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Commun Biol. 2019 Jul 2;2:247. doi: 10.1038/s42003-019-0495-2. eCollection 2019.

Lactate from astrocytes fuels learning-induced mRNA translation in excitatory and inhibitory neurons.

Author information

1
1Center for Neural Science, New York University, New York, NY 10003 USA.
2
2Present Address: Department of Biochemistry, Faculty of Medicine, Graduate School of Medicine & Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama, 930-0194 Japan.

Abstract

Glycogenolysis and lactate transport from astrocytes to neurons is required for long-term memory formation, but the role of this lactate is poorly understood. Here we show that the Krebs cycle substrates pyruvate and ketone body B3HB can functionally replace lactate in rescuing memory impairment caused by inhibition of glycogenolysis or expression knockdown of glia monocarboxylate transporters (MCTs) 1 and 4 in the dorsal hippocampus of rats. In contrast, either metabolite is unable to rescue memory impairment produced by expression knockdown of MCT2, which is selectively expressed by neurons, indicating that a critical role of astrocytic lactate is to provide energy for neuronal responses required for long-term memory. These responses include learning-induced mRNA translation in both excitatory and inhibitory neurons, as well as expression of Arc/Arg3.1. Thus, astrocytic lactate acts as an energy substrate to fuel learning-induced de novo neuronal translation critical for long-term memory.

KEYWORDS:

Astrocyte; Consolidation; Learning and memory; Neuroscience

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