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首页> 外文期刊>Neuron >Pathway-Specific Remodeling of Thalamostriatal Synapses in Parkinsonian Mice
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Pathway-Specific Remodeling of Thalamostriatal Synapses in Parkinsonian Mice

机译：帕金森病小鼠丘脑突触特定于途径的重塑

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Movement suppression in Parkinson's disease (PD) is thought to arise from increased efficacy of the indirect pathway basal ganglia circuit, relative to the direct pathway. However, the underlying pathophysiological mechanisms remain elusive. To examine whether changes in the strength of synaptic inputs to these circuits contribute to this imbalance, we obtained paired whole-cell recordings from striatal direct-and indirect-pathway medium spiny neurons (dMSNs and iMSNs) and optically stimulated inputs from sensorimotor cortex or intralaminar thalamus in brain slices from control and dopamine-depleted mice. We found that dopamine depletion selectively decreased synaptic strength at thalamic inputs to dMSNs, suggesting that thalamus drives asymmetric activation of basal ganglia circuitry underlying parkinsonian motor impairments. Consistent with this hypothesis, in vivo chemogenetic and optogenetic inhibition of thalamostriatal terminals reversed motor deficits in dopamine-depleted mice. These results implicate thalamostriatal projections in the pathophysiology of PD and support interventions targeting thalamus as a potential therapeutic strategy.
机译：帕金森氏病（PD）的运动抑制被认为是由于相对于直接途径，间接途径的基底神经节回路的功效增强。然而，潜在的病理生理机制仍然难以捉摸。为了检查突触输入到这些电路的强度的变化是否导致这种不平衡，我们从纹状体直接和间接途径中突棘神经元（dMSN和iMSN）以及感觉运动皮层或层内的光刺激输入获得了成对的全细胞记录对照和多巴胺缺乏小鼠的脑切片中的丘脑。我们发现，多巴胺的消耗选择性地降低了丘脑输入dMSNs的突触强度，提示丘脑驱动了帕金森氏运动障碍基础的基底神经节回路的不对称激活。与该假设相一致，体内化学和光遗传学抑制丘脑末梢末端逆转了多巴胺缺乏小鼠的运动功能障碍。这些结果暗示了丘脑基底膜在PD的病理生理中的预测，并支持针对丘脑的干预作为一种潜在的治疗策略。

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