That led to my pharmacogenetic project, which I continued in my own lab.
What questions are you addressing with that project?
There is evidence that there are inhibitory neurons in the spinal cord that under normal conditions tonically prevent touch information from activating pain circuits.
But in conditions with neuropathic pain, this level of inhibition may decrease, either because the interneurons that are responsible for inhibiting this connection die, or because they reduce their release of GABA [gamma-aminobutyric acid], for instance, or glycine.
Then we use the spared nerve injury model of neuropathic pain that Shannon Shields developed in Allan’s lab to see whether increasing interneuron activity alleviates mechanical allodynia. Our approach uses a method developed by Bryan Roth’s lab at the University of North Carolina [Chapel Hill, US].