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Abstract：
Cortical-basal ganglia (CBG) circuits are critical for motor learning and performance, and are a major site of pathology. In songbirds, a CBG circuit regulates moment-by-moment variability in song and also enables song plasticity. Studies have shown that variable burst firing in LMAN, the output nucleus of this CBG circuit, actively drives acute song variability, but whether and how LMAN drives long-lasting changes in song remains unclear. Here, we ask whether chronic pharmacological augmentation of LMAN bursting is sufficient to drive plasticity in birds singing stereotyped songs. We show that altered LMAN activity drives cumulative changes in acoustic structure, timing, and sequencing over multiple days, and induces repetitions and silent pauses reminiscent of human stuttering. Changes persisted when LMAN was subsequently inactivated, indicating plasticity in song motor regions. Following cessation of pharmacological treatment, acoustic features and song sequence gradually recovered to their baseline values over a period of days to weeks. Together, our findings show that augmented bursting in CBG circuitry drives plasticity in well-learned motor skills, and may inform treatments for basal ganglia movement disorders.
摘要：
皮质-基底神经节（CBG）回路对于运动学习和表现至关重要，是病理的主要部位。在鸣鸟中，CBG电路调节歌曲的瞬间可变性，并使歌曲的可塑性。研究表明，LMAN中的可变爆发射击，这个CBG电路的输出核心，积极驱动急性歌曲变异性，但是LMAN是否以及如何推动歌曲的持久变化尚不清楚。这里,我们询问LMAN爆裂的慢性药理学增强是否足以驱动唱定型歌曲的鸟类的可塑性。我们表明，改变的LMAN活动驱动声学结构的累积变化，定时,并进行了多天的测序，并引起重复和沉默的停顿，让人想起人类的口吃。当LMAN随后被停用时，变化仍然存在，表明歌曲运动区域的可塑性。停止药物治疗后，声学特征和歌曲序列在几天到几周的时间内逐渐恢复到基线值。一起,我们的研究结果表明，CBG电路中的增强爆裂驱动了学习良好的运动技能的可塑性，并可能告知基底神经节运动障碍的治疗。
