Control of cleft glutamate concentration and glutamate spill-out by perisynaptic glia: uptake and diffusion barriers.

Most glutamatergic synapses in the mammalian central nervous system are covered by thin astroglial processes that exert a dual action on synaptically released glutamate: they form physical barriers that oppose diffusion and they carry specific transporters that remove glutamate from the extracellula...

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Autor principal:	Jean-Pierre Kessler
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/23db57c3437f459c988a7baaccb946b7
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spelling	oai:doaj.org-article:23db57c3437f459c988a7baaccb946b72021-11-18T09:00:16ZControl of cleft glutamate concentration and glutamate spill-out by perisynaptic glia: uptake and diffusion barriers.1932-620310.1371/journal.pone.0070791https://doaj.org/article/23db57c3437f459c988a7baaccb946b72013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23951010/?tool=EBIhttps://doaj.org/toc/1932-6203Most glutamatergic synapses in the mammalian central nervous system are covered by thin astroglial processes that exert a dual action on synaptically released glutamate: they form physical barriers that oppose diffusion and they carry specific transporters that remove glutamate from the extracellular space. The present study was undertaken to investigate the dual action of glia by means of computer simulation. A realistic synapse model based on electron microscope data and Monte Carlo algorithms were used for this purpose. Results show (1) that physical obstacles formed by glial processes delay glutamate exit from the cleft and (2) that this effect is efficiently counteracted by glutamate uptake. Thus, depending on transporter densities, the presence of perisynaptic glia may result in increased or decreased glutamate transient in the synaptic cleft. Changes in temporal profiles of cleft glutamate concentration induced by glia differentially impact the response of the various synaptic and perisynaptic receptor subtypes. In particular, GluN2B- and GluN2C-NMDA receptor responses are strongly modified while GluN2A-NMDA receptor responses are almost unaffected. Thus, variations in glial transporter expression may allow differential tuning of NMDA receptors according to their subunit composition. In addition, simulation data suggest that the sink effect generated by transporters accumulation in the vicinity of the release site is the main mechanism limiting glutamate spill-out. Physical obstacles formed by glial processes play a comparatively minor role.Jean-Pierre KesslerPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 8, p e70791 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jean-Pierre Kessler Control of cleft glutamate concentration and glutamate spill-out by perisynaptic glia: uptake and diffusion barriers.
description	Most glutamatergic synapses in the mammalian central nervous system are covered by thin astroglial processes that exert a dual action on synaptically released glutamate: they form physical barriers that oppose diffusion and they carry specific transporters that remove glutamate from the extracellular space. The present study was undertaken to investigate the dual action of glia by means of computer simulation. A realistic synapse model based on electron microscope data and Monte Carlo algorithms were used for this purpose. Results show (1) that physical obstacles formed by glial processes delay glutamate exit from the cleft and (2) that this effect is efficiently counteracted by glutamate uptake. Thus, depending on transporter densities, the presence of perisynaptic glia may result in increased or decreased glutamate transient in the synaptic cleft. Changes in temporal profiles of cleft glutamate concentration induced by glia differentially impact the response of the various synaptic and perisynaptic receptor subtypes. In particular, GluN2B- and GluN2C-NMDA receptor responses are strongly modified while GluN2A-NMDA receptor responses are almost unaffected. Thus, variations in glial transporter expression may allow differential tuning of NMDA receptors according to their subunit composition. In addition, simulation data suggest that the sink effect generated by transporters accumulation in the vicinity of the release site is the main mechanism limiting glutamate spill-out. Physical obstacles formed by glial processes play a comparatively minor role.
format	article
author	Jean-Pierre Kessler
author_facet	Jean-Pierre Kessler
author_sort	Jean-Pierre Kessler
title	Control of cleft glutamate concentration and glutamate spill-out by perisynaptic glia: uptake and diffusion barriers.
title_short	Control of cleft glutamate concentration and glutamate spill-out by perisynaptic glia: uptake and diffusion barriers.
title_full	Control of cleft glutamate concentration and glutamate spill-out by perisynaptic glia: uptake and diffusion barriers.
title_fullStr	Control of cleft glutamate concentration and glutamate spill-out by perisynaptic glia: uptake and diffusion barriers.
title_full_unstemmed	Control of cleft glutamate concentration and glutamate spill-out by perisynaptic glia: uptake and diffusion barriers.
title_sort	control of cleft glutamate concentration and glutamate spill-out by perisynaptic glia: uptake and diffusion barriers.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/23db57c3437f459c988a7baaccb946b7
work_keys_str_mv	AT jeanpierrekessler controlofcleftglutamateconcentrationandglutamatespilloutbyperisynapticgliauptakeanddiffusionbarriers
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Control of cleft glutamate concentration and glutamate spill-out by perisynaptic glia: uptake and diffusion barriers.

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