Reduced spinal microglial activation and neuropathic pain after nerve injury in mice lacking all three nitric oxide synthases
Author Information
Author(s): Kuboyama Kazuya, Tsuda Makoto, Tsutsui Masato, Toyohara Yumiko, Tozaki-Saitoh Hidetoshi, Shimokawa Hiroaki, Yanagihara Nobuyuki, Inoue Kazuhide
Primary Institution: Department of Molecular and System Pharmacology, Graduate School of Pharmaceutical Sciences, University of Kyushu, Fukuoka, Japan
Hypothesis
The NOS/NO pathway contributes to behavioral pain responses evoked by tissue injury and nerve injury.
Conclusion
The study shows that the NOS/NO pathway is important for spinal microglial activation and tactile allodynia after nerve injury.
Supporting Evidence
- Both iNOS-/- and n/i/eNOS-/- mice showed reduced pain behaviors compared to wild-type mice.
- Nerve injury-induced tactile allodynia was significantly suppressed in n/i/eNOS-/- mice.
- Pharmacological inhibition of NOSs improved tactile allodynia after nerve injury.
Takeaway
Mice without certain enzymes that produce nitric oxide feel less pain after nerve injuries, suggesting that these enzymes are important for pain signaling.
Methodology
The study used various pain assays on mice lacking different nitric oxide synthase genes to assess pain responses.
Participant Demographics
Male mice, including wild-type and genetically modified strains.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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