The basolateral amygdala (BLA) sends excitatory projections to the nucleus accumbens (NAc) and regulates motivated behaviors partially by activating NAc medium spiny neurons (MSNs). Here, we characterized a feedforward inhibition circuit, through which BLA-evoked activation of NAc shell (NAcSh) MSNs was fine-tuned by GABAergic monosynaptic innervation from adjacent fast-spiking interneurons (FSIs). Specifically, BLA-to-NAcSh projections predominantly innervated NAcSh FSIs compared with MSNs and triggered action potentials in FSIs preceding BLA-mediated activation of MSNs. Due to these anatomical and temporal properties, activation of the BLA-to-NAcSh projection resulted in a rapid FSI-mediated inhibition of MSNs, timing-contingently dictating BLA-evoked activation of MSNs. Cocaine self-administration selectively and persistently up-regulated the presynaptic release probability of BLA-to-FSI synapses, entailing enhanced FSI-mediated feedforward inhibition of MSNs upon BLA activation. Experimentally enhancing the BLA-to-FSI transmission in vivo expedited the acquisition of cocaine self-administration. These results reveal a previously unidentified role of an FSI-embedded circuit in regulating NAc-based drug seeking and taking.

中文翻译：

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伏伏核前馈抑制回路促进可卡因的自我管理

基底外侧杏仁核（BLA）将兴奋性投射发送到伏伏核（NAc），并通过激活NAc中棘状神经元（MSN）来部分调节动机行为。在这里，我们表征了前馈抑制电路，通过该电路可通过邻近快加中子神经元（FSI）的GABA能单突触神经对BLA引起的NAc壳（NAcSh）MSNs的激活进行微调。具体而言，与MSN相比，BLA到NAcSh的预测主要支配了NAcSh FSI，并在BLA介导的MSN激活之前触发了FSI中的动作电位。由于这些解剖和时间特性，BLA到NAcSh投影的激活导致了FSI介导的MSN的快速抑制，在时间上决定了BLA引起的MSN激活。可卡因的自我管理选择性地和持续地上调了BLA到FSI突触的突触前释放可能性，从而增强了BLA激活后FSI介导的MSN的前馈抑制作用。通过实验增强体内从BLA到FSI的传播，加快了可卡因自我管理的获得。这些结果揭示了FSI嵌入式电路在调节基于NAc的药物寻找和服用中的作用尚未确定。