@Murph, Naviaux says "testing the hypothesis that purinergic signaling is chronically increased in the MIA model of ASD cannot be achieved by measuring tissue or plasma concentrations of nucleotides like ATP and ADP. The relevant concentration of nucleotides is confined to a thin shell, or pericellular halo, that defines the unstirred water layer (UWL) around the effector cells where receptors and their ligands meet. Concentrations of metabolites in the UWL can be 1000-fold higher than in plasma or interstitial fluid . Hence, we selected purinergic receptor downregulation as a surrogate for chronic hyperpurinergia."
(There's a risk of making a goof of yourself when you have some data but shaky understanding of the actual systems the numbers refer to - I've certainly taken that risk! Just looking back at my earlier posts in this thread I can see glaring misunderstandings and mistakes. I'm learning at the sort of rapid rate that's probably only possible when you start at the beginning!!)
Anyway, does cd39 also only operate in the pericellular halo? Surely not, right? So the low serum levels of adenosine may still indicate cd39 shortfall? I am left wondering how the high serum ratios of ATP:AMP:adenosine can be interpreted.
Also, is there evidence of purinergic receptor downregulation in mecfs? Those Light studies seem to show up-regulation...