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A Critical Role of Basolateral Amygdala to Nucleus Accumbens Projection in Sleep Regulation of Reward Seeking
Biological Psychiatry ( IF 9.6 ) Pub Date : 2020-06-01 , DOI: 10.1016/j.biopsych.2019.10.027
Yao Wang 1 , Zheng Liu 2 , Li Cai 2 , Rong Guo 2 , Yan Dong 1 , Yanhua H Huang 2
Affiliation  

BACKGROUND Sleep impacts reward-motivated behaviors partly by retuning the brain reward circuits. The nucleus accumbens (NAc) is a reward processing hub sensitive to acute sleep deprivation. Glutamatergic transmission carrying reward-associated signals converges in the NAc and regulates various aspects of reward-motivated behaviors. The basolateral amygdala projection (BLAp) innervates broad regions of the NAc and critically regulates reward seeking. METHODS Using slice electrophysiology, we measured how acute sleep deprivation alters transmission at BLAp-NAc synapses in male C57BL/6 mice. Moreover, using SSFO (stabilized step function opsin) and DREADDs (designer receptors exclusively activated by designer drugs) (Gi) to amplify and reduce transmission, respectively, we tested behavioral consequences following bidirectional manipulations of BLAp-NAc transmission. RESULTS Acute sleep deprivation increased sucrose self-administration in mice and altered the BLAp-NAc transmission in a topographically specific manner. It selectively reduced glutamate release at the rostral BLAp (rBLAp) onto ventral and lateral NAc (vlNAc) synapses, but spared caudal BLAp onto medial NAc synapses. Furthermore, experimentally facilitating glutamate release at rBLAp-vlNAc synapses suppressed sucrose reward seeking. Conversely, mimicking sleep deprivation-induced reduction of rBLAp-vlNAc transmission increased sucrose reward seeking. Finally, facilitating rBLAp-vlNAc transmission per se did not promote either approach motivation or aversion. CONCLUSIONS Sleep acts on rBLAp-vINAc transmission gain control to regulate established reward seeking but does not convey approach motivation or aversion on its own.

中文翻译:

基底外侧杏仁核对伏隔核投射在寻求奖励的睡眠调节中的关键作用

背景睡眠部分地通过重新调整大脑奖赏回路来影响奖赏驱动的行为。伏隔核 (NAc) 是一个对急性睡眠剥夺敏感的奖励处理中心。携带奖励相关信号的谷氨酸能传输会聚在 NAc 中并调节奖励驱动行为的各个方面。基底外侧杏仁核投射 (BLAp) 支配 NAc 的广泛区域并严格调节奖励寻求。方法使用切片电生理学,我们测量了急性睡眠剥夺如何改变雄性 C57BL/6 小鼠中 BLAp-NAc 突触的传递。此外,使用 SSFO(稳定阶跃函数视蛋白)和 DREADDs(由设计药物专门激活的设计受体)(Gi)分别放大和减少传输,我们测试了双向操作 BLAp-NAc 传输后的行为后果。结果 急性睡眠剥夺增加了小鼠的蔗糖自我给药,并以特定于地形的方式改变了 BLAp-NAc 传输。它选择性地减少了前侧 BLAp (rBLAp) 释放到腹侧和外侧 NAc (vlNAc) 突触上的谷氨酸盐,但不会将尾部 BLAp 释放到内侧 NAc 突触上。此外,通过实验促进 rBLAp-vlNAc 突触的谷氨酸释放抑制了蔗糖奖励寻求。相反,模仿睡眠剥夺引起的 rBLAp-vlNAc 传输减少会增加蔗糖奖励寻求。最后,促进 rBLAP-vlNAc 传输本身并没有促进接近动机或厌恶。
更新日期:2020-06-01
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