Decreased metabolic response to visual stimulation in the superior colliculus of mice lacking the glial glutamate transporter GLT-1

During a specific task, an increase in glucose utilization anatomically restricted to the functionally activated region(s) is a landmark of brain physiology. While this response represents the biological bases for functional brain imaging, the underlying signalling pathway(s) are still not fully characterized. Recent evidence suggests that glial glutamate (re)uptake plays a key role. We provide evidence that the metabolic response to synaptic activation (i.e. enhancement of glucose uptake) is decreased in the superior colliculus during visual stimulation in young adult mice deficient in the glial glutamate transporter GLT-1. A similar reduction was not observed in the glial glutamate transporter GLAST-knockout mice. Consistent with our previous observation obtained in the somatosensory cortex, our data suggest that a metabolic crosstalk takes place between neurons and astrocytes in the adult brain which would be regulated by synaptic activity and mediated by GLT-1.