Fig. 2: Astrocytic GLUT1 deletion does not affect sensorimotor, learning or memory functions.
From: Astrocytic GLUT1 deletion in adult mice enhances glucose metabolism and resilience to stroke
a Experimental timeline: Behavioral tests were conducted 60, 75, and 90 days post-tamoxifen treatment, with a one-week rest between tests. b Sensorimotor performance (gait, ledge, hindlimb clasping, and horizontal wire test) was comparable between Ctrl (n = 11) and cKO (n = 11) mice (p = 0.5295, two-sided unpaired t-test). c Left: Barnes maze setup with 22 holes, one escape hole, and visual cues. Right: Experimental timeline with a 4-day acquisition phase (arrowheads indicate sessions), followed by a day 5 memory test with the target hole sealed. d Both Ctrl (n = 11) and cKO (n = 11) mice showed a significant decrease in latency to find the target hole from day 1 to day 4 (Ctrl: β = -93.71 s, cKO: β = −91.05 s, each p < 0.0001, two-sided paired t-test), with no genotype differences in spatial learning (Finteraction(3,60) = 0.6990, p = 0.5563, two-way ANOVA). e On day 5, Ctrl (n = 11) and cKO (n = 11) mice preferentially identified the target hole over an adjacent hole (Ctrl: β = 3.6, p = 0.0027; cKO: β = 4.3, p = 0.0003, two-sided paired t-test), indicating intact memory retrieval in cKO mice. f Locomotor performance on day 5 was comparable between Ctrl (7.9 ± 0.5 m; n = 11) and cKO (7.5 ± 0.5 m; n = 11, p = 0.5979, two-sided unpaired t-test). g Passive avoidance setup with bright and dark compartments. Memory retention was measured by latency to enter the dark compartment 1 h and 24 h post-acquisition. Both Ctrl (n = 11) and cKO (n = 10) mice showed increased latency at 1 h (Ctrl: β = 52.27 s, p = 0.0015; cKO: β = 54.90 s, p = 0.0126) and 24 h (Ctrl: β = 27.09 s, p = 0.058; cKO: β = 22.10 s, p = 0.0040), with no genotype differences (Finteraction(2,38) = 0.08586, p = 0.9179, two-way ANOVA). Data are represented as mean ± SEM. Source data are provided as a Source Data file.
