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首页> 外文期刊>Cell Reports >Coordinated Regulation of Synaptic Plasticity at Striatopallidal and Striatonigral Neurons Orchestrates Motor Control
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Coordinated Regulation of Synaptic Plasticity at Striatopallidal and Striatonigral Neurons Orchestrates Motor Control

机译：纹状体顶神经和纹状体神经元的突触可塑性的协调调节协调运动控制。

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The basal ganglia play a critical role in shaping motor behavior. For this function, the activity of medium spiny neurons (MSNs) of the striatonigral and striatopallidal pathways must be integrated. It remains unclear whether the activity of the two pathways is primarily coordinated by synaptic plasticity mechanisms. Using a model of Parkinson's disease, we determined the circuit and behavioral effects of concurrently regulating cell-type-specific forms of corticostriatal long-term synaptic depression (LTD) by inhibiting small-conductance Ca^2^+-activated K^+ channels (SKs) of the dorsolateral striatum. At striatopallidal synapses, SK channel inhibition rescued the disease-linked deficits in endocannabinoid (eCB)-dependent LTD. At striatonigral cells, inhibition of these channels counteracted a form of adenosine-mediated LTD by activating the ERK cascade. Interfering with eCB-, adenosine-, and ERK signaling in vivo alleviated motor abnormalities, which supports that synaptic modulation of striatal pathways affects behavior. Thus, our results establish a central role of coordinated synaptic plasticity at MSN subpopulations in motor control.
机译：基底神经节在塑造运动行为中起关键作用。为实现此功能，必须整合纹状体神经和纹状体神经通路的中棘神经元（MSN）的活性。尚不清楚这两个途径的活动是否主要由突触可塑性机制协调。我们使用帕金森氏病模型，通过抑制小传导性Ca ^ 2 ^ +激活的K ^ +通道，确定了同时调节皮质类固醇长期突触抑制（LTD）的细胞类型特异性形式的电路和行为效应（背外侧纹状体。在纹状体蛛网膜突触处，SK通道抑制可以挽救依赖于内源性大麻素（eCB）的LTD中与疾病有关的缺陷。在纹状体黑素细胞中，这些通道的抑制通过激活ERK级联反应抵消了腺苷介导的LTD形式。在体内干扰eCB-，腺苷和ERK信号可减轻运动异常，这支持纹状体途径的突触调节影响行为。因此，我们的研究结果确立了运动控制中MSN亚群协同突触可塑性的重要作用。

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