Task-related "cortical" bursting depends critically on basal ganglia input and is linked to vocal plasticity
Task-related "cortical" bursting depends critically on basal ganglia input and is linked to vocal plasticity
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DOI：
10.1073/pnas.1216308110
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发表时间：
2013-03-19
影响因子：
11.1
通讯作者：
Doupe, Allison J.
中科院分区：
文献类型：
--
作者：
Kojima, Satoshi;Kao, Mimi H.;Doupe, Allison J.
基底神经节-丘脑皮层回路对运动控制和运动学习至关重要。传统上，基底神经节核被认为通过增加或减少皮质放电率来调节运动行为，基底神经节疾病被认为反映了异常的整体活动水平。最近的研究表明，相反，运动障碍源于异常的放电模式，并导致假设手术治疗，如苍白球切开术，主要通过消除病理性放电模式。然而，令人惊讶的是，关于基底神经节通常如何影响任务相关的皮层活动以调节运动行为，以及基底神经节的病变如何影响皮层放电特性，我们知之甚少。在这里，我们调查了这些问题的鸣禽电路，哺乳动物基底神经节丘脑皮层电路，但专门为唱歌有惊人的同源性。这个回路的“皮质”流出核是歌曲可塑性所必需的，通常在唱歌和歌曲锁定的爆发性放电期间表现出增加的放电。我们发现，纹状体苍白球核在这个电路的病变阻止听力依赖的歌曲变化。这些基底神经节病变也剥夺了皮质流出神经元在唱歌时的模式爆发放电，而不改变它们的自发或唱歌相关的放电率。总而言之，这些结果表明，基底神经节不是对于正常的皮质放电率至关重要，而是对于驱动特定于任务的皮质放电模式（包括爆发）至关重要。此外，这种模式化的爆发似乎对运动可塑性至关重要。因此，我们的研究结果为旨在通过使放电模式正常化来治疗基底神经节运动障碍的疗法提供了支持。
Basal ganglia-thalamocortical circuits are critical for motor control and motor learning. Classically, basal ganglia nuclei are thought to regulate motor behavior by increasing or decreasing cortical firing rates, and basal ganglia diseases are assumed to reflect abnormal overall activity levels. More recent studies suggest instead that motor disorders derive from abnormal firing patterns, and have led to the hypothesis that surgical treatments, such as pallidotomy, act primarily by eliminating pathological firing patterns. Surprisingly little is known, however, about how the basal ganglia normally influence task-related cortical activity to regulate motor behavior, and how lesions of the basal ganglia influence cortical firing properties. Here, we investigated these questions in a songbird circuit that has striking homologies to mammalian basal ganglia-thalamocortical circuits but is specialized for singing. The "cortical" outflow nucleus of this circuit is required for song plasticity and normally exhibits increased firing during singing and song-locked burst firing. We found that lesions of the striato-pallidal nucleus in this circuit prevented hearing-dependent song changes. These basal ganglia lesions also stripped the cortical outflow neurons of their patterned burst firing during singing, without changing their spontaneous or singing-related firing rates. Taken together, these results suggest that the basal ganglia are essential not for normal cortical firing rates but for driving task-specific cortical firing patterns, including bursts. Moreover, such patterned bursting appears critical for motor plasticity. Our findings thus provide support for therapies that aim to treat basal ganglia movement disorders by normalizing firing patterns.