Related Experiment Video
Updated: Sep 27, 2025
Combining Imaging and Electrophysiology to Visualize and Record Spreading Depolarizations in Mice
Published on: October 4, 2024
Spatiotemporal Patterns of Spreading Depolarization and its Correlation with Brain Injury During the Acute Stage of
Zelong Zheng1, Jinbiao Luo1, Zhikai Cao1
1The Department of Neurosurgery, Guangzhou First People's Hospital, School of Medicine, South China University of Technology, Panfu Road No.1, Guangdong 510180, China.
Objective:
Spreading depolarization (SD) has been regarded as one cause of neuronal injury in subarachnoid hemorrhage (SAH). However, SD in the hyperacute phase of SAH is still unclear. The objective of this study was to detect real-time spatial-temporal patterns of SD, assess the effect of SD on cerebral blood flow, and test the relationship between SD and brain injury in the acute phase of SAH.
Methods:
Twenty-eight mice were separated into two groups: 16 animals in the SAH group and 12 animals in the sham group. Experimental SAH was done with an endovascular filament perforation model. Changes in optical reflection were registered with intrinsic optical signal imaging (IOSI) after SAH. Spatial-temporal patterns of SDs were analyzed and brain injury including brain edema and infarction was tested.
Results:
Totally, 117 SDs occurred after SAH. According to the hemodynamic response and duration, SDs could be classified into Type I (short SD), Type II (intermediate SD), and Type III (persistent SD). Most of SDs originated from the somatosensory and visual cortex. SDs demonstrated distinct spreading patterns. Moreover, the number and duration of SDs associated with brain water content (p < 0.05, p < 0.01). SDs, especially, persistent SDs associated with infarct volume in the hyperacute phase of SAH (p < 0.001, p < 0.001).
Conclusion:
Our results suggest that SD occurs with a high incidence during the acute stage of SAH in mice. And the lissencephalic mouse brain is capable of different SD propagation patterns. Additionally, SD may aggravate brain edema and induce brain infarction, contributing to early brain injury after SAH.
