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Store-operated calcium entry in the satellite glial cells of rat sympathetic ganglia

  • Sohyun Kim (Department of Physiology, Laboratory of Molecular Neurophysiology, Yonsei University Wonju College of Medicine) ;
  • Seong Jun Kang (Department of Physiology, Laboratory of Molecular Neurophysiology, Yonsei University Wonju College of Medicine) ;
  • Huu Son Nguyen (Department of Physiology, Laboratory of Molecular Neurophysiology, Yonsei University Wonju College of Medicine) ;
  • Seong-Woo Jeong (Department of Physiology, Laboratory of Molecular Neurophysiology, Yonsei University Wonju College of Medicine)
  • Received : 2023.12.04
  • Accepted : 2023.12.17
  • Published : 2024.01.01

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.

Keywords

Acknowledgement

We thank Professors Kyu-Sang Park and Seung-Kuy Cha for proofreading this manuscript.

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