Store-operated calcium entry in the satellite glial cells of rat sympathetic ganglia
10.4196/kjpp.2024.28.1.93
- Author:
Sohyun KIM
1
;
Seong Jun KANG
;
Huu Son NGUYEN
;
Seong-Woo JEONG
Author Information
1. Department of Physiology, Laboratory of Molecular Neurophysiology, Yonsei University Wonju College of Medicine, Wonju 26426, Korea
- Publication Type:Original Article
- From:The Korean Journal of Physiology and Pharmacology
2024;28(1):93-103
- CountryRepublic of Korea
- Language:EN
-
Abstract:
Satellite glial cells (SGCs), a major type of glial cell in the autonomic ganglia, closely envelop the cell body and even the synaptic regions of a single neuron with a very narrow gap. This structurally unique organization suggests that autonomic neurons and SGCs may communicate reciprocally. Glial Ca2+ signaling is critical for controlling neural activity. Here, for the first time we identified the machinery of store-operated Ca2+ entry (SOCE) which is critical for cellular Ca2+ homeostasis in rat sympathetic ganglia under normal and pathological states. Quantitative realtime PCR and immunostaining analyses showed that Orai1 and stromal interaction molecules 1 (STIM1) proteins are the primary components of SOCE machinery in the sympathetic ganglia. When the internal Ca2+ stores were depleted in the absence of extracellular Ca2+ , the number of plasmalemmal Orai1 puncta was increased in neurons and SGCs, suggesting activation of the Ca2+ entry channels. Intracellular Ca2+imaging revealed that SOCE was present in SGCs and neurons; however, the magnitude of SOCE was much larger in the SGCs than in the neurons. The SOCE was significantly suppressed by GSK7975A, a selective Orai1 blocker, and Pyr6, a SOCE blocker.Lipopolysaccharide (LPS) upregulated the glial fibrillary acidic protein and Toll-like receptor 4 in the sympathetic ganglia. Importantly, LPS attenuated SOCE via downregulating Orai1 and STIM1 expression. In conclusion, sympathetic SGCs functionally express the SOCE machinery, which is indispensable for intracellular Ca2+ signaling.The SOCE is highly susceptible to inflammation, which may affect sympathetic neuronal activity and thereby autonomic output.
