Unbound MEDLINE

Glutamate receptors modulate sodium-dependent and calcium-independent vitamin C bidirectional transport in cultured avian retinal cells. Journal of neurochemistry [J Neurochem] Journal article

 
TitleGlutamate receptors modulate sodium-dependent and calcium-independent vitamin C bidirectional transport in cultured avian retinal cells.
Author(s)Portugal CC, Miya VS, da Costa Calaza K, Santos RA, Paes-de-Carvalho R 
InstitutionDepartment of Neurobiology and Program of Neurosciences, Institute of Biology, Fluminense Federal University, Niterói, RJ 24001-970, Brazil.
SourceJ Neurochem 2008 Nov 17.
AbstractVitamin C is transported in the brain by sodium vitamin C co-transporters (SVCT-2) for ascorbate and glucose transporters for dehydroascorbate (DHA). Here we have studied the expression of SVCT-2 and the uptake and release of [(14)C] ascorbate in chick retinal cells. SVCT-2 immunoreactivity was detected in rat and chick retina, specially in amacrine cells and in cells in the ganglion cell layer. Accordingly, SVCT-2 was expressed in cultured retinal neurons, but not in glial cells. [(14)C] ascorbate uptake was saturable and inhibited by sulfinpyrazone or sodium-free medium, but not by treatments that inhibit DHA transport. Glutamate-stimulated vitamin C release was not inhibited by the glutamate transport inhibitor L-beta-threo-benzylaspartate, indicating that vitamin C release was not mediated by glutamate uptake. Also, ascorbate had no effect on [(3)H] D-aspartate release, ruling out a glutamate/ascorbate exchange mechanism. Kainate or NMDA stimulated the release, effects blocked by their respective antagonists 6,7-initroquinoxaline-2,3- dione (DNQX) or (5R,2S) - (1) - 5 - methyl -10,11- dihydro- 5H- dibenzo [a,d] cyclohepten- 5,10- imine hydrogen maleate (MK-801). However, DNQX, but not MK801 or 2-amino-5-phosphonopentanoic acid, blocked the stimulation by glutamate. Interestingly, DNQX prevented the stimulation by NMDA, suggesting that the effect of NMDA was mediated by glutamate release and stimulation of non-NMDA receptors. The effect of glutamate was neither dependent on external calcium nor inhibited by 1,2-bis (2-aminophenoxy) ethane-N',N',N',N',-tetraacetic acid tetrakis (acetoxy-methyl ester) (BAPTA-AM), an internal calcium chelator, but was inhibited by sulfinpyrazone or by the absence of sodium. In conclusion, retinal cells take up and release vitamin C, probably through SVCT-2, and the release can be stimulated by NMDA or non-NMDA glutamate receptors.
LanguageENG
Pub Type(s)JOURNAL ARTICLE
PubMed ID19054286
  
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