ArticleCNS neuroscience & therapeutics2025
Impaired WNT3/IGF-1 Signaling in Dorsal Dentate Gyrus Contributes to Chronic Pain-Related Cognitive Impairment.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Prelimbic cortex layer 5 GABAergic neurons mediate chronic pain and memory impairment by regulating excitatory/inhibitory imbalance.The journal of headache and pain · 2026Article
- Impaired WNT3/IGF-1 Signaling in Dorsal Dentate Gyrus Contributes to Chronic Pain-Related Cognitive Impairment.CNS neuroscience & therapeutics · 2025Article
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9 authors.
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Abstract
backgroundNeuropathic pain is frequently accompanied by cognitive deficits, but the neural circuits and molecular mechanisms linking nociceptive hypersensitivity to cognitive dysfunction remain incompletely understood. The hippocampal dentate gyrus (DG), a critical hub for adult neurogenesis and memory encoding, is emerging as a key substrate integrating pain processing and cognitive impairment, but how peripheral nerve injury disrupts DG homeostasis remains unclear.
methodsIn this study, we used the spared nerve injury (SNI) mouse model to investigate the cellular and molecular mechanisms underlying comorbid neuropathic pain and cognitive deficits. Behavioral assessments, stereotaxic viral/drug delivery, Western blot, immunofluorescence staining, whole-cell patch-clamp recordings, ELISA, and primary astrocyte culture were employed to characterize phenotypic changes and regulatory pathways in the dorsal DG.
resultsWe found that SNI induced persistent mechanical hypersensitivity and cognitive impairment in mice, which was associated with reduced neurogenesis (decreased nestin
conclusionOur findings identify that decreased WNT3 secretion from astrocytes in dorsal DG integrates nociceptive and cognitive dysfunction after nerve injury via crosstalking with the IGF-1/AKT pathway. Targeting this WNT3/IGF-1 axis may represent a promising therapeutic strategy for neuropathic pain and its cognitive sequelae.
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