The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
P2Y12Receptors in Spinal Microglia Are Required for Neuropathic Pain after Peripheral Nerve Injury
Open accessAbstract
Extracellular nucleotides have been implicated as signaling molecules used by microglia to sense adverse physiological conditions, such as neuronal damage. They act through purinoceptors, especially the G-protein-coupled P2Y receptor P2Y 12 R. Emerging evidence has indicated that activated spinal microglia responding to nerve injury are key cellular intermediaries in the resulting highly debilitating chronic pain state, namely neuropathic pain. However, the role of microglial P2Y 12 Rs in neuropathic pain remains unknown. Here, we show that the level of P2Y 12 R mRNA expression was markedly increased in the spinal cord ipsilateral to the nerve injury and that this expression was highly restricted to ionized binding calcium adapter molecule 1-positive microglia. An increase in the immunofluorescence of P2Y 12 R protein in the ipsilateral spinal cord was also observed after nerve injury, and P2Y 12 R-positive cells were double labeled with the microglial marker OX-42. Blocking spinal P2Y 12 R by the intrathecal administration of its antagonist AR-C69931MX prevented the development of tactile allodynia (pain hypersensitivity to innocuous stimuli), a hallmark of neuropathic pain syndrome. Furthermore, mice lacking P2ry12(P2ry 12−/−) displayed impaired tactile allodynia after nerve injury without any change in basal mechanical sensitivity. Moreover, a single intrathecal administration of AR-C69931MX or oral administration of clopidogrel (a P2Y 12 R blocker clinically in use) to nerve-injured rats produced a striking alleviation of existing tactile allodynia. Together, our findings indicate that activation of P2Y 12 Rs in spinal microglia may be a critical event in the pathogenesis of neuropathic pain and suggest that blocking microglial P2Y 12 R might be a viable therapeutic strategy for treating neuropathic pain.
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Cites
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Self-citationP2X4 receptors induced in spinal microglia gate tactile allodynia after nerve injury
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Cited by
Cellular and Molecular Mechanisms of Pain
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Microglia emerge as central players in brain disease
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Models and Mechanisms of Hyperalgesia and Allodynia
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Pathological pain and the neuroimmune interface
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Metadata
- Authors
- Tozaki-Saitoh, H., Tsuda, M., Miyata, H., Ueda, K., Kohsaka, S., & Inoue, K.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2008-05-07
- Volume
- 28
- Issue
- 19
- Pages
- 4949-4956
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2006261709
- Cited by
- 278
- References
- 31
- FWCI
- 13.47
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- CoChat. (2026). Citation check: P2Y12Receptors in Spinal Microglia Are Required for Neuropathic Pain after Peripheral Nerve Injury. https://app.cochat.ai/papers/10.1523/jneurosci.0323-08.2008
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- Tozaki-Saitoh, H., Tsuda, M., Miyata, H., Ueda, K., Kohsaka, S., & Inoue, K. (2008). P2Y12Receptors in Spinal Microglia Are Required for Neuropathic Pain after Peripheral Nerve Injury. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.0323-08.2008
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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