Abstract
Neuron-glia interactions are essential for synaptic function, and glial glutamate (re)uptake plays a key role at glutamatergic synapses. In knockout mice, for either glial glutamate transporters, GLAST or GLT-1, a classical metabolic response to synaptic activation (i.e., enhancement of glucose utilization) is decreased at an early functional stage in the somatosensory barrel cortex following activation of whiskers. Investigation in vitro demonstrates that glial glutamate transport represents a critical step for triggering enhanced glucose utilization, but also lactate release from astrocytes through a mechanism involving changes in intracellular Na(+) concentration. These data suggest that a metabolic crosstalk takes place between neurons and astrocytes in the developing cortex, which would be regulated by synaptic activity and mediated by glial glutamate transporters.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Amino Acid Transport System X-AG / genetics
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Amino Acid Transport System X-AG / metabolism
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Amino Acid Transport System X-AG / physiology*
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Animals
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Animals, Newborn
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Aspartic Acid / metabolism
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Astrocytes / physiology*
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Blotting, Western
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Cells, Cultured
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Cerebral Cortex / growth & development*
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Cerebral Cortex / physiology*
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Deoxyglucose / metabolism
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Efferent Pathways / physiology
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Excitatory Amino Acid Transporter 2 / genetics
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Excitatory Amino Acid Transporter 2 / metabolism
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Glycolysis / physiology
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Immunohistochemistry
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Lactic Acid / metabolism
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Neuroglia / physiology*
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Neurons / physiology*
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Physical Stimulation
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Receptor Cross-Talk / physiology*
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Somatosensory Cortex / physiology
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Synapses / physiology
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Vibrissae / innervation
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Vibrissae / physiology
Substances
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Amino Acid Transport System X-AG
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Excitatory Amino Acid Transporter 2
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Aspartic Acid
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Lactic Acid
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Deoxyglucose