Skip to content
DraconiticResearch
Search Sources API
181,716 studies31 sourcesUpdated 51 min ago
Peer-reviewedCC BY 4.0International Journal of Molecular Sciences

PM2.5 Exposure Disrupts Sympathetic Neurotransmission by Impairing Voltage-Gated Ca2+ Channels and Remodeling Satellite Glia in the Superior Cervical Ganglion

  • Phuong Anh Do1,2,3
  • Huu Son Nguyen1,2,3,4
  • Seung-Kuy Cha1,2,3,5
5 affiliations
  1. 1Department of Physiology, Yonsei University Wonju College of Medicine, Wonju 26426, Republic of Korea
  2. 2Department of Global Medical Science, Yonsei University Wonju College of Medicine, Wonju 26426, Republic of Korea
  3. 3Organelle Medicine Research Center, Yonsei University Wonju College of Medicine, Wonju 26426, Republic of Korea
  4. 4Vinmec Research Institute of Stem Cell and Gene Technology, College of Health Sciences, VinUniversity, Hanoi 100000, Vietnam
  5. 5Institute of Mitochondrial Medicine, Yonsei University Wonju College of Medicine, Wonju 26426, Republic of Korea
Read full textPDFDOICite

Abstract

Airborne fine particulate matter (PM2.5) exposure is associated with central neuroinflammation and autonomic dysfunction, but its effects on peripheral sympathetic ganglia remain poorly defined. Here, we examined the effects of central PM2.5 administration and direct PM2.5 exposure on the superior cervical ganglion (SCG), a primary sympathetic relay governing cephalic noradrenergic outflow. Intracerebroventricular (ICV) administration of PM2.5 increased hypothalamic TNF-α and IL-6 levels and reduced presynaptic synaptophysin expression, while SCG tyrosine hydroxylase expression remained unchanged. In a complementary ex vivo model, direct PM2.5 exposure reduced norepinephrine (NE) accumulation in the culture medium of isolated SCGs without significantly altering tissue NE content. Mechanistically, live-cell Ca2+ imaging revealed attenuated depolarization-evoked Ca2+ responses in SCG neurons following either 24-h direct exposure or in vivo ICV administration. Whole-cell patch-clamp recordings further demonstrated reduced voltage-gated Ca2+ channel (VGCC) current density in neurons isolated from ICV PM2.5-treated rats. This functional reduction was not accompanied by significant changes in the SCG mRNA levels of the examined pore-forming Cavα1 subunits. In parallel, ICV PM2.5 administration increased GFAP and Kir4.1 protein levels and enhanced perineuronal GFAP immunoreactivity, consistent with satellite glial cell reactivity. Together, these findings identify impaired neuronal Ca2+ signaling and accompanying glial alterations in the SCG following PM2.5 exposure. The reductions in extracellular NE accumulation and VGCC function across complementary exposure models support a potential contribution of impaired Ca2+-dependent secretion to PM2.5-associated sympathetic dysfunction.

Related

  1. Satellite-derived air pollution exposure during pregnancy and preterm birth in South-West Oltenia
    ML Cara, A Becheru, AL Golli +3
    The European Journal of Public HealthPeer-reviewedCC BY-NC 4.0Full textPharmacology & toxicologyPMCEurope PMC
  2. A corticopapillary Gdf15 response links maladaptive collecting duct remodeling to polyuria during lithium exposure
    L. Zerarga, M. Himbert, M. Try +22
    bioRxivPreprintCC BYFull textPharmacology & toxicologybioRxiv
  3. Occupational endotoxin exposure, DNA methylation changes, and immune-cell remodeling: an epigenome-wide association study in two cohorts
    H. Wang, M. L. Rahman, C. E. Breeze +16
    medRxivPreprintCC0Full textEpidemiology & public healthmedRxiv
  4. Rhythms of mood: Bidirectional regulation of molecular clocks and neurotransmission in affective disorders
    Xin-Ling Wang, Tsvetan Serchov
    Neuroscience and Biobehavioral ReviewsPeer-reviewedCC BY 4.0Full text2 citedPhysiologyHALHAL
  5. Corticosteroids drive oral candidiasis by impairing type-17 immunity without inducing interferon-gammopathy
    Ashira Lubkin, Abigail Fellows, Lucas dos Santos Dias +2
    mBioPeer-reviewedPublisher termsFull textInfectious diseaseCrossref

Cite

BibTeXRIS
BibTeX
@article{do2026pm25,
  title = {{PM2.5 Exposure Disrupts Sympathetic Neurotransmission by Impairing Voltage-Gated Ca2+ Channels and Remodeling Satellite Glia in the Superior Cervical Ganglion}},
  author = {Phuong Anh Do and Huu Son Nguyen and Seung-Kuy Cha},
  journal = {International Journal of Molecular Sciences},
  year = {2026},
  month = oct,
  doi = {10.3390/ijms27209184},
  url = {https://www.mdpi.com/1422-0067/27/20/9184},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - PM2.5 Exposure Disrupts Sympathetic Neurotransmission by Impairing Voltage-Gated Ca2+ Channels and Remodeling Satellite Glia in the Superior Cervical Ganglion
AU  - Phuong Anh Do
AU  - Huu Son Nguyen
AU  - Seung-Kuy Cha
PY  - 2026
DA  - 2026/10/01
JO  - International Journal of Molecular Sciences
DO  - 10.3390/ijms27209184
UR  - https://www.mdpi.com/1422-0067/27/20/9184
AB  - Airborne fine particulate matter (PM2.5) exposure is associated with central neuroinflammation and autonomic dysfunction, but its effects on peripheral sympathetic ganglia remain poorly defined. Here, we examined the effects of central PM2.5 administration and direct PM2.5 exposure on the superior cervical ganglion (SCG), a primary sympathetic relay governing cephalic noradrenergic outflow. Intracerebroventricular (ICV) administration of PM2.5 increased hypothalamic TNF-α and IL-6 levels and reduced presynaptic synaptophysin expression, while SCG tyrosine hydroxylase expression remained unchanged. In a complementary ex vivo model, direct PM2.5 exposure reduced norepinephrine (NE) accumulation in the culture medium of isolated SCGs without significantly altering tissue NE content. Mechanistically, live-cell Ca2+ imaging revealed attenuated depolarization-evoked Ca2+ responses in SCG neurons following either 24-h direct exposure or in vivo ICV administration. Whole-cell patch-clamp recordings further demonstrated reduced voltage-gated Ca2+ channel (VGCC) current density in neurons isolated from ICV PM2.5-treated rats. This functional reduction was not accompanied by significant changes in the SCG mRNA levels of the examined pore-forming Cavα1 subunits. In parallel, ICV PM2.5 administration increased GFAP and Kir4.1 protein levels and enhanced perineuronal GFAP immunoreactivity, consistent with satellite glial cell reactivity. Together, these findings identify impaired neuronal Ca2+ signaling and accompanying glial alterations in the SCG following PM2.5 exposure. The reductions in extracellular NE accumulation and VGCC function across complementary exposure models support a potential contribution of impaired Ca2+-dependent secretion to PM2.5-associated sympathetic dysfunction.
SN  - 1422-0067
ER  -