Extended Data Fig. 3: Cav1-knockout mice have attenuated vasodilation but normal neural activity and neurovascular coupling kinetics.
From: Caveolae in CNS arterioles mediate neurovascular coupling
a–d, Maximum percentage change in dilation response (a) and baseline diameter (b) latency to maximum change in arteriolar dilation (c), time to peak dilation (d) in Cav1+/+ (n = 193 arterioles, 40 capillaries, 5 mice), Cav1+/− (n = 123 arterioles, 40 capillaries, 5 mice), and Cav1−/− mice (n = 153 arterioles, 31 capillaries, 5 mice). e, f, Latency to maximum red blood cell flow velocity (e) and time to peak red blood cell flow (f) in Cav1+/+ (n = 193 arterioles, 40 capillaries, 5 mice), Cav1+/− (n = 123 arterioles, 40 capillaries, 5 mice) and Cav1−/− mice (n = 153 arterioles, 31 capillaries, 5 mice). g, h, Maximum percentage change in GCaMP6s (g) and latency to peak change in GCaMPs (h) in Cav1+/+;Thy1-GCaMP6s (n = 78 field of views of the neuropils, 5 mice) and Cav1−/−;Thy1-GCaMP6s (n = 78 neuropils, 5 mice). Each circle represents an individual trial of GCaMP6s signal. i, Baseline diameter to absolute maximum diameter response during whisker stimulation in Cav1+/+ and Cav1−/− mice. j, Tail-cuff blood pressure measurements between Cav1+/+ (n = 5 mice) and Cav1−/− mice (n = 5 mice). Statistical significance was determined by a one-way nested ANOVA with a post hoc Bonferroni multiple comparison adjustment for a–f, a nested unpaired, two-tailed t-test for g, h, and two-tailed Mann–Whitney U test for j. All data are mean ± s.e.m.
