Yeh I just had another look at that. I think what's confusing now is, is this type II synapse increase upon noise trauma the actual act of sensitization? Or is sensitization something yet again different?
The part about OHCs retaining normal sensitivity would suggest to me that that they don't yet suffer synapse disconnection.
Then it goes on to say that type IIs are excited by and could become sensitized by ATP.
So is it like a 2 point attack on the type IIs? First they become hyper-connected to the OHC with the new synapses, and then they become sensitized by a flood of ATP? Or a combination of the 2 that causes sensitization.
'Here, we have examined OHC ribbon synapses 7 days after noise exposure. The model presented assumes that OHCs retain normal sensitivity. Also, it is known that acute tissue damage initiates spreading waves of activity among supporting cells via the release of ATP. Type II afferents are excited by ATP, and could become sensitized in the presence of ATP as is observed in somatic nociceptors. Tissue damage caused by acoustic trauma also induces a prolonged inflammatory response.'
I think there's a couple of pieces of research that can be linked together quite well in a new experiment. First the research with the deaf mice that still showed type II sensitization due to noise trauma (I'm not sure if anyone ever uncovered the paper for this but its mentioned
here), then there's the latest one that you found on the extra ribbon synapses
here. I'll spend some time reading them over the next couple of days to see how they could collaborated together in a possible 'setback' experiment.