PDF(Pubmed)
Abstract：
The potential brain mechanism underlying resilience to socially transferred allodynia remains unknown. Here, we utilize a well-established socially transferred allodynia paradigm to segregate male mice into pain-susceptible and pain-resilient subgroups. Brain screening results show that ventral tegmental area glutamatergic neurons are selectively activated in pain-resilient mice as compared to control and pain-susceptible mice. Chemogenetic manipulations demonstrate that activation and inhibition of ventral tegmental area glutamatergic neurons bi-directionally regulate resilience to socially transferred allodynia. Moreover, ventral tegmental area glutamatergic neurons that project specifically to the nucleus accumbens shell and lateral habenula regulate the development and maintenance of the pain-resilient phenotype, respectively. Together, we establish an approach to explore individual variations in pain response and identify ventral tegmental area glutamatergic neurons and related downstream circuits as critical targets for resilience to socially transferred allodynia and the development of conceptually innovative analgesics.
摘要：
潜在的大脑机制对社会转移的异常性疼痛的恢复力仍然未知。这里,我们利用公认的社会转移异常性疼痛范式,将雄性小鼠分为疼痛易感和疼痛弹性亚组.脑筛查结果表明，与对照组和疼痛易感小鼠相比，疼痛弹性小鼠的腹侧被盖区谷氨酸能神经元被选择性激活。化学遗传学操作表明，腹侧被盖区谷氨酸能神经元的激活和抑制双向调节对社会转移的异常性疼痛的弹性。此外，腹侧被盖区谷氨酸能神经元，特别是投射到伏隔核壳和侧突，调节疼痛弹性表型的发展和维持，分别。一起,我们建立了一种方法来探索疼痛反应的个体差异，并将腹侧被盖区谷氨酸能神经元和相关的下游回路确定为社会转移异常性疼痛恢复力和概念创新镇痛药开发的关键目标。
