一般认为外部信息传入小脑皮层后兴奋浦肯野细胞（PC），而我们前期研究发现感觉刺激诱发分子层中间神经元（MLI）放电，而PC出现抑制、放电暂停；阻断GABAA受体活性后,感觉刺激诱发PC产生单纯性放电，提示感觉刺激引起MLI同步放电而导致PC抑制。为了进一步明确感觉刺激诱发PC抑制、MLI兴奋的突触和时空机制，我们拟应用双通道记录（在体膜片钳或细胞贴附式记录）、组织化学和神经药理学手段，研究小鼠小脑皮层各种神经元在感觉信息传递过程中的相互关系，明确感觉刺激诱发PC抑制和中间神经元兴奋的突触、网络及时空机制，揭示MLI在小脑皮层感觉信息传递过程中是否同步活动；研究兴奋性谷氨酸和GABAA受体激动剂和阻断剂对在小脑皮层感觉信息传递的影响，明确感觉信息传递的递质与受体机制。最后，阐明小脑皮层神经元对感觉信息传递的突触与时空机制，完善拥有自主知识产权的小脑感觉信息传递与整合理论。

The classical theory asserts that sensory information coming from outside induces excitation of Purkinje cells (PC). However, we found that sensory stimulation failed to fire PCs, but induced spike firing in molecular layer interneurons (MLI), resulted in an inhibition with a pause of spike firing in PCs. Blockade GABAA receptor activity, the same stimulation induced simple spike firing in PCs. Our present results suggested that MLIs exhibited more faster and sensitive and synchronous responses than PCs. To understand the synaptic and temperal-spatial mechanisms of the sensory stimulation-induced inhibition of PCs and excitation of MLIs, we will use duo- electrophysiological recording (in vivo patch-clamp or cell-attached recording), histochemistry and neuropharmacology methods to study the interactions of various cerebellar cortical neurons during the sensory information processing. We aim to understand the synaptic, neuronal network and temperal-spatial mechanisms of the sensory stimulation-induced inhibition of PCs and excitation of MLIs, and reveal whether the MLIs exhibited synchronous activity during the sensory information transmissing. We also study the effects of the antagonist and antagonist of glutamate and GAGA on the sensory information transmission in cerebellar cortex, and to understand the synaptic and receptor's mechanisms of the sensory information transmission in cerebellar cortex. Together, our goal is to understand the synaptic and temperal and spatial mechanisms of sensory information transmission in cerebellar cortex, and to accomplish our theory of sensory information transmitting and integrating in cerebellar cortex.