Taurine Transporter Regulation in Hippocampal Neurons

Olson, James E.; Martinho, Eduardo

doi:10.1007/978-0-387-33504-9_34

Cited by 6 publications

(4 citation statements)

References 43 publications

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“…Our observation that hypotonicity reduces the V max for taurine uptake in SH‐SY5Y cells without an effect on the K m is in agreement with the results of a recent study of primary hippocampal neurons in which taurine uptake was also attenuated (by 48%) in response to a 30% reduction in osmolarity (Olson and Martinho 2006a). Although the mechanism underlying the reduction of TauT activity under basal hypoosmotic conditions remains to be determined, possibilities to be considered include the involvement of a tyrosine kinase (Olson and Martinho 2006b) and internalization of the transporter (Han et al. 2006).…”

Section: Discussionmentioning

confidence: 99%

Muscarinic receptor regulation of osmosensitive taurine transport in human SH‐SY5Y neuroblastoma cells

Foster

Vitvitsky

Banerjee

et al. 2008

Journal of Neurochemistry

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The ability of G-protein-coupled receptors to regulate osmosensitive uptake of the organic osmolyte, taurine, into human SH-SY5Y neuroblastoma cells has been examined. When monitored under isotonic conditions and in the presence of physiologically relevant taurine concentrations (1-100 µM), taurine influx was mediated exclusively by a Na + -dependent, highaffinity (K m =2.5 µM) saturable transport mechanism (V max =0.087 nmol/mg protein/min). Reductions in osmolarity of >20% (attained under conditions of a constant NaCl concentration) resulted in an inhibition of taurine influx (>30%) that could be attributed to a reduction in V max , whereas the K m for uptake remained unchanged. Inclusion of the muscarinic cholinergic agonist, oxotremorine-M (Oxo-M), also resulted in an attenuation of taurine influx (EC 50~0 .7 µM). Although Oxo-M-mediated inhibition of taurine uptake could be observed under isotonic conditions (~25-30%), the magnitude of inhibition was significantly enhanced by hypotonicity (~55-60%), a result that also reflected a reduction in the V max , but not the K m , for taurine transport. Oxo-M-mediated inhibition of taurine uptake was dependent upon the availability of extracellular Ca 2+ but was independent of protein kinase C activity. In addition to Oxo-M, inclusion of either thrombin or sphingosine 1-phosphate also attenuated volume-dependent taurine uptake. The ability of Oxo-M to inhibit the influx of taurine was attenuated by 4-[(2-butyl-6,7-dichloro-2-cyclopentyl-2,3-dihydro-1-oxo-1H-inden-5-yl)oxy]butanoic acid (DCPIB), an inhibitor of the volume-sensitive organic osmolyte and anion channel. DCPIB also prevented receptormediated changes in the efflux and influx of K + under hypoosmotic conditions. The results suggest that muscarinic receptor activation can regulate both the volume-dependent efflux and uptake of taurine and that these events may be functionally coupled.

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Section: Discussionmentioning

confidence: 99%

Muscarinic receptor regulation of osmosensitive taurine transport in human SH‐SY5Y neuroblastoma cells

Foster

Vitvitsky

Banerjee

et al. 2008

Journal of Neurochemistry

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“…Mechanisms responsible for reduced taurine transporter activity in osmotically swollen cultured neurons are not clear from these studies; however, preliminary data suggest tyrosine kinase activity is required (Olson and Martinho in press). For kidney cells, retina, and astrocytes, activation of PKC leads to decreased carrier‐mediated taurine accumulation (Loo et al .…”

Section: Discussionmentioning

confidence: 99%

“…Our data suggest neurons rapidly down‐regulate the taurine transporter when osmotically swollen. These data have been presented in preliminary form (Olson and Martinho 2003; Olson and Martinho in press).…”

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confidence: 99%

Regulation of taurine transport in rat hippocampal neurons by hypo‐osmotic swelling

Olson¹,

Martinho

2006

Journal of Neurochemistry

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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 K m of 30.0 ± 8.8 lM (mean ± SE) and J max 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 J max of the saturable transport pathway by approximately 48%, increases K diff 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.

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“…They show marked homology with each other and also with the transporters of established neurotransmitters (Smith et al, 1992;Uchida et al, 1992). The distribution of mRNA for the rat TAUT is more or less universal within the CNS and among different types of cells, both glial cells and neurons (Borden et al, 1995;Lake and Orlowski, 1996;Kang, 2000;Olson and Martinho, 2006), though the two different clones TAUT-1 and TAUT-2 are differently localized (Pow et al, 2002). TAUT-1 is detectable in the rat pituicytes, cerebellar Purkinje cells, and in photoreceptors and bipolar cells in the retina.…”

Section: Uptakementioning

confidence: 99%

Handbook of Neurochemistry and Molecular Neurobiology

2008

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Additionally, the whole set will be available upon completion under The electronic version of the whole set will be available under The print and electronic bundle of the whole set will be available under ISBN: 978-0-387-35478-1 ß 2008 Springer Science+Business Media, LLC.All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC., 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. springer.comPrinted on acid-free paper SPIN: 11416593 2109 -5 4 3 2 1 0 PrefaceThe brain is the organ that collects information from the environment, processes and stores the information, and generates behavior as and when needed. In essence, the brain makes us who we are. For this reason, understanding the biology of brain function is a great challenge and a major goal of modern science. The brain is one of the last great frontiers in science, and the unraveling of its mysteries is comparable in complexity to efforts in space exploration. Therefore, it was not a surprise that the U.S. Congress proclaimed the 1990s the ''Decade of the Brain,'' a movement also introduced by several other countries, thereby giving a chance for neuroscientists to focus on this topic and to have better conditions for their research.A fundamental goal of neuroscience is to understand how neurons generate behavior and the pathophysiology of different mental and neurological diseases. This requires, among other things, information about where these neurons are located, how they are connected, and how they communicate with each other in various physiological and pathophysiological conditions.At the end of the nineteenth century, the great neuroanatomist Santiago Ramon y Cajal recognized that neurons are the individual signaling elements of the brain. In this book, we focus on these nerve cells of the brain and the chemical molecules that allow them to talk to each other. The discovery of intercellular communication through endogenous molecules is a milestone in the history of science. It makes the brain a unique organ.Our aim is to describe recent discoveries about the basic operations of the brain and to provide an introduction to the adaptations for specific types of information processing. For example, at a chemical synapse, the presynaptic terminal liberates a transmitter substance that acts on the postsynaptic process. Thus, a synapse converts a presynaptic electrical signal into a chemical signal and back into a postsynaptic electrical signal.Cur...

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Taurine Transporter Regulation in Hippocampal Neurons

Cited by 6 publications

References 43 publications

Muscarinic receptor regulation of osmosensitive taurine transport in human SH‐SY5Y neuroblastoma cells

Muscarinic receptor regulation of osmosensitive taurine transport in human SH‐SY5Y neuroblastoma cells

Regulation of taurine transport in rat hippocampal neurons by hypo‐osmotic swelling

Handbook of Neurochemistry and Molecular Neurobiology

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