苏州大学Guang-Yin Xu等研究人员合作发现，丘脑核仁谷氨酸能神经元通过5-HT2B受体介导小鼠大肠内脏疼痛。这一研究成果于2024年5月13日在线发表在国际学术期刊《神经科学通报》上。

研究人员发现Re谷氨酸能神经元中5-HT2B受体的高表达促进了结直肠内脏痛的发生。具体来说，研究人员发现新生儿母体剥夺（NMD）小鼠表现出内脏痛觉亢进，并增强了Re脑区的自发突触传递。结肠直肠扩张（CRD）刺激可诱导NMD小鼠Re脑区大量c-Fos表达，主要是在谷氨酸能神经元中。此外，对Re脑区谷氨酸能神经元活动的光遗传学操作改变了CON和NMD小鼠的结肠直肠内脏疼痛反应。

此外，研究人员还证明了Re谷氨酸能神经元上的5-HT2B受体表达上调，并最终促进了NMD小鼠的结直肠内脏痛。这些研究结果表明，Re谷氨酸能神经元上的5HT2B受体在调节结直肠内脏疼痛中起着关键作用。

附：英文原文

Title: Thalamic Nucleus Reuniens Glutamatergic Neurons Mediate Colorectal Visceral Pain in Mice via 5-HT2B Receptors

Author: Li, Di, Du, Han, Qu, Shu-Ting, Wu, Jing-Lai, Li, Yong-Chang, Xu, Qi-Ya, Chen, Xia, Dai, Xiao-Xuan, Xu, Ji-Tian, Wang, Qian, Xu, Guang-Yin

Issue&Volume: 2024-05-13

Abstract: Irritable bowel syndrome (IBS) is a common functional bowel disorder characterized by abdominal pain and visceral hypersensitivity. Reducing visceral hypersensitivity is the key to effectively relieving abdominal pain in IBS. Increasing evidence has confirmed that the thalamic nucleus reuniens (Re) and 5-hydroxytryptamine (5-HT) neurotransmitter system play an important role in the development of colorectal visceral pain, whereas the exact mechanisms remain largely unclear. In this study, we found that high expression of the 5-HT2B receptors in the Re glutamatergic neurons promoted colorectal visceral pain. Specifically, we found that neonatal maternal deprivation (NMD) mice exhibited visceral hyperalgesia and enhanced spontaneous synaptic transmission in the Re brain region. Colorectal distension (CRD) stimulation induced a large amount of c-Fos expression in the Re brain region of NMD mice, predominantly in glutamatergic neurons. Furthermore, optogenetic manipulation of glutamatergic neuronal activity in the Re altered colorectal visceral pain responses in CON and NMD mice. In addition, we demonstrated that 5-HT2B receptor expression on the Re glutamatergic neurons was upregulated and ultimately promoted colorectal visceral pain in NMD mice. These findings suggest a critical role of the 5HT2B receptors on the Re glutamatergic neurons in the regulation of colorectal visceral pain.

DOI: 10.1007/s12264-024-01207-0

Source: https://link.springer.com/article/10.1007/s12264-024-01207-0