Astrocytic GABA transporter activity modulates excitatory neurotransmission

Kim Boddum, Thomas P. Jensen, Vincent Magloire, Uffe Kristiansen, Dmitri A. Rusakov (), Ivan Pavlov () and Matthew C. Walker ()
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Kim Boddum: UCL Institute of Neurology, University College London, Queen Square
Thomas P. Jensen: UCL Institute of Neurology, University College London, Queen Square
Vincent Magloire: UCL Institute of Neurology, University College London, Queen Square
Uffe Kristiansen: Faculty of Health and Medical Sciences, University of Copenhagen, Universitetsparken 2
Dmitri A. Rusakov: UCL Institute of Neurology, University College London, Queen Square
Ivan Pavlov: UCL Institute of Neurology, University College London, Queen Square
Matthew C. Walker: UCL Institute of Neurology, University College London, Queen Square

Nature Communications, 2016, vol. 7, issue 1, 1-10

Abstract: Abstract Astrocytes are ideally placed to detect and respond to network activity. They express ionotropic and metabotropic receptors, and can release gliotransmitters. Astrocytes also express transporters that regulate the extracellular concentration of neurotransmitters. Here we report a previously unrecognized role for the astrocytic GABA transporter, GAT-3. GAT-3 activity results in a rise in astrocytic Na+ concentrations and a consequent increase in astrocytic Ca2+ through Na+/Ca2+ exchange. This leads to the release of ATP/adenosine by astrocytes, which then diffusely inhibits neuronal glutamate release via activation of presynaptic adenosine receptors. Through this mechanism, increases in astrocytic GAT-3 activity due to GABA released from interneurons contribute to 'diffuse' heterosynaptic depression. This provides a mechanism for homeostatic regulation of excitatory transmission in the hippocampus.

Date: 2016
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DOI: 10.1038/ncomms13572

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