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Direct neuronal glucose uptake heralds activity-dependent increases in cerebral metabolism

Lundgaard, Iben LU ; Li, Baoman ; Xie, Lulu ; Kang, Hongyi ; Sanggaard, Simon ; Haswell, John D.R. ; Sun, Wei ; Goldman, Siri ; Blekot, Solomiya and Nielsen, Michael LU , et al. (2015) In Nature Communications 6.
Abstract

Metabolically, the brain is a highly active organ that relies almost exclusively on glucose as its energy source. According to the astrocyte-to-neuron lactate shuttle hypothesis, glucose is taken up by astrocytes and converted to lactate, which is then oxidized by neurons. Here we show, using two-photon imaging of a near-infrared 2-deoxyglucose analogue (2DG-IR), that glucose is taken up preferentially by neurons in awake behaving mice. Anaesthesia suppressed neuronal 2DG-IR uptake and sensory stimulation was associated with a sharp increase in neuronal, but not astrocytic, 2DG-IR uptake. Moreover, hexokinase, which catalyses the first enzymatic steps in glycolysis, was highly enriched in neurons compared with astrocytes, in mouse as... (More)

Metabolically, the brain is a highly active organ that relies almost exclusively on glucose as its energy source. According to the astrocyte-to-neuron lactate shuttle hypothesis, glucose is taken up by astrocytes and converted to lactate, which is then oxidized by neurons. Here we show, using two-photon imaging of a near-infrared 2-deoxyglucose analogue (2DG-IR), that glucose is taken up preferentially by neurons in awake behaving mice. Anaesthesia suppressed neuronal 2DG-IR uptake and sensory stimulation was associated with a sharp increase in neuronal, but not astrocytic, 2DG-IR uptake. Moreover, hexokinase, which catalyses the first enzymatic steps in glycolysis, was highly enriched in neurons compared with astrocytes, in mouse as well as in human cortex. These observations suggest that brain activity and neuronal glucose metabolism are directly linked, and identiy the neuron as the principal locus of glucose uptake as visualized by functional brain imaging.

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publishing date
type
Contribution to journal
publication status
published
subject
in
Nature Communications
volume
6
article number
6807
publisher
Nature Publishing Group
external identifiers
  • pmid:25904018
  • scopus:84928526146
ISSN
2041-1723
DOI
10.1038/ncomms7807
language
English
LU publication?
no
id
8a69fa20-453e-4a4d-bdf9-51ecbfdabd8c
date added to LUP
2019-05-16 16:44:46
date last changed
2024-03-19 08:09:56
@article{8a69fa20-453e-4a4d-bdf9-51ecbfdabd8c,
  abstract     = {{<p>Metabolically, the brain is a highly active organ that relies almost exclusively on glucose as its energy source. According to the astrocyte-to-neuron lactate shuttle hypothesis, glucose is taken up by astrocytes and converted to lactate, which is then oxidized by neurons. Here we show, using two-photon imaging of a near-infrared 2-deoxyglucose analogue (2DG-IR), that glucose is taken up preferentially by neurons in awake behaving mice. Anaesthesia suppressed neuronal 2DG-IR uptake and sensory stimulation was associated with a sharp increase in neuronal, but not astrocytic, 2DG-IR uptake. Moreover, hexokinase, which catalyses the first enzymatic steps in glycolysis, was highly enriched in neurons compared with astrocytes, in mouse as well as in human cortex. These observations suggest that brain activity and neuronal glucose metabolism are directly linked, and identiy the neuron as the principal locus of glucose uptake as visualized by functional brain imaging.</p>}},
  author       = {{Lundgaard, Iben and Li, Baoman and Xie, Lulu and Kang, Hongyi and Sanggaard, Simon and Haswell, John D.R. and Sun, Wei and Goldman, Siri and Blekot, Solomiya and Nielsen, Michael and Takano, Takahiro and Deane, Rashid and Nedergaard, Maiken}},
  issn         = {{2041-1723}},
  language     = {{eng}},
  month        = {{04}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Nature Communications}},
  title        = {{Direct neuronal glucose uptake heralds activity-dependent increases in cerebral metabolism}},
  url          = {{http://dx.doi.org/10.1038/ncomms7807}},
  doi          = {{10.1038/ncomms7807}},
  volume       = {{6}},
  year         = {{2015}},
}