Document Detail

Regulation of taurine transport in rat hippocampal neurons by hypo-osmotic swelling.
MedLine Citation:
PMID:  16478528     Owner:  NLM     Status:  MEDLINE    
Taurine, an important mediator of cellular volume regulation in the central nervous system, is accumulated into neurons and glia by means of a highly specific sodium-dependent membrane transporter. During hyperosmotic cell shrinkage, net cellular taurine content increases as taurine transporter activity is enhanced via elevated gene expression of the transporter protein. In hypo-osmotic conditions, taurine is rapidly lost from cells by means of taurine-conducting membrane channels. We reasoned that changes in taurine transporter activity also might accompany cell swelling to minimize re-accumulation of taurine from the extracellular space. Thus, we determined the kinetic and pharmacological characteristics of neuronal taurine transport and the response to osmotic swelling. Accumulation of radioactive taurine is strongly temperature dependent and occurs via saturable and non-saturable pathways. At concentrations of taurine expected in extracellular fluid in vivo, 98% of taurine accumulation would occur via the saturable pathway. This pathway obeys Michaelis-Menten kinetics with a Km of 30.0 +/- 8.8 microm (mean +/- SE) and Jmax of 2.1 +/- 0.2 nmol/mg protein min. The saturable pathway is dependent on extracellular sodium with an effective binding constant of 80.0 +/- 3.1 mm and a Hill coefficient of 2.1 +/- 0.1. This pathway is inhibited by structural analogues of taurine and by the anion channel inhibitors, 4,4'-diisothiocyanostilbene-2, 2'-disulfonic acid (DIDS) and 5-nitro-2-(3 phenylpropylamino) benzoic acid (NPPB). NPPB, but not DIDS, also reduces the ATP content of the cell cultures. Osmotic swelling at constant extracellular sodium concentration reduces the Jmax of the saturable transport pathway by approximately 48%, increases Kdiff for the non-saturable pathway by 77%, but has no effect on cellular ATP content. These changes in taurine transport occurring in swollen neurons in vivo would contribute to net reduction of taurine content and resulting volume regulation.
James E Olson; Eduardo Martinho
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of neurochemistry     Volume:  96     ISSN:  0022-3042     ISO Abbreviation:  J. Neurochem.     Publication Date:  2006 Mar 
Date Detail:
Created Date:  2006-02-15     Completed Date:  2006-05-11     Revised Date:  2013-06-07    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  England    
Other Details:
Languages:  eng     Pagination:  1375-89     Citation Subset:  IM    
Department of Emergency Medicine, Wright State University School of Medicine, Cox Institute, Kettering, Ohio 45429, USA.
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MeSH Terms
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / pharmacology
Adenosine Triphosphate / metabolism
Cells, Cultured
Dose-Response Relationship, Drug
Embryo, Mammalian
Glial Fibrillary Acidic Protein / metabolism
Hippocampus / cytology*
Immunohistochemistry / methods
Intracellular Fluid / metabolism*
Neurons / metabolism*
Osmolar Concentration
Penicillamine / analogs & derivatives,  metabolism
Phosphopyruvate Hydratase / metabolism
Protein Transport / physiology
Sodium / pharmacokinetics
Taurine / metabolism*
Time Factors
Grant Support
Reg. No./Substance:
0/Glial Fibrillary Acidic Protein; 0/S-nitro-N-acetylpenicillamine; 107-35-7/Taurine; 52-67-5/Penicillamine; 53005-05-3/4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; 56-65-5/Adenosine Triphosphate; 7440-23-5/Sodium; EC Hydratase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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