title: Contribution of astrocytic glutamate and GABA uptake to corticostriatal information processing.
abstract: The astrocytes, active elements of the tripartite synapse, remove most of the neurotransmitter that spills over the synaptic cleft. Neurotransmitter uptake operated by astrocytes contributes to the strength and timing of synaptic inputs. The striatum, the main input nucleus of basal ganglia, extracts pertinent cortical signals from the background noise and relays cortical information toward basal ganglia output structures. We investigated the role of striatal astrocytic uptake in the shaping of corticostriatal transmission.We performed dual patch-clamp recordings of striatal output neuron (the medium-sized spiny neurons, MSNs)–astrocyte pairs while stimulating the somatosensory cortex. Cortical activity evoked robust synaptically activated transporter-mediated currents (STCs) in 78% of the recorded astrocytes. STCs originated equally from the activities of glutamate transporters and GABA transporters (GATs). Astrocytic STCs reflected here a presynaptic release of neurotransmitters. STCs displayed a large magnitude associated with fast kinetics, denoting an efficient neurotransmitter clearance at the corticostriatal pathway. Inhibition of glutamate transporters type-1 (GLT-1) and GATs decreased the corticostriatal synaptic transmission, through, respectively, desensitization of AMPA receptors and activation of GABAA receptor. STCs displayed a bidirectional short-term plasticity (facilitation for paired-pulse intervals less than 100 ms and depression up to 1 s).We report a genuine facilitation of STCs for high-frequency cortical activity, which could strengthen the detection properties of cortical activity operated by MSNs. MSN EPSCs showed a triphasic short-term plasticity, which was modified by the blockade of GLT-1 or GATs. We show here that neurotransmitter uptake by astrocytes plays a key role in the corticostriatal information processing.
authors.affiliation: Dynamic and Pathophysiology of Neuronal Networks, INSERM U667, College de France, 75005 Paris, France.
authors.forename: Valérie
authors.initials: V
authors.lastname: Goubard
authors.forename: Elodie
authors.initials: E
authors.lastname: Fino
authors.forename: Laurent
authors.initials: L
authors.lastname: Venance
mesh_terms: D000200:Action Potentials; D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism*; D001479:Basal Ganglia / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D004558:Electric Stimulation; D027342:Excitatory Amino Acid Transporter 2 / Q000037:antagonists & inhibitors / Q000378:metabolism*; D019706:Excitatory Postsynaptic Potentials; D050485:GABA Plasma Membrane Transport Proteins / Q000187:drug effects / Q000378:metabolism*; D018698:Glutamic Acid / Q000378:metabolism*; D007700:Kinetics; D009434:Neural Pathways / Q000378:metabolism; D009473:Neuronal Plasticity; D018377:Neurotransmitter Agents / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D017729:Presynaptic Terminals / Q000378:metabolism; D051381:Rats; D011930:Reaction Time; D013003:Somatosensory Cortex / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D027342:Excitatory Amino Acid Transporter 2; D050485:GABA Plasma Membrane Transport Proteins; D018377:Neurotransmitter Agents; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid