Pseudorabies Virus (PRV) was used as trans-synaptic retrograde tracer. AAV-hM4D(Gi) was used for chemogenetics manipulation. (From
BrainVTA)
The viruses used in this article from BrainVTA are in the table below
|
Pseudorabies Virus (PRV) |
PRV-CAG-EGFP |
|
Chemogenetics |
PT-0153 rAAV-hSyn-hM4D(Gi)-EGFP-WPRE-hGH pA |
|
Control |
PT-0241 rAAV-hSyn-EGFP-WPRE-hGH pA |
Yuhong Wang, Wanli Jiang, Hu Chen, Huixin Zhou, Zhihao Liu, Zihan Liu, Zhihao Liu, Yuyang Zhou, Xiaoya Zhou, Lilei Yu, Hong Jiang
Pub Date: 2021-03-04,
DOI: 10.3389/fcvm.2021.668387,
Email: [email protected]
Background: Circadian rhythms have a considerable impact on the daily physiology of the heart, and their disruption causes pathology. Several studies have revealed that circadian disruption impaired cardiac remodeling after myocardial infarction (MI); however, the underlying brain-heart mechanisms remain unknown. We aim to discuss whether circadian disruption facilitates cardiac remodeling after MI by activating sympathetic nervous system. Methods: Rats were randomly divided into three groups: Sham group (Sham), MI group (MI), and MI+ circadian disruption group (MI+Dis); rats were treated with PRV injections for trans-synaptic retrograde tracing; rats were randomly divided into two groups: MI+ circadian disruption + Empty Vector+ CNO (Empty Vector), and MI+ circadian disruption + hM4D(Gi)+ CNO (hM4D(Gi)). Results: Circadian disruption significantly facilitated cardiac remodeling after MI with lower systolic function, larger left ventricular volume, and aggravated cardiac fibrosis. Cardiac sympathetic remodeling makers and serum norepinephrine levels were also significantly increased by circadian disruption. PRV virus-labeled neurons were identified in the SCG, PVN, and SCN regions. Ganglionic blockade via DREADD technique suppressed the activity of sympathetic nervous system and significantly alleviated the disruption-related cardiac dysfunction. Conclusion: Circadian disruption adversely affected cardiac remodeling after MI possibly by activating sympathetic nervous system, and suppressing sympathetic activity can attenuate this disruption-related cardiac dysfunction.
Figure 1. Sympathetic ganglionic blockade by DREADD.
The study is aimed to explore the underlying brain-heart mechanisms on circadian rhythms. Using PRV for trans-synaptic retrograde tracing, the authors explored whether circadian disruption facilitates cardiac remodeling after MI by activating sympathetic nervous system. The results showed that circadian disruption adversely affected cardiac remodeling after MI possibly by activating sympathetic nervous system, and suppressing sympathetic activity can attenuate this disruption-related cardiac dysfunction.
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