| pubmed-article:15951392 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15951392 | lifeskim:mentions | umls-concept:C0005528 | lld:lifeskim |
| pubmed-article:15951392 | lifeskim:mentions | umls-concept:C0061609 | lld:lifeskim |
| pubmed-article:15951392 | lifeskim:mentions | umls-concept:C0439780 | lld:lifeskim |
| pubmed-article:15951392 | lifeskim:mentions | umls-concept:C1832873 | lld:lifeskim |
| pubmed-article:15951392 | lifeskim:mentions | umls-concept:C1555029 | lld:lifeskim |
| pubmed-article:15951392 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:15951392 | pubmed:dateCreated | 2005-8-29 | lld:pubmed |
| pubmed-article:15951392 | pubmed:abstractText | Glycine is a coagonist at the N-methyl-D-aspartate receptor. Changes in extracellular glycine concentration may modulate N-methyl-D-aspartate receptor function and excitatory synaptic transmission. The GLYT1 glycine transporter is present in glia surrounding excitatory synapses, and plays a key role in regulating extracellular glycine concentration. We investigated the kinetic and other biophysical properties of GLYT1b, stably expressed in CHO cells, using whole-cell patch-clamp techniques. Application of glycine produced an inward current, which decayed within a few seconds to a steady-state level. When glycine was removed, a transient outward current was observed, consistent with reverse transport of accumulated glycine. The outward current was enhanced by elevating intracellular or lowering extracellular [Na(+)], and was modulated by changes in extracellular [glycine] and time of glycine application. We developed a model of GLYT1b function, which accurately describes the time course of the transporter current under a range of experimental conditions. The model predicts that glial uptake of glycine will decay toward zero during a sustained period of elevated glycine concentration. This property of GLYT1b may permit spillover from glycinergic terminals to nearby excitatory terminals during a prolonged burst of inhibitory activity, and reverse transport may extend the period of elevated glycine concentration beyond the end of the inhibitory burst. | lld:pubmed |
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| pubmed-article:15951392 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15951392 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15951392 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:15951392 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15951392 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:15951392 | pubmed:issn | 0006-3495 | lld:pubmed |
| pubmed-article:15951392 | pubmed:author | pubmed-author:ClementsJohn... | lld:pubmed |
| pubmed-article:15951392 | pubmed:author | pubmed-author:VandenbergRob... | lld:pubmed |
| pubmed-article:15951392 | pubmed:author | pubmed-author:AubreyKarin... | lld:pubmed |
| pubmed-article:15951392 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15951392 | pubmed:volume | 89 | lld:pubmed |
| pubmed-article:15951392 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15951392 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15951392 | pubmed:pagination | 1657-68 | lld:pubmed |
| pubmed-article:15951392 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:15951392 | pubmed:meshHeading | pubmed-meshheading:15951392... | lld:pubmed |
| pubmed-article:15951392 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:15951392 | pubmed:articleTitle | Dynamics of forward and reverse transport by the glial glycine transporter, glyt1b. | lld:pubmed |
| pubmed-article:15951392 | pubmed:affiliation | Department of Pharmacology, Institute for Biomedical Research, University of Sydney, NSW 2006, Australia. aubrey@biologie.ens.fr | lld:pubmed |
