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Updated: Feb 7, 2026

Location, Dissection, and Analysis of the Murine Stellate Ganglion
Published on: December 22, 2020
Mast cells modulate the pathogenesis of leptin-induced left stellate ganglion activation in canines
Yuhong Wang1, Lilei Yu1, Guannan Meng1
1Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute, Wuhan University, Hubei Key Laboratory of Cardiology, Wuhan, Hubei, PR China.
Background:
Leptin is an adipocytokine predominantly secreted by adipose tissue that participates in immune modulation. Mast cells are important immune cells that are related to altered sympathetic activity. Previous study has shown that leptin promotes activation of the left stellate ganglion (LSG) directly via the leptin receptor. This study aims to investigate whether mast cells play a key role in indirect activation.
Methods:
Twenty-eight canines were randomly divided into 3 groups: the control group (saline, n = 8), leptin group (leptin, n = 9), and DSCG group (disodium cromoglycate plus leptin, n = 11). Drugs were locally microinjected into the LSG. The function and neural activity of the LSG were evaluated to investigate LSG activation. Tryptase was adopted to identify activated mast cells in the LSG.
Results:
Compared with the control group, leptin injection (18 μg) markedly increased the function and neural activity of the LSG. Leptin also upregulated c-fos, nerve growth factor (NGF), and tryptase expression in the LSG. However, these effects of leptin were attenuated by pre-injection of DSCG (25 mg). Additionally, the immunofluorescence analysis revealed that many mast cells were present in the LSG and that those cells were located close to sympathetic neurons. The presence of leptin receptors on the mast cells was verified.
Conclusions:
Immune mast cells play an important supplementary role in the pathogenesis of leptin-induced LSG activation.
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