The perception of visceral pain is a complex process involving the spinal cord and higher order brain structures. Increasing evidence implicates the gut microbiota as a key regulator of brain and behavior, yet it remains to be determined if gut bacteria play a role in visceral sensitivity. We used germ-free mice (GF) to assess visceral sensitivity, spinal cord gene expression and pain-related brain structures. GF mice displayed visceral hypersensitivity accompanied by increases in Toll-like receptor and cytokine gene expression in the spinal cord, which were normalized by postnatal colonization with microbiota from conventionally colonized (CC). In GF mice, the volumes of the anterior cingulate cortex (ACC) and periaqueductal grey, areas involved in pain processing, were decreased and enlarged, respectively, and dendritic changes in the ACC were evident. These findings indicate that the gut microbiota is required for the normal visceral pain sensation.

译文

:内脏痛的感觉是一个复杂的过程,涉及脊髓和高级大脑结构。越来越多的证据表明肠道菌群是大脑和行为的关键调节因子,但肠道细菌是否在内脏敏感性中起作用尚待确定。我们使用无菌小鼠(GF)评估内脏敏感性,脊髓基因表达和与疼痛相关的脑结构。 GF小鼠表现出内脏超敏反应,并伴随着脊髓Toll样受体和细胞因子基因表达的增加,这可以通过用常规定殖的(CC)菌群在出生后定植来实现。在GF小鼠中,前扣带回皮质(ACC)和导水管周围灰色的体积(参与疼痛处理的区域)分别减小和增大,并且ACC中的树突状变化是明显的。这些发现表明,肠道菌群是正常内脏痛感所必需的。

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