Literature DB >> 19054286

Glutamate receptors modulate sodium-dependent and calcium-independent vitamin C bidirectional transport in cultured avian retinal cells.

Camila Cabral Portugal1, Vivian Sayuri Miya, Karin da Costa Calaza, Rochelle Alberto Martins Santos, Roberto Paes-de-Carvalho.   

Abstract

Vitamin C is transported in the brain by sodium vitamin C co-transporter 2 (SVCT-2) for ascorbate and glucose transporters for dehydroascorbate. 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 dehydroascorbate 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. 2-Carboxy-3-carboxymethyl-4-isopropenylpyrrolidine (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 MK-801 or 2-amino-5-phosphonopentanoic acid (APV), 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.

Entities:  

Mesh:

Substances:

Year:  2008        PMID: 19054286     DOI: 10.1111/j.1471-4159.2008.05786.x

Source DB:  PubMed          Journal:  J Neurochem        ISSN: 0022-3042            Impact factor:   5.372


  13 in total

1.  Allosteric modulation of retinal GABA receptors by ascorbic acid.

Authors:  Cecilia I Calero; Evan Vickers; Gustavo Moraga Cid; Luis G Aguayo; Henrique von Gersdorff; Daniel J Calvo
Journal:  J Neurosci       Date:  2011-06-29       Impact factor: 6.167

2.  Corticostriatal dysfunction and glutamate transporter 1 (GLT1) in Huntington's disease: interactions between neurons and astrocytes.

Authors:  Ana María Estrada-Sánchez; George V Rebec
Journal:  Basal Ganglia       Date:  2012-07-01

3.  Positive modulation of the α9α10 nicotinic cholinergic receptor by ascorbic acid.

Authors:  J C Boffi; C Wedemeyer; M Lipovsek; E Katz; D J Calvo; A B Elgoyhen
Journal:  Br J Pharmacol       Date:  2013-02       Impact factor: 8.739

4.  Nitric oxide modulates sodium vitamin C transporter 2 (SVCT-2) protein expression via protein kinase G (PKG) and nuclear factor-κB (NF-κB).

Authors:  Camila Cabral Portugal; Thaísa Godinho da Encarnação; Renato Socodato; Sarah Rodrigues Moreira; Dan Brudzewsky; António Francisco Ambrósio; Roberto Paes-de-Carvalho
Journal:  J Biol Chem       Date:  2011-10-31       Impact factor: 5.157

5.  Glutathione induces GABA release through P2X7R activation on Müller glia.

Authors:  Hércules Rezende Freitas; Ricardo A de Melo Reis
Journal:  Neurogenesis (Austin)       Date:  2017-02-06

6.  Reduced-serum vitamin C and increased uric acid levels in normal-tension glaucoma.

Authors:  Kenya Yuki; Dogru Murat; Itaru Kimura; Yuichiro Ohtake; Kazuo Tsubota
Journal:  Graefes Arch Clin Exp Ophthalmol       Date:  2009-09-08       Impact factor: 3.117

7.  Corticostriatal dysfunction underlies diminished striatal ascorbate release in the R6/2 mouse model of Huntington's disease.

Authors:  Jenelle L Dorner; Benjamin R Miller; Emma L Klein; Alexander Murphy-Nakhnikian; Rachel L Andrews; Scott J Barton; George V Rebec
Journal:  Brain Res       Date:  2009-07-16       Impact factor: 3.252

8.  Up-regulation of GLT1 reverses the deficit in cortically evoked striatal ascorbate efflux in the R6/2 mouse model of Huntington's disease.

Authors:  Benjamin R Miller; Jenelle L Dorner; Kendra D Bunner; Thomas W Gaither; Emma L Klein; Scott J Barton; George V Rebec
Journal:  J Neurochem       Date:  2012-03-28       Impact factor: 5.372

9.  Combination Therapy with Sulfasalazine and Valproic Acid Promotes Human Glioblastoma Cell Death Through Imbalance of the Intracellular Oxidative Response.

Authors:  Carlos Gustavo Garcia; Suzana Assad Kahn; Luiz Henrique Medeiros Geraldo; Igor Romano; Ivan Domith; Deborah Christinne Lima E Silva; Fernando Dos Santos Assunção; Marcos José Ferreira; Camila Cabral Portugal; Jorge Marcondes de Souza; Luciana Ferreira Romão; Annibal Duarte Pereira Netto; Flávia Regina Souza Lima; Marcelo Cossenza
Journal:  Mol Neurobiol       Date:  2018-01-19       Impact factor: 5.590

10.  Dopamine Promotes Ascorbate Release from Retinal Neurons: Role of D1 Receptors and the Exchange Protein Directly Activated by cAMP type 2 (EPAC2).

Authors:  Thaísa Godinho da Encarnação; Camila Cabral Portugal; Caio Eduardo Nogueira; Felipe Nascimento Santiago; Renato Socodato; Roberto Paes-de-Carvalho
Journal:  Mol Neurobiol       Date:  2018-02-23       Impact factor: 5.590

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.