Spinal NKCC1 blockade inhibits TRPV1-dependent referred allodynia
2007
Blocking NKCC1 Reduces Pain Sensitivity in Mice
Sample size: 6
publication
10 minutes
Evidence: moderate
Author Information
Author(s): Mark H Pitcher, Theodore J Price, Jose M Entra, Fernando Cervero
Primary Institution: McGill University
Hypothesis
Does spinal NKCC1 mediate referred allodynia in response to a visceral inflammatory stimulus?
Conclusion
Spinal NKCC1 and TRPV1 are critical for referred allodynia mediated by a painful visceral stimulus.
Supporting Evidence
- Intrathecal injection of bumetanide inhibited referred allodynia evoked by capsaicin.
- Bumetanide was effective when injected before or up to 4 hours after allodynia establishment.
- The TRPV1 antagonist AMG 9810 also inhibited referred allodynia in the model.
- NADA, a TRPV1 agonist, evoked stroking allodynia that was blocked by AMG 9810.
- Bumetanide inhibited NADA-evoked stroking allodynia, linking NKCC1 to TRPV1 activity.
Takeaway
When scientists blocked a specific protein in the spine, it helped reduce pain caused by inflammation in mice.
Methodology
Mice received intrathecal injections of NKCC1 inhibitor bumetanide and TRPV1 antagonist AMG 9810, followed by capsaicin injections to induce pain.
Limitations
The study was conducted on mice, which may not fully represent human pain mechanisms.
Participant Demographics
Male C57BL6 mice, 20-25 g.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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