The brain is the most energy-demanding organ of our body in proportion to its size. Within it, neurons are the prime energy consumers, but they are not alone in the brain. While the classical view of brain energetics pointed at blood-borne glucose as the main source for neuronal energy metabolism, it is now admitted that lactate is also playing a key role. The Astrocyte-Neuron Lactate Shuttle (ANLS) in which astrocytes take up glucose from the blood, store it as glycogen, and/or convert and release it under the form of lactate, is a parallel energy source. Whether neurons preferentially use glucose or lactate as an energy source according to their activity remains an open debate. To tackle this issue, we took advantage of a viral approach to downregulate either glucose transporters on neurons (i.e. GLUT3) or lactate transporters on neurons (i.e. MCT2) or astrocytes (i.e. MCT4) in layer IV of the somatosensory cortex of adult rats. Four weeks later, we performed neuron patch-clamp electrophysiological recordings in whole cell configuration in acute brain slices to investigate the impact of downregulating each transporter on miniature excitatory synaptic currents. Downregulating MCT4, potentially involved in activity-dependent release of lactate but not in basal release, had no impact neither on the frequency, nor amplitude of miniature excitatory currents. Surprisingly, the downregulation of neuronal GLUT3 also had no impact on miniature activity. Whether impairing directly the neuronal uptake of lactate through MCT2 would affect miniature activity is an open question we are investigating now.