Loss of spinal substance P pain transmission in neuropathic pain
Author Information
Author(s): Inoue Makoto, Yamaguchi Asuka, Kawakami Megumi, Chun Jerold, Ueda Hiroshi
Primary Institution: Nagasaki University Graduate School of Biomedical Sciences
Hypothesis
Is the loss of pain transmission through C-fiber neurons mediated by LPA1 receptor activation following nerve injury?
Conclusion
The study concludes that the loss of spinal substance P transmission via C-fibers is mediated through the activation of LPA1 receptor and RhoA.
Supporting Evidence
- The loss of C-fiber responses was observed with nociceptive flexor responses in nerve-injured mice.
- SP signal in the dorsal horn was markedly reduced in nerve-injured mice.
- All changes were abolished in LPA1-/- mice or with RhoA inhibitor pretreatment.
Takeaway
When nerves are injured, a special signal called LPA makes it hard for the body to feel pain through certain nerves, but blocking this signal can help.
Methodology
The study used male Std-ddY mice and LPA1-/- mice, performing nerve injury and measuring pain responses through substance P injections and immunohistochemistry.
Participant Demographics
Male Std-ddY mice and LPA1-/- mice weighing 20–22 g.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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