Source:http://linkedlifedata.com/resource/pubmed/id/17944872
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rdf:type | |
lifeskim:mentions |
umls-concept:C0017890,
umls-concept:C0025914,
umls-concept:C0026809,
umls-concept:C0030685,
umls-concept:C0037925,
umls-concept:C0039067,
umls-concept:C0391871,
umls-concept:C0441712,
umls-concept:C0596902,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1420215,
umls-concept:C1522485,
umls-concept:C1708632,
umls-concept:C1963578
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pubmed:issue |
6
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pubmed:dateCreated |
2007-12-11
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pubmed:abstractText |
Glycine release has been rarely studied. The aim of this work was to characterize the release of the amino acid from spinal cord glycinergic nerve endings selectively pre-labeled through glycine transporters of the GLYT2 type. Purified mouse spinal cord synaptosomes were incubated with [(3)H]glycine in the presence of the GLYT1 blocker N-[(3R)-3-([1,1'-biphenyl]-4-yloxy)-3-(4-fluorophenyl)propyl]-N-methylglycine hydrochloride and exposed in superfusion to varying concentrations of KCl, 4-aminopyridine (4-AP), or veratridine. KCl (< or = 15 micromol/L), 4-AP (up to 1 mmol/L), and veratridine (< or = 0.3 micromol/L)-provoked [(3)H]glycine release by external Ca2+-dependent, botulinum toxin C(1)-sensitive, exocytosis. The overflows evoked by higher concentrations of K+ or veratridine involved external Ca2+-independent mechanisms of different nature. Only the overflow evoked by 3 or 10 micromol/L veratridine occurred totally (3 micromol/L) or in part (10 micromol/L) by transporter reversal, being sensitive to the GLYT2 blockers 4-benzyloxy-3,5-dimethoxy-N-[1-(dimethylaminociclopentyl)-methyl] benzamide or O-[(2-benzyloxyphenyl-3-flurophenyl)methyl]-l-serine; in contrast, the external Ca2+-independent [(3)H]glycine overflow provoked by 50 mmol/L K+ was transporter-independent. This component of K+-evoked overflow and the GLYT2-independent portion of the 10 micromol/L veratridine-evoked overflow, were largely sensitive to the vesicle depletor bafilomycin or BAPTA-AM and were prevented by blocking the mitochondrial Na+/Ca2+ exchanger with 7-chloro-5-(2-chlorophenyl)-1,5-dihydro-4,1-benzothiazepin-2(3H)-one, indicating the involvement of exocytosis triggered by intraterminal mitochondrial Ca2+ ions.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Glycine,
http://linkedlifedata.com/resource/pubmed/chemical/Glycine Plasma Membrane Transport...,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium,
http://linkedlifedata.com/resource/pubmed/chemical/Slc6a5 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Calcium Exchanger,
http://linkedlifedata.com/resource/pubmed/chemical/Tritium,
http://linkedlifedata.com/resource/pubmed/chemical/Veratridine
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1471-4159
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
103
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2439-48
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pubmed:meshHeading |
pubmed-meshheading:17944872-Animals,
pubmed-meshheading:17944872-Calcium,
pubmed-meshheading:17944872-Calcium Signaling,
pubmed-meshheading:17944872-Exocytosis,
pubmed-meshheading:17944872-Glycine,
pubmed-meshheading:17944872-Glycine Plasma Membrane Transport Proteins,
pubmed-meshheading:17944872-Mice,
pubmed-meshheading:17944872-Mitochondria,
pubmed-meshheading:17944872-Neural Inhibition,
pubmed-meshheading:17944872-Potassium,
pubmed-meshheading:17944872-Presynaptic Terminals,
pubmed-meshheading:17944872-Sodium-Calcium Exchanger,
pubmed-meshheading:17944872-Spinal Cord,
pubmed-meshheading:17944872-Synaptic Transmission,
pubmed-meshheading:17944872-Synaptosomes,
pubmed-meshheading:17944872-Tritium,
pubmed-meshheading:17944872-Veratridine
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pubmed:year |
2007
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pubmed:articleTitle |
Mechanisms of [(3)H]glycine release from mouse spinal cord synaptosomes selectively labeled through GLYT2 transporters.
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pubmed:affiliation |
Department of Experimental Medicine, Pharmacology and Toxicology Section, University of Genoa, Genoa, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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