Figure 4.

Glucose but not lactate supports neurotransmitter homeostasis. The ability of cultured (glutamatergic) cerebellar neurons to perform re-uptake of release D-[³H]aspartate (pre-loaded marker of glutamate release) during superfusion is diminished in the presence of lactate as compared to the presence of glucose (data from Bak et al., 2006). This is evidenced by an increase in the apparent pulsatile NMDA-induced release of D-[³H]aspartate in the presence of lactate; however, since this increase was abolished by the additional presence of the glutamate transport blocker TBOA, it most likely reflects a diminished ability to take up a fraction of the released D-[³H]aspartate. Experimentally, cultured cerebellar neurons were superfused and the depolarization-coupled release of preloaded D-[³H]aspartate evoked by 30 s pulses of NMDA (300 μ M) plus potassium (15 mM) was quantified (see Bak et al., 2006 for details). The effect of TBOA (100 μ M) on the release in the presence of glucose (2.5 mM, black and open bars) or lactate (1 mM, hatched and gray bars) was investigated. The release in the presence of glucose alone was used as a reference and normalized to 100 (black bar). The results are averages ± SD. Statistically significant differences were calculated using One-Way ANOVA followed by a Tukey–Kramer post hoc test. ^*Significantly different from the other three conditions (P < 0.01).