Moreover, energy deprivation and cell death/dysfunction can considerably elevate the concentration of choline in the extracellular space [89–91] providing a large source of this endogenous α7 nAChR agonist as has been recently demonstrated by direct measurements of choline/ACh levels in the ischemic core and penumbra in the MCAO model of ischemic stroke in rats [92]. This evidence concerns the gene CHRNA7 and ischemic stroke.