I have a hypothesis that activation of TRPA1 is involved in the patogenesis of ME.
And now, nice people have written this paper:
Reactive oxygen species enhance excitatory synaptic transmission in rat spinal dorsal horn neurons by activating TRPA1 and TRPV1 channels
The nice people have made highlights:
- ROS enhance excitatory synaptic transmission in rat spinal dorsal horn neurons
- These excitatory effects are induced by the activation of TRPA1 and TRPV1 channels
- ROS in the spinal cord can play an important role in central sensitization
We all have in mind Julia Newtons research that shows that the cells from ME patients produced on average 20 times as much acid when exercised.
And more nice people have written another fine paper:
The molecular basis for species-specific activation of human TRPA1 by protons involves poorly conserved residues within transmembrane domains 5 and 6
And quote from there:
Background: Extracellular acidosis mediates pain and inflammation by activating sensory afferent neurons
Results: Protons activate and sensitize human TRPA1 in a strongly species-specific manner encoded by transmembrane domains 5 and 6.
Conclusion: Our data identify TRPA1 as an ion channel likely to mediate acid-induced pain in humans.
Significance: Protons are the first known endogenous agonists of TRPA1 with species-specificity for human TRPA1.
If only all those nice people will do a little research on ME.....
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