect to those rebound depolarizing neurons. Together, this study will interpret a new mechanism underlying chronic pain and suggest potential targets for clinical treatment of chronic pain.