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减少抑制性突触传输到条形状神经元可能是与衰老相关的运动技能缺陷的基础

Qiang Shan¹, Xiaoxuan Yu¹, Xiaoli Lin¹

¹Laboratory for Synaptic Plasticity, Shantou University Medical College, Shantou, Guangdong 515041, China.

Neurobiology of disease

|June 28, 2024

概括

老龄化通过减少大脑中的突触抑制来损害运动技能. 这项研究发现,向脊侧条体 (DLS) 中的腺氨酸A2A受体可以恢复老年小鼠的运动功能.

科学领域:

神经科学是一个神经科学.
衰老研究研究衰老研究
突触性可塑性突触性可塑性

背景情况:

衰老与增加的运动缺陷有关,影响诸如帕金森病 (PD) 和亨廷顿病 (HD) 等疾病.
与年龄相关的运动技能下降背后的精确突触机制仍然不清楚.
脊侧条纹体 (DLS) 在运动控制中起着至关重要的作用.

研究的目的:

调查与年龄相关的运动缺陷的功能突触基础.
为了确定在DLS中突触传输的特定变化,有助于老化中的运动障碍.
探索恢复老年人的运动功能的潜在治疗点.

主要方法:

在年轻和年老的小鼠中进行行为测试 (旋转杆,梁行走,杆测试).
电生理学记录以评估DLS神经元中的突触传输疗效.
使用腺A2A受体 (A2A R) 激动剂和抗剂进行药理学操纵.

主要成果:

年龄较大的小鼠在运动技能的表现上表现出显著的损伤.
电生理学揭示了与年龄相关的抑制性突触传输到DLS间接通路中等状神经元 (iMSNs) 的衰减,表明了无抑制.
通过A2A R激动剂/对抗剂对DLSiMSN活性进行药理学调节,分别模仿或逆转年轻和老年小鼠的运动缺陷.

结论:

在DLSiMSN中抑制性突触可塑性的功能性减少有助于与年龄相关的运动缺陷.
在DLS中这种突触消抑制提供了一个潜在的神经基础,解释为什么衰老是神经退行性运动疾病的危险因素.
在DLS中准A2A R可能提供一种改善与衰老相关的运动障碍的策略.

关键词:

衰老的衰老衰老的衰老亨廷顿病就是亨廷顿病.抑制突触传输的抑制作用运动技巧运动技巧帕金森病的疾病.直体间接通道 - 直体间接通道

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