基底外侧杏仁核
边缘下皮质
慢性疼痛
光遗传学
神经科学
扁桃形结构
痛觉过敏
导水管周围灰质
焦虑
伤害
医学
神经病理性疼痛
心理学
前额叶皮质
受体
内科学
中枢神经系统
精神科
认知
中脑
作者
Feng Gao,Jie Huang,Guobin Huang,Qiang-Long You,Shan Yao,Shuoxian Zhao,Jian Liu,Chunqing Wu,Gui-Fu Chen,Shimin Liu,Zhou Yu,Yue Zhou,Yuping Ning,Shenquan Liu,Bingjie Hu,Xiangdong Sun
摘要
Chronic pain can cause both hyperalgesia and anxiety symptoms. However, how the two components are encoded in the brain remains unclear. The prelimbic cortex (PrL), a critical brain region for both nociceptive and emotional modulations, serves as an ideal medium for comparing how the two components are encoded. We report that PrL neurons projecting to the basolateral amygdala (PrLBLA) and those projecting to the ventrolateral periaqueductal gray (PrLl/vlPAG) were segregated and displayed elevated and reduced neuronal activity, respectively, during pain chronicity. Consistently, optogenetic suppression of the PrL-BLA circuit reversed anxiety-like behaviors, whereas activation of the PrL-l/vlPAG circuit attenuated hyperalgesia in mice with chronic pain. Moreover, mechanistic studies indicated that elevated TNF-α/TNFR1 signaling in the PrL caused increased insertion of GluA1 receptors into PrLBLA neurons and contributed to anxiety-like behaviors in mice with chronic pain. Together, these results provide insights into the circuit and molecular mechanisms in the PrL for controlling pain-related hyperalgesia and anxiety-like behaviors.
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