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J Physiol Volume 586, Number 5, 1337-1349, March 1, 2008 DOI: 10.1113/jphysiol.2007.144154
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NEUROSCIENCE

Glutamate receptor-dependent increments in lactate, glucose and oxygen metabolism evoked in rat cerebellum in vivo

 Kirsten Caesar1, Parastoo Hashemi2, Aicha Douhou3, Gilles Bonvento3, Martyn G. Boutelle2, Anne B. Walls4 and Martin Lauritzen1,5

1 Department of Neuroscience and Pharmacology
4 Department of Pharmaceutical Sciences, University of Copenhagen, Copenhagen, Denmark
2 Department of Bioengineering, Imperial College London, London, UK
3 Commissariat à l'Energie Atomique, Direction des Sciences du Vivant, Institut d'Imagerie Biomédicale, Centre National de la Recherche Scientifique, Unité de Recherche Associée 2210, Orsay, France
5 Department of Clinical Neurophysiology, Glostrup Hospital, 2600 Glostrup, Denmark

Neuronal activity is tightly coupled with brain energy metabolism. Numerous studies have suggested that lactate is equally important as an energy substrate for neurons as glucose. Lactate production is reportedly triggered by glutamate uptake, and independent of glutamate receptor activation. Here we show that climbing fibre stimulation of cerebellar Purkinje cells increased extracellular lactate by 30% within 30 s of stimulation, but not for briefer stimulation periods. To explore whether lactate production was controlled by pre- or postsynaptic events we silenced AMPA receptors with CNQX. This blocked all evoked rises in postsynaptic activity, blood flow, and glucose and oxygen consumption. CNQX also abolished rises in lactate concomitantly with marked reduction in postsynaptic currents. Rises in lactate were unaffected by inhibition of glycogen phosphorylase, suggesting that lactate production was independent of glycogen breakdown. Stimulated lactate production in cerebellum is derived directly from glucose uptake, and coupled to neuronal activity via AMPA receptor activation.

(Received 30 August 2007; accepted after revision 7 January 2008; first published online 10 January 2008)
Corresponding author M. Lauritzen: Department of Clinical Neurophysiology, Glostrup Hospital, Nordre Ringvej, DK-2600 Glostrup, Denmark. Email: marl{at}glo.regionh.dk

K. Caesar and P. Hashemi contributed equally to this work.


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