Fig. 7: Activity-induced axonal glucose consumption rate is reduced in Kir4.1 cKO mice.
From: Oligodendrocyte–axon metabolic coupling is mediated by extracellular K+ and maintains axonal health
a, Time-course traces of 50-Hz-evoked axonal glucose dynamics showing differences in glucose level changes between cKO (n = 16) and control (n = 11) mice. b, During stimulation, glucose levels decreased at a rate of 2.7 ± 0.6% min−1 in controls (n = 11) but remained stable (0.1 ± 0.2% min−1) in cKO (n = 16; ***P = 0.0002, two-sided unpaired t test). c, After stimulation, glucose levels increased above the initial baseline values in both genotypes but were significantly higher in cKO (3.2 ± 0.3%) than in controls (1.4 ± 0.4%; ***P = 0.0006, two-sided unpaired t test). d–g, Assessment of glucose consumption rate changes from 0.1- to 50-Hz stimulations in control (n = 6) and cKO (n = 7) mice. d, Decline slopes are indicated by dashed lines. e, Axonal glucose consumption rates significantly increased upon 50-Hz stimulation (Stim 50 Hz) in controls (0.1 versus 50 Hz, **P = 0.0022, two-sided paired t test) and in cKO (0.1 versus 50 Hz, ***P < 0.0001, two-sided paired t test). f, Glucose consumption rate during 50-Hz stimulation was 40 ± 15% lower in cKO than in controls (*P = 0.0208, two-sided unpaired t test). g, Fold change in glucose consumption from 0.1 to 50 Hz was comparable between genotypes (8.5 ± 2 in controls and 8.5 ± 1 in cKO, P = 0.9858, two-sided unpaired t test). Data are represented as mean ± s.e.m.
