Fig. 2

Deletion of CD36 in BAM rescues neurovascular dysfunction in 15-month-old Tg2576 mice. A WT → Tg2576 chimeras exhibit an attenuated increase in CBF during whisker stimulation (functional hyperemia), which is completely restored in CD36^−/− → Tg2576 chimeras. B CBF responses to neocortical application of the mechanistically distinct endothelium-dependent vasodilators acetylcholine, bradykinin, and the Ca²⁺ ionophore A23187 are attenuated in WT → Tg2576 chimeras and are restored in CD36^−/− → Tg2576 chimeras. C The attenuation of CBF responses to neocortical application the NO donor SNAP in WT → Tg2576 is normalized in CD36^−/− → Tg2576 chimeras. CBF responses to adenosine are not attenuated in WT → Tg2576 and remain normal in CD36^−/− → Tg2576 chimeras D: CBF response to the potent vasodilator hypercapnia has a trend toward to attenuation in WT → Tg2576 which was not observed in CD36^−/− → Tg2576 chimeras. N = 5/group; two-way ANOVA with Tukey’s test; data presented as mean ± SEM