Nucleus Accumbens Tac1-Expressing Neurons Mediate Stress-Induced Anhedonia-like Behavior in Mice
Nucleus Accumbens Tac1-Expressing Neurons Mediate Stress-Induced Anhedonia-like Behavior in Mice
复制标题
表达 Tac1 的伏核神经元介导小鼠应激诱发的快感缺失样行为
DOI：
10.1016/j.celrep.2020.108343
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发表时间：
2020-11-03
期刊：
影响因子：
8.8
通讯作者：
Zhu, Xiao-Juan
中科院分区：
文献类型：
--
作者：
He, Zi-Xuan;Yin, Yue-Yue;Zhu, Xiao-Juan
重度抑郁症（MDD）主要表现为两种症状：抑郁情绪和快感缺乏，这表明不同的神经回路可能调节MDD。然而，这些与抑郁症相关的个体症状的潜在回路仍然难以捉摸。在这里，我们确定了一个离散的电路速激肽前体1（Tac 1）表达的神经元在核腹侧苍白球（NAc）的外侧壳，这项目，并有助于压力诱导的快感缺失样行为。选择性抑制和激活Tac1（NAc）神经元双向调节应激敏感性，揭示了NAc中的Tac1神经元对调节快感缺失样行为至关重要。我们发现，VP神经元的一个亚群接收抑制输入Tac1（NAc）神经元，并表现出敏感小鼠的兴奋性下降。此外，神经激肽1受体的抑制促进了对社会压力的易感性。总的来说，我们的研究揭示了一个离散的电路调节小鼠的快感缺乏样行为。
Major depressive disorder (MDD) presents with two primary symptoms: depressed mood and anhedonia, which suggests that distinct neuronal circuits may regulate MDD. However, the underlying circuits of these individual symptoms linked to depression remain elusive. Herein, we identify a discrete circuit of tachykinin precursor 1 (Tac1)-expressing neurons in the nucleus accumbens (NAc) lateral shell, which project to ventral pallidum and contribute to stress-induced anhedonia-like behavior. Selective inhibition and activation of Tac1(NAc) neurons bidirectionally modulate stress susceptibility, revealing that Tac1 neurons in the NAc are critical for regulating anhedonia-like behaviors. We find that a subpopulation of VP neurons receives inhibitory inputs from Tac1(NAc) neurons and exhibits decreased excitability in susceptible mice. Furthermore, the inhibition of the neurokinin 1 receptor promotes susceptibility to social stress. Overall, our study reveals a discrete circuit regulating anhedonia-like behavior in mice.