CaMK II信号转导通路参与前扣带回皮质调节IBS大鼠的内脏痛觉
基本信息
结项摘要
内脏高敏感是肠易激综合征（IBS）最重要的发病机制。我们的前期研究证实，被致敏的前扣带回皮质（ACC）参与易化（增强）调节IBS大鼠的内脏痛觉（包括内脏痛感觉和相关情绪），并发现其内CaMK II表达显著增加。CaMK II被认为参与伤害性刺激的感觉处理和神经突触可塑性的形成。为明确CaMK II信号转导通路与ACC调节IBS大鼠内脏痛觉作用的关联，本研究拟采用体内RNA干扰静默ACC内α-CaMK II表达的方法，观察其对IBS大鼠1）由等级压力结直肠扩张（CRD）诱导的内脏运动反射（VMR）定量评估的内脏疼痛感觉的影响；和2）由CRD相关的条件位置回避（CPA）得分来评估的痛相关情绪的影响，以证实我们提出的CaMK II信号转导通路参与ACC调节IBS大鼠内脏痛觉的假设。
项目摘要
项目成果
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数据更新时间：2023-05-31
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