A new pathway for lactate production in the CNS

摘要

Lactate has long been considered to be a potentially damaging final metabolite of anaerobic glycolysis and has received little interest by neuroscientists. Interest in lactate began to increase with the demonstration of non-oxidative glucose consumption (i.e. glycolysis) in the activated brain by a landmark PET study (Fox et al. 1988). Numerous studies have since measured lactate with the consensus that sustained focal neural activity in the CNS is inevitably accompanied by an increase in extracellular lactate (Prichard et al. 1988; Mangia etal. 2007). In this context, Pellerin & Magistretti (1994) proposed that lactate may not be a metabolic dead-end product but rather the dominant oxidative substrate for neurons. The formulation of theastrocyte-neuron lactate shuttle hypothesis has generated tremendous interest in the cellular source and fate of lactate, to the point that 'lactate, has become a contentious term and is frequently associated with academic disputes. In this issue of The Journal of Physiology, Caesar et al. (2008) open a new perspective on the generation of extracellular lactate. As is often the case, this intriguing study advances the field but also raises more questions than it answers.