正常衰老限制脑卒中后皮层网络重组和行为恢复。

IF 4.5
Asher Albertson, Ryan M Bowen, Kyrillos Ayoub, Rose Leon-Alvarado, Brendon Wang, Roman Pati, Adam Q Bauer, Jin-Moo Lee
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引用次数: 0

摘要

背景:虽然年龄的增长与中风后较差的恢复有关,但人们对衰老如何影响中风后神经元回路和网络的重组知之甚少。方法:采用宽视场钙显像比较幼龄(3月龄)和老年(18月龄)Thy1-GCaMP6f小鼠前爪体感觉皮层局灶性光血栓性中风后的皮质网络动力学和行为恢复情况。结果:年轻和年老小鼠在中风后都出现了明显的躯体运动缺陷,但只有年轻小鼠表现出明显的行为恢复。虽然年轻和老年小鼠在中风后的基线前爪诱发反应幅度及其轨迹上存在差异,但这些电路的时间动态在年轻和老年小鼠中风前后都是相似的。与老年小鼠相比,年轻小鼠表现出更好的半球刺激锁定保真度、双侧相干性和皮质夹带的基线测量,这些在中风后显著下降;这种趋势在老年小鼠中不存在。最后,只有幼鼠在中风后表现出躯体感觉和躯体运动功能连接的显著恢复。结论:这些结果提示衰老和中风引起的神经网络退化具有相似性,并突出了这两个过程中神经网络的脆弱性。我们的研究结果还表明中风幸存者慢性缺陷的潜在网络水平基础。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
EXPRESS: Normal Aging Limits Cortical Network Reorganization and Behavioral Recovery after Experimental Stroke.

Background: Although advancing age is associated with worse recovery after stroke, little is known about how aging influences post-stroke reorganization of neuronal circuits and networks.

Methods: We used wide-field calcium imaging to compare cortical network dynamics and behavioral recovery after focal photothrombotic stroke in forepaw somatosensory cortex in young (3-month-old) and aged (18-month-old) Thy1-GCaMP6f mice.

Results: Both young and aged mice developed significant somatomotor deficits after stroke, but only young mice exhibited substantial behavioral recovery. While young and aged mice showed differences in baseline forepaw-evoked response amplitudes and their trajectories after stroke, the temporal dynamics of these circuits were comparable both before and after stroke between young and aged mice. Relative to aged mice, young mice demonstrated superior baseline measures of hemispheric stimulus-locked fidelity, bilateral coherence, and cortical entrainment, that declined significantly after stroke; this trend was absent in aged mice. Finally, only young mice showed significant recovery of somatosensory and somatomotor functional connectivity after stroke.

Conclusions: These results suggest similarities in neuronal network degradation caused by aging and stroke and highlight the vulnerability of neuronal networks in both processes. Our findings also indicate a potential network-level basis for chronic deficits in stroke survivors.

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