Chronic postoperative pain induces contextual fear extinction dysfunction through hippocampal NMDAR/BDNF/TrkB signaling pathway in mice Article Swipe
Jiawei Zhang
,
Xiaoting Zheng
,
Gaoyan Zhang
,
Zixi Cheng
,
Yinuo Liu
,
Lei Zhang
,
Jiqian Zhang
,
Xuesheng Liu
,
Zhilai Yang
·
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1038/s41398-025-03417-0
YOU?
·
· 2025
· Open Access
·
· DOI: https://doi.org/10.1038/s41398-025-03417-0
Post-traumatic stress disorder (PTSD) is a common disorder in clinical practice, characterized by various manifestations, with fear extinction dysfunction being a typical one. Postoperative persistent pain, a form of chronic pain following surgical procedures, significantly affects patients' quality of life. Clinical studies have demonstrated the comorbidity between chronic pain and PTSD; however, the molecular mechanisms underlying this comorbidity remain unclear. Researches have shown that brain-derived neurotrophic factor (BDNF) and N-methyl-D-aspartate glutamate receptors (NMDARs) are crucial in fear extinction dysfunction. Thus, we established a skin/muscle incision and retraction (SMIR) mice model to explore the roles of hippocampal NMDARs and BDNF signaling pathways in fear extinction following postoperative persistent pain. We found that SMIR mice exhibited contextual fear extinction dysfunction, potentially caused by a down-regulated NMDARs/ERK/CREB/BDNF signaling pathway and impaired synaptic plasticity in the hippocampus. Hippocampal injection of the NMDARs agonist NMDA promoted extinction learning and retrieval of extinction memory, activating the NMDARs/ERK/CREB/BDNF signaling pathway, and restoring lost dendritic spines. Simultaneous hippocampal administration of NMDA and the TrkB inhibitor ANA-12 promoted the learning process of fear extinction without enhancing the retrieval of extinction memory, while re-inducing dendritic spine loss. In summary, we conclude that postoperative persistent pain impairs synaptic plasticity by downregulating the NMDARs/ERK/CREB/BDNF signaling pathway, thereby inducing contextual fear extinction dysfunction. These findings may partially explain the mechanisms underlying the comorbidity between chronic pain and PTSD.
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- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1038/s41398-025-03417-0
- https://www.nature.com/articles/s41398-025-03417-0.pdf
- OA Status
- gold
- References
- 73
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4411370817
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W4411370817Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1038/s41398-025-03417-0Digital Object Identifier
- Title
-
Chronic postoperative pain induces contextual fear extinction dysfunction through hippocampal NMDAR/BDNF/TrkB signaling pathway in miceWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2025Year of publication
- Publication date
-
2025-06-17Full publication date if available
- Authors
-
Jiawei Zhang, Xiaoting Zheng, Gaoyan Zhang, Zixi Cheng, Yinuo Liu, Lei Zhang, Jiqian Zhang, Xuesheng Liu, Zhilai YangList of authors in order
- Landing page
-
https://doi.org/10.1038/s41398-025-03417-0Publisher landing page
- PDF URL
-
https://www.nature.com/articles/s41398-025-03417-0.pdfDirect link to full text PDF
- Open access
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YesWhether a free full text is available
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-
goldOpen access status per OpenAlex
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https://www.nature.com/articles/s41398-025-03417-0.pdfDirect OA link when available
- Concepts
-
Tropomyosin receptor kinase B, Hippocampal formation, NMDA receptor, Neuroscience, Extinction (optical mineralogy), Chronic pain, Medicine, Psychology, Schizophrenia (object-oriented programming), Hippocampus, Internal medicine, Psychiatry, Neurotrophic factors, Receptor, Biology, PaleontologyTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
- References (count)
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73Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| publication_date | 2025-06-17 |
| publication_year | 2025 |
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| abstract_inverted_index.by | 12, 120, 198 |
| abstract_inverted_index.in | 8, 75, 101, 130 |
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| abstract_inverted_index.we | 80, 189 |
| abstract_inverted_index.and | 49, 68, 85, 97, 126, 143, 153, 163, 223 |
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| abstract_inverted_index.may | 212 |
| abstract_inverted_index.the | 44, 52, 92, 131, 136, 149, 164, 169, 177, 200, 215, 218 |
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| abstract_inverted_index.NMDA | 139, 162 |
| abstract_inverted_index.SMIR | 111 |
| abstract_inverted_index.TrkB | 165 |
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| abstract_inverted_index.caused | 119 |
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| abstract_inverted_index.factor | 66 |
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| abstract_inverted_index.between | 46, 220 |
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| abstract_inverted_index.explore | 91 |
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| abstract_inverted_index.molecular | 53 |
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| institutions_distinct_count | 9 |
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