皮层扩散性抑制诱导清醒小鼠丘脑腹后内侧核的传播性激活。
Cortical spreading depression induces propagating activation of the thalamus ventral posteromedial nucleus in awake mice.
机构信息
Britton Chance Center and MoE Key Laboratory for Biomedical Photonics, Wuhan National Laboratory for Optoelectronics, Huazhong University of Science and Technology, Wuhan, China.
Research Unit of Multimodal Cross Scale Neural Signal Detection and Imaging, Chinese Academy of Medical Sciences, HUST-Suzhou Institute for Brainsmatics, JITRI, Suzhou, China.
出版信息
J Headache Pain. 2022 Jan 24;23(1):15. doi: 10.1186/s10194-021-01370-z.
BACKGROUND
As the relay centre for processing sensory information, the thalamus may involve in the abnormal sensory procedure caused by cortical spreading depression (CSD). However, few studies have focused on the transient response of thalamus during CSD. Our study aimed to investigate the neuronal activity of mouse thalamus ventral posteromedial nucleus (VPM) during CSD by in vivo micro-endoscopic fluorescence imaging of the genetic calcium probe GCaMP6s expressed in excitatory glutamatergic neurons.
METHODS
Thirty-four transgenic VGluT2-GCaMP6s mice were used in the experiments. An endoscope was inserted into the VPM for image acquisition. CSD was induced by KCl topically applied unilaterally on the cranial dura. Data were acquired in awake (ipsilateral or contralateral VPM, saline instead of KCl, MK-801 treatment) and anaesthetized (isoflurane, pentobarbital) states. Statistical analysis was performed using analysis of variance (ANOVA) by SPSS.
RESULTS
We found that after CSD induced in ipsilateral motor cortex, the neuronal activity increased and propagated from the posterior-lateral to the anterior-medial part of the VPM with an average speed of 3.47 mm/min. When CSD was induced in visual cortex, the response propagated in opposite direction, from the anterior-medial to the posterior-lateral part of the VPM. Aanaesthetics resulted in the suppression of VPM activation induced by CSD. No significant VPM activation was detected when CSD was induced in contralateral cortex or KCl was replaced by saline. When 5 mM MK-801 was applied to the dura, the electrode failed to record the DC shift of CSD, and there was no significant VPM activation after KCl application.
CONCLUSION
CSD induced propagating activation of the ipsilateral VPM in awake mice. The response might correlate to the cortical location where CSD was induced and might be affected by anaesthetics. No significant VPM activation was detected in saline and mk801 experiment results indicated that this VPM activation is due to CSD rather than mouse motion or direct effect of the KCl applying to the intact dura. This finding suggests the potential involvement of thalamus in the migraine auras.
背景
作为处理感觉信息的中继中心，丘脑可能参与皮质扩散性抑制（CSD）引起的异常感觉过程。然而，很少有研究关注 CSD 期间丘脑的瞬时反应。我们的研究旨在通过活体显微镜荧光成像技术，观察表达在兴奋性谷氨酸能神经元中的遗传钙探针 GCaMP6s，研究 CSD 期间小鼠丘脑腹后内侧核（VPM）的神经元活动。
方法
实验中使用了 34 只转基因 VGluT2-GCaMP6s 小鼠。通过插入 VPM 的内窥镜进行图像采集。CSD 通过在颅顶硬脑膜单侧施加 KCl 诱导。在清醒（同侧或对侧 VPM，用生理盐水代替 KCl，MK-801 处理）和麻醉（异氟烷、戊巴比妥）状态下采集数据。使用 SPSS 的方差分析（ANOVA）进行统计分析。
结果
我们发现，在同侧运动皮层诱导 CSD 后，神经元活动增加，并从 VPM 的后外侧向前内侧传播，平均速度为 3.47mm/min。当 CSD 在视觉皮层诱导时，反应以相反的方向传播，从 VPM 的前内侧到后外侧。麻醉剂导致 CSD 诱导的 VPM 激活受到抑制。当 CSD 在对侧皮层诱导或用生理盐水代替 KCl 时，未检测到 VPM 激活。当在硬脑膜上施加 5mM MK-801 时，电极未能记录到 CSD 的 DC 偏移，并且在施加 KCl 后没有明显的 VPM 激活。
结论
在清醒小鼠中，CSD 诱导同侧 VPM 的传播激活。该反应可能与诱导 CSD 的皮质位置相关，并且可能受到麻醉剂的影响。在生理盐水和 mk801 实验中未检测到明显的 VPM 激活，表明这种 VPM 激活是由于 CSD 引起的，而不是由于小鼠运动或 KCl 直接施加到完整硬脑膜引起的。这一发现表明丘脑可能参与偏头痛先兆。
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