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Cell. 2011 Mar 4;144(5):810-23. doi: 10.1016/j.cell.2011.02.018.

Astrocyte-neuron lactate transport is required for long-term memory formation.

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1
Department of Neuroscience, Mount Sinai School of Medicine, New York, New York 10029, USA.

Abstract

We report that, in the rat hippocampus, learning leads to a significant increase in extracellular lactate levels that derive from glycogen, an energy reserve selectively localized in astrocytes. Astrocytic glycogen breakdown and lactate release are essential for long-term but not short-term memory formation, and for the maintenance of long-term potentiation (LTP) of synaptic strength elicited in vivo. Disrupting the expression of the astrocytic lactate transporters monocarboxylate transporter 4 (MCT4) or MCT1 causes amnesia, which, like LTP impairment, is rescued by L-lactate but not equicaloric glucose. Disrupting the expression of the neuronal lactate transporter MCT2 also leads to amnesia that is unaffected by either L-lactate or glucose, suggesting that lactate import into neurons is necessary for long-term memory. Glycogenolysis and astrocytic lactate transporters are also critical for the induction of molecular changes required for memory formation, including the induction of phospho-CREB, Arc, and phospho-cofilin. We conclude that astrocyte-neuron lactate transport is required for long-term memory formation.

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PMID:
21376239
PMCID:
PMC3073831
DOI:
10.1016/j.cell.2011.02.018
[Indexed for MEDLINE]
Free PMC Article

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