CLONIDINE-INDUCED SPRINAL ACETYLCHOLINE RESEARCH

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。本协议是疼痛中心拨款的一部分，重点关注疼痛本身，特别是慢性神经性疼痛，如何改变对传统和非传统镇痛药的反应。神经纤维将疼痛信息传递到大脑的方式被认为在手术后和慢性疼痛中发生了变化。由于这个原因，一些药物比那些手术后或慢性疼痛的人更能缓解突然疼痛的健康人群的疼痛。目前可用的止痛药可能不能缓解所有类型的疼痛，或者可能只是在产生副作用和潜在并发症的剂量下缓解疼痛。该方案的目的是了解鞘内可乐定增加效力和功效的机制，通过观察健康个体在使用可乐定之前和之后的脑脊液，以及观察患有慢性神经性神经疼痛的人的脑脊液。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This protocol is part of a Pain Center Grant that focuses on how pain itself, especially chronic neuropathic pain, alters the response to traditional and non-traditional analgesics. The way that nerve fibers carry the information of pain to the brain is thought to change after surgery and in chronic pain. For this reason, some medicines work better to relieve pain in healthy people who have a sudden painful injury compared to those after surgery or those with chronic pain. Currently available pain medications may not relieve all types of pain or may relieve pain only at doses that produce side effects and potential complications. The aim of this protocol is to understand the mechanisms by which intrathecal clonidine increases in potency and efficacy by looking at the cerebrospinal fluid of healthy individuals before and after clonidine administration as well as looking at the spinal fluid of people that have chronic neuropathic nerve pain.