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September 10, 2025Cellular SignallingOpen Access

GPR55 activation alleviates cognitive dysfunction caused by neuropathic pain through modulation of microglia polarization and synaptic plasticity via the CaMKKβ/AMPK/SOCS3 signaling pathway

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Authors

FZFengtian ZhaoTongji HospitalXZXiaoyu ZhangTongji HospitalTLTengteng LiuNanjing Agricultural University

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Overview

Pharmacological activation of GPR55 mitigates cognitive deficits in neuropathic pain, suggesting its potential therapeutic role in neuroinflammation and microglial polarization.

Key Points

  • GPR55 activation alleviates cognitive dysfunction, improving memory in a neuropathic pain model.
  • Activation shifts microglial polarization toward the neuroprotective M2 phenotype, reducing neuroinflammation.
  • The CaMKKβ/AMPK/SOCS3 signaling pathway is involved in modulating synaptic plasticity and neuroinflammation.
  • These findings support GPR55 as a potential target for treating cognitive deficits linked to neuropathic pain.

Cite This Study

Zhao et al. (2025) studied this question.

synapsesocial.com/papers/68c1cc4754b1d3bfb60f4e3fhttps://doi.org/10.1016/j.cellsig.2025.112070
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Activation of GPR55 alleviates neuropathic pain and chronic inflammation2024 · 3 citations
  2. 2Activation of <scp>GPR35</scp> in the Anterior Cingulate Cortex Alleviates Neuropathic Pain and Depression‐Related Behavior2026
  3. 3Activation of GPR55 Ameliorates Maternal Separation-Induced Learning and Memory Deficits by Augmenting 5-HT Synthesis in the Dorsal Raphe Nucleus of Juvenile Mice2024 · 3 citations
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