6月24日のNeuroClubを担当します、神経科学研究部の吉本です。
下記の論文を紹介いたします。
40 Hz light flickering alleviates chronic pain via adenosine signaling
in the retina-amygdala pathway
Jiawang Chen, Tao Xu, Chenchen Zhang, Li Li, Yan He, Zhaoxia Sun,
Jiasheng He, Zhimo Yao, Peng Cai, Yipeng Huang, Fenfen Ye, Wei Guo,
Manli Jia, Jia Qu, Jiang-Fan Chen & Yi Zhang
Cell Res. 2026 Jun;36(6):440-461. doi: 10.1038/s41422-026-01227-7.
ttps://www.nature.com/articles/s41422-026-01227-7
(先頭にhを付け足してください)
Abstract
Chronic pain affects over 20% of the global population, yet frontline
treatments remain limited in efficacy and are often hampered by serious
side effects. In search of novel and effective neuromodulation
alternatives, we discovered that 40 Hz flickering light effectively
alleviates inflammatory and neuropathic pain in mice. We identified the
retina-central amygdala (CeA) pathway as a critical conduit for the
analgesic effects of 40 Hz flickering light. Using circuit-specific
manipulations, we demonstrated that activation of the retina-CeA pathway
is both sufficient to mimic and necessary to mediate the analgesic
outcomes of 40 Hz light stimulation. In terms of mechanism, we found
that 40 Hz light flickering significantly increases extracellular
adenosine levels in the CeA. Local pharmacological blockade of
equilibrative nucleoside transporters prevented this adenosine increase
and abolished the analgesic effects of 40 Hz light flickering, whereas
focal adenosine infusion phenocopied the light-induced analgesia. Both
interventions required A2A receptor signaling to suppress nociceptive
responses. Furthermore, we found that hyperalgesia could be destabilized
in the CeA and reversed by 40 Hz light stimulation or adenosine infusion,
mirroring memory reconsolidation processes and implicating the CeA as a
key locus for pain memory erasure. Collectively, our findings
demonstrate the multifaceted therapeutic benefits of 40 Hz light
flickering as a novel non-invasive approach for pain management and
reveal a distinct retina-CeA circuit and adenosine signaling mechanism
for control of chronic pain and pain memory.
よろしくお願いいたします。
東京慈恵会医科大学 神経科学研究部
吉本 凌