Whereas energy function in the aging brain and their related neurodegenerative diseases has been explored in some detail, there is limited knowledge about molecular mechanisms and brain networks of energy metabolism during infancy and childhood. In this review we describe current insights on physiological brain energetics at prenatal and neonatal stages, and in childhood. We then describe the main groups of inborn errors of energy metabolism affecting the brain. Of note, scarce basic neuroscience research in this field limits the opportunity for these disorders to provide paradigms of energy utilization during neurodevelopment. Finally, we report energy metabolism disturbances in well-known non-metabolic neurodevelopmental disorders. As energy metabolism is a fundamental biological function, brain energy utilization is likely altered in most neuropediatric diseases. Precise knowledge on mechanisms of brain energy disturbance will open the possibility of metabolic modulation therapies regardless of disease etiology.
The transport of lactate and pyruvate between glial cells and neurons plays an important role in the nervous system metabolic coupling. However, the mechanisms and characteristics that underlie the transport of monocarboxylates (MC-T) in vivo are poorly described. Here we use Drosophila expressing genetically-encoded FRET sensors to provide an ex vivo characterization of the MC-T in motor neurons and glial cells from the ventral nerve cord. We show that lactate/pyruvate transport on glial cells is coupled to protons and is more efficient than in neurons. Glial cells maintain higher levels of intracellular lactate generating a positive gradient towards neurons. Moreover, our results show that under increased activity lactate and pyruvate rise on motor neurons and suggest that this depends on the transfer of lactate from glial cells mediated in part by the previously described MC transporter Chaski, giving support to the in vivo glia to neurons lactate shuttling during activity.
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