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Peer-reviewedCC BY 4.0Neuroscience bulletin

Small-Conductance Ca2+-Activated K+ Channels and Their Regulation of Excitability of Autonomic Neurons

  • Renjun Wang1,2
  • Zhengwei Li1
  • Andrew D. Chapp2
  • Min Lin3
  • Dong-Shu Du4
  • Zhiying Shan2
  • Zixi Jack Cheng5
  • Qing-Hui Chen2
5 affiliations
  1. 1Department of Biotechnology, School of Life Science, Jilin Normal University, Siping 136000, China
  2. 2Department of Kinesiology and Integrative Physiology, Michigan Technological University, Houghton, MI 49931-1200, USA
  3. 3Department of Neuroscience, Evelyn F. and William L. McKnight Brain Institute, University of Florida, Gainesville, FL 32611, USA
  4. 4School of Life Sciences, Shanghai University, Shanghai 200444, China
  5. 5Biomolecular Science Center, College of Medicine, Burnett School of Biomedical Sciences, University of Central Florida, Orlando, FL 32816, USA
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Abstract

Dyshomeostasis of the autonomic nervous system (ANS) drives chronic illnesses including hypertension, heart failure, diabetes mellitus, metabolic syndrome, Parkinson’s disease, and traumatic brain injury. Abnormal neuronal excitability within central nervous system (CNS) nuclei is a major cause of ANS dysfunction. Small-conductance calcium-activated potassium (SK) channels govern excitability in central autonomic nuclei, sustaining neuronal excitation-inhibition balance via medium afterhyperpolarization potentials (mAHP)-mediated negative feedback. This review describes SK channels’ molecular structure and electrophysiology, maps central sympathetic-parasympathetic neuroanatomical pathways, and highlights pathological impacts of the dysfunction of SK channels among the hypothalamic paraventricular nucleus (PVN) and nucleus ambiguus (NA). It also summarizes SK channels-centered regulatory approaches: epigenetics (DNA methylation, miRNA modulation), post-translational modification (phosphorylation, ubiquitination), protein interaction, metabolites, and synthetic exogenous agonists and antagonists. These results offer a theoretical basis and candidate targets to decode the neurogenic hypertension and diabetes mechanisms and facilitate bench-to-clinic translation.

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Cite

BibTeXRIS
BibTeX
@article{wang2026smallconductance,
  title = {{Small-Conductance Ca2+-Activated K+ Channels and Their Regulation of Excitability of Autonomic Neurons}},
  author = {Renjun Wang and Zhengwei Li and Andrew D. Chapp and Min Lin and Dong-Shu Du and Zhiying Shan and Zixi Jack Cheng and Qing-Hui Chen},
  journal = {Neuroscience bulletin},
  year = {2026},
  month = sep,
  doi = {10.1007/s12264-026-01715-1},
  url = {https://doi.org/10.1007/s12264-026-01715-1},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Small-Conductance Ca2+-Activated K+ Channels and Their Regulation of Excitability of Autonomic Neurons
AU  - Renjun Wang
AU  - Zhengwei Li
AU  - Andrew D. Chapp
AU  - Min Lin
AU  - Dong-Shu Du
AU  - Zhiying Shan
AU  - Zixi Jack Cheng
AU  - Qing-Hui Chen
PY  - 2026
DA  - 2026/09/18
JO  - Neuroscience bulletin
DO  - 10.1007/s12264-026-01715-1
UR  - https://doi.org/10.1007/s12264-026-01715-1
AB  - Dyshomeostasis of the autonomic nervous system (ANS) drives chronic illnesses including hypertension, heart failure, diabetes mellitus, metabolic syndrome, Parkinson’s disease, and traumatic brain injury. Abnormal neuronal excitability within central nervous system (CNS) nuclei is a major cause of ANS dysfunction. Small-conductance calcium-activated potassium (SK) channels govern excitability in central autonomic nuclei, sustaining neuronal excitation-inhibition balance via medium afterhyperpolarization potentials (mAHP)-mediated negative feedback. This review describes SK channels’ molecular structure and electrophysiology, maps central sympathetic-parasympathetic neuroanatomical pathways, and highlights pathological impacts of the dysfunction of SK channels among the hypothalamic paraventricular nucleus (PVN) and nucleus ambiguus (NA). It also summarizes SK channels-centered regulatory approaches: epigenetics (DNA methylation, miRNA modulation), post-translational modification (phosphorylation, ubiquitination), protein interaction, metabolites, and synthetic exogenous agonists and antagonists. These results offer a theoretical basis and candidate targets to decode the neurogenic hypertension and diabetes mechanisms and facilitate bench-to-clinic translation.
SN  - 1673-7067
SN  - 1995-8218
ER  -