Figure 2.

Activity-dependent glucose trafficking through astroglial networks sustain normal and pathological neuronal activity. (A) Sample pictures showing that the fluorescent glucose derivative 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxyglucose (2-NBDG, green) trafficking in astrocytes is decreased when neuronal activity is inhibited with tetrodotoxin (TTX) (B) and increased during epileptiform activity (in 0 Mg²⁺-picrotoxin) (C) as compared with control conditions (A). Scale bar, 50 μm. Insets, corresponding spontaneous activity of hippocampal CA1 pyramidal cells recorded in current clamp in control, TTX (0.5 μm, 1–4 h), and 0 Mg²⁺-picrotoxin (100 μm, 1–4 h) conditions. Scale bar, 20 mV, 9 s. (D,E) Glucose supply through astrocytic networks sustains basal synaptic transmission and epileptiform activity during exogenous glucose deprivation (EGD). Sample traces of extracellular field potentials recorded in hippocampal slices showing that intracellular glucose (20 mM) delivery to astrocytic networks (+Glucose astrocytes) through the patch pipette inhibits the depression of fEPSP amplitude (D) and epileptiform activity (E) induced by exogenous glucose deprivation (0 glucose, 30 min) in wild-type mice. Scale bars (D) 0.2 mV, 5 ms and (E) 0.3 mV, 20 s. Adapted, with permission, from Rouach et al. (2008) (A–E).