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Astroglial glutamate transporters in the brain: Regulating neurotransmitter homeostasis and synaptic transmission
Author(s) -
MurphyRoyal Ciaran,
Dupuis Julien,
Groc Laurent,
Oliet Stéphane H. R.
Publication year - 2017
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.24029
Subject(s) - glutamate receptor , neurotransmission , neuroscience , glutamatergic , excitotoxicity , neurotransmitter , biology , synaptic cleft , neurotransmitter receptor , metabotropic glutamate receptor , astrocyte , neurotransmitter agents , central nervous system , receptor , biochemistry
Astrocytes, the major glial cell type in the central nervous system (CNS), are critical for brain function and have been implicated in various disorders of the central nervous system. These cells are involved in a wide range of cerebral processes including brain metabolism, control of central blood flow, ionic homeostasis, fine‐tuning synaptic transmission, and neurotransmitter clearance. Such varied roles can be efficiently carried out due to the intimate interactions astrocytes maintain with neurons, the vasculature, as well as with other glial cells. Arguably, one of the most important functions of astrocytes in the brain is their control of neurotransmitter clearance. This is particularly true for glutamate whose timecourse in the synaptic cleft needs to be controlled tightly under physiological conditions to maintain point‐to‐point excitatory transmission, thereby limiting spillover and activation of more receptors. Most importantly, accumulation of glutamate in the extracellular space can trigger excessive activation of glutamatergic receptors and lead to excitotoxicity, a trademark of many neurodegenerative diseases. It is thus of utmost importance for both physiological and pathophysiological reasons to understand the processes that control glutamate time course within the synaptic cleft and regulate its concentrations in the extracellular space. © 2017 Wiley Periodicals, Inc.