Scholarlink

<p>Ischemic stroke (IS) commonly results in long-term disability, largely due to alterations in neuronal networks. In repeatable rodent IS model under naturalistic conditions, the difficulty of capturing single-cell neuronal activities and how this solves a long-standing challenge is still remained. Here, we combined a photothrombotic stroke model with head-mounted miniaturized two-photon microscopy (mTPM) to achieve longitudinal, real-time imaging of GABAergic neurons in the contralesional primary motor cortex (M1) in freely moving mice. We observed pronounced reductions in calcium dynamics in GABAergic neurons. These calcium dynamics emerged as early as day 3 post-stroke and persisted through day 19, despite no detectable gross motor deficits. Our findings highlight subtle cortical dysfunction persists despite normal gross motor function, underscoring the need for finer behavioral tests. This approach offered a powerful tool to bridge the gap between cellular-level dysfunction and macroscopic behaviors after focal ischemic&#xa0;stroke.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

A Freely Moving Photothrombotic Stroke Model Reveals Sustained Dysfunction of GABAergic Neuron in Contralesional Cortex Using Miniaturized Two-Photon Microscopy

  • 期刊论文

  • 发表日期：

    2025年3月10日

查看全文
  • Jin Chuanyang,
  • Dai Hui,
  • Dai Dechun,
  • Zhang Jianbin

摘要

Ischemic stroke (IS) commonly results in long-term disability, largely due to alterations in neuronal networks. In repeatable rodent IS model under naturalistic conditions, the difficulty of capturing single-cell neuronal activities and how this solves a long-standing challenge is still remained. Here, we combined a photothrombotic stroke model with head-mounted miniaturized two-photon microscopy (mTPM) to achieve longitudinal, real-time imaging of GABAergic neurons in the contralesional primary motor cortex (M1) in freely moving mice. We observed pronounced reductions in calcium dynamics in GABAergic neurons. These calcium dynamics emerged as early as day 3 post-stroke and persisted through day 19, despite no detectable gross motor deficits. Our findings highlight subtle cortical dysfunction persists despite normal gross motor function, underscoring the need for finer behavioral tests. This approach offered a powerful tool to bridge the gap between cellular-level dysfunction and macroscopic behaviors after focal ischemic stroke.