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Peer-reviewedCC BYEMBO Reports

Upregulation of AK7 in ACC-VTA glutamatergic projections contributes to chronic inflammation pain in male mice

  • Jie Huang1
  • Meng-Ge Li2
  • Ru-Yu Yan3
  • Zhen-Hua Xu2
  • Chen-Hao Zhang2
  • Ying Cao2
  • Xiao-Dong Xu1
  • Yong-Chang Li2
  1. 1Department of Pharmacy, The Zhangjiagang Affiliated Hospital of Soochow University
  2. 2Center of Translational Medicine, The Zhangjiagang Affiliated Hospital of Soochow University
  3. 3Jiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of Neuroscience, Soochow University
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Abstract

Chronic inflammation pain is a complex pathological condition involving multiple mechanisms in both the peripheral and central nervous systems. Growing evidence indicates that an imbalance in central nervous system function plays a crucial role in the progression of chronic pain, yet the underlying neural circuits and molecular targets remain largely unclear. Here we identify the anterior cingulate cortex (ACC) as a key mediator in chronic inflammation pain. Noxious stimulation significantly increases c-Fos expression and calcium activity in both the ACC and the ventral tegmental area (VTA). Upregulation of adenosine kinase 7 (AK7) in ACC glutamatergic neurons emerges as an important factor in pain pathogenesis: interfering with AK7 expression reduces neuronal activity in the ACC and VTA and alleviates pain-related behaviors, while overexpressing AK7 enhances neuronal activity in these regions and exacerbates pain. Further experiments demonstrate that modulating the activity of VTA glutamatergic neurons can correspondingly reverse the effects of AK7 manipulation on pain phenotypes. In summary, our findings demonstrate that upregulation of AK7 in ACC promotes chronic pain through the ACC-VTA neural circuit.

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Cite

BibTeXRIS
BibTeX
@article{huang2026upregulation,
  title = {{Upregulation of AK7 in ACC-VTA glutamatergic projections contributes to chronic inflammation pain in male mice}},
  author = {Jie Huang and Meng-Ge Li and Ru-Yu Yan and Zhen-Hua Xu and Chen-Hao Zhang and Ying Cao and Xiao-Dong Xu and Yong-Chang Li},
  journal = {EMBO Reports},
  year = {2026},
  month = sep,
  doi = {10.1038/s44319-026-00940-z},
  url = {https://doi.org/10.1038/s44319-026-00940-z},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Upregulation of AK7 in ACC-VTA glutamatergic projections contributes to chronic inflammation pain in male mice
AU  - Jie Huang
AU  - Meng-Ge Li
AU  - Ru-Yu Yan
AU  - Zhen-Hua Xu
AU  - Chen-Hao Zhang
AU  - Ying Cao
AU  - Xiao-Dong Xu
AU  - Yong-Chang Li
PY  - 2026
DA  - 2026/09/01
JO  - EMBO Reports
DO  - 10.1038/s44319-026-00940-z
UR  - https://doi.org/10.1038/s44319-026-00940-z
AB  - Chronic inflammation pain is a complex pathological condition involving multiple mechanisms in both the peripheral and central nervous systems. Growing evidence indicates that an imbalance in central nervous system function plays a crucial role in the progression of chronic pain, yet the underlying neural circuits and molecular targets remain largely unclear. Here we identify the anterior cingulate cortex (ACC) as a key mediator in chronic inflammation pain. Noxious stimulation significantly increases c-Fos expression and calcium activity in both the ACC and the ventral tegmental area (VTA). Upregulation of adenosine kinase 7 (AK7) in ACC glutamatergic neurons emerges as an important factor in pain pathogenesis: interfering with AK7 expression reduces neuronal activity in the ACC and VTA and alleviates pain-related behaviors, while overexpressing AK7 enhances neuronal activity in these regions and exacerbates pain. Further experiments demonstrate that modulating the activity of VTA glutamatergic neurons can correspondingly reverse the effects of AK7 manipulation on pain phenotypes. In summary, our findings demonstrate that upregulation of AK7 in ACC promotes chronic pain through the ACC-VTA neural circuit.
SN  - 1469-3178
ER  -