Overexpression of neuronal calcium sensor-1 to promote axonal regeneration

脊髓损伤（SCI）患者通常会留下严重的感觉、运动和自主神经功能缺陷。在拟议的研究中，我们的目标是测试这一假设，即添加钙传感器蛋白;神经元钙传感器-1（NCS-1）可以使成年神经再生。这种小分子参与胚胎大脑和脊髓中轴突的生长和突触（神经的布线和通信点）的形成。这种分子通常仅在胚胎神经系统中表达，除了正常生长外，胚胎神经系统在损伤后也能够显著再生。我们计划在成年大鼠的两种SCI模型中增加受损神经的NCS-1含量。这两种模型之间的差异将使我们能够研究不同机制的贡献，这些机制可能是NCS-1增加引起的任何功能恢复的基础。在临床上，SCI后神经元损伤的治疗因需要稳定患者而延迟，因此我们将测试在损伤后而不是同时增加NCS-1是否可以诱导恢复。我们希望这项工作可以为SCI的治疗提供新的选择。

Patients with spinal cord injury (SCI) are often left with severe sensory, motor and autonomic functional deficits. In the proposed research we aim to test the hypothesis that adding a calcium sensor protein; neuronal calcium sensor-1 (NCS-1) can enable adult nerves to regenerate. This small molecule is involved in the growth of axons and formation of synapses (the wiring and communication points of nerves) in the embryonic brain and spinal cord. This molecule is usually only expressed in the embryonic nervous system which, as well as normal growth, is also capable of significant regeneration after injury. We plan to increase the NCS-1 content of injured nerves in two models of SCI in the adult rat. The differences between the two models will allow us to examine the contribution of different mechanisms that may underlie any functional recovery caused by the increase in NCS-1. Clinically the treatment of the neuronal injury following SCI is delayed by the need to stabilise the patient, therefore we will test if increasing NCS-1 after as opposed to at the same time as the injury can induce recovery. We hope this work may contribute to new treatment options in SCI.