Research Paper Volume 13, Issue 14 pp 18033—18050

β-amyloid monomers drive up neuronal aerobic glycolysis in response to energy stressors


Figure 3. Inhibition of Aβ release or blockade of IGF-IRs prevent kainate-stimulated lactate release. Following 2 hours of glucose deprivation, 3 mM glucose was added to neuronal cultures. A treatment with kainate (KA, 100 μM) stimulated glucose uptake after 10 min (A) and lactate release after 40 min (B). Glucose consumption was measured as glucose (mg/dl) remaining in the incubation buffer 10 minutes following re-addition. With respect to the initial 3 mM glucose concentration, no glucose uptake occurred within 10 min unless KA was added. The IGF-IR antagonist, PPP (500 nM), and γ-secretase inhibitor IX (γ-Sec Inh, 100 nM) prevented kainate-stimulated lactate release at 40 min (B). Bars represent the means ± SEM of 4 determinations. In (A) p < 0.001 vs. *control (CTRL) or **KA alone. In (B) p < 0.001 vs. *CTRL or #KA alone; one-way ANOVA with post hoc Fisher LSD multiple comparison method.