如何有效地改善和治疗以阿尔茨海默症为代表的认知功能障碍疾病一直是神经科学界所关注的重要问题。新近的研究认为，突触可塑性调节产生的长时程增强在形成学习记忆功能的同时，有可能作为阿尔茨海默症治疗的重要手段。通过前期研究和预实验，我们发现内源性多肽神经降压素(Neurotensin)通过抑制钾离子通道可诱导海马颗粒细胞去极化并增加突触间兴奋性递质释放，但其促进神经兴奋性增强的突触前机制，和其是否具有改善认知功能的作用仍需进一步研究。本课题辅以膜片钳、光遗传学、行为学等实验手段，将深入探索Neurotensin通过促进递质囊泡转运从而调节神经元兴奋性的突触传递机制，力求证实其在增强神经元兴奋性的基础上可产生长时程增强并改善认知功能障碍这一假说。本研究以Neurotensin或其受体作为新型药物或干预靶点，为未来将其应用于认知功能障碍类疾病的临床治疗奠定了基础，有着积极的理论和临床意义。

It is a significant issue in neuroscience that how to efficiently improve and cure the cognitive disorders, such as Alzheimer's disease. It is found in recent research that the synaptic plasticity and long-term potentiation could enhance learning and memory function, which could also be an important means to treat Alzheimer's disease. The results in our publication and pre-experiments showed that, neurotensinergic excited dentate gyrus granule cells via Gαq-coupled inhibition of TASK-3 channels. However, the pre-synaptic mechanism of promoting neuronal excitability, and whether it can improve cognitive function require further study. This study would explore in-depth of neurotensin which facilitates neuronal excitability by increasing the size of readily releasable pool and releasing probability, supplemented by patch clamp, light genetics, neurobehavioral test and other experimental methods. It would demonstrate the hypothesis that neurotensin could enhance neuronal excitability, produce long-term potentiation and improve cognitive dysfunction ultimately. This research could also provide the basis for future research on clinical treatment of cognitive disorders upon neurotensin or its acceptor as new drugs. It could be meaningful in both theoretical and clinical area.