Abstract
Research over the last couple of decades has provided novel insights into lactate neurobiology and the implications of lactate transport-driven neuroenergetics in health and diseases of peripheral nerve and the brain. The expression pattern of lactate transporters in glia and neurons has now been described, though notable controversies and discrepancies remain. Importantly, down- and up-regulation experiments are underway to better understand the function of these transporters in different systems. Lactate transporters in peripheral nerves are important for maintenance of axon and myelin integrity, motor end-plate integrity, the development of diabetic peripheral neuropathy (DPN), and the functional recovery following nerve injuries. Similarly, brain energy metabolism and functions ranging from development to synaptic plasticity to axonal integrity are also dependent on lactate transport primarily between glia and neurons. This review is focused on critically analysing the expression pattern and the functions of lactate transporters in peripheral nerves and the brain and highlighting their role in glia-neuron metabolic crosstalk in physiological and pathological conditions.
Highlights
Though reported two centuries ago in exhausted animal muscle as a waste product, recent evidence and new lines of investigation have redefined the biology of lactate (L-lactate or lactic acid)
This study reported that Schwann cell-specific MCT1 is necessary for long-term maintenance of motor endplate integrity, which was not investigated in our Schwann cellspecific MCT1 null mice, while MCT4 appears largely dispensable for the support of motor neurons (Boucanova et al, 2020)
Consistent with an earlier study using sciatic nerve explants to demonstrate the dependence of axons on lactate for metabolic energy (Brown et al, 2012), we demonstrated that axons in an injured condition, following crush of the sciatic nerve, depend on MCT1 for transport of lactate as an energy substrate (Morrison et al, 2015)
Summary
Though reported two centuries ago in exhausted animal muscle as a waste product, recent evidence and new lines of investigation have redefined the biology of lactate (L-lactate or lactic acid). Lactic acid, which is hydrophilic and a weak acid, donates hydrogen ions (H+) and the resultant product, a hydroxy monocarboxylic acid anion, referred to as lactate, is the conjugate base of lactic acid. Pyruvate under both anaerobic and aerobic (Warburg effect; Warburg et al, 1927) conditions is metabolized by lactate dehydrogenase (LDH) to lactic acid. Lactic acid dissociates almost completely to lactate and H+. Growing evidence acknowledges lactate as an active metabolite capable of moving
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