Distribution of two splice variants of the glutamate transporter GLT1 in the retinas of humans, monkeys, rabbits, rats, cats, and chickens

Reye, Peter; Sullivan, Rodney N.; Fletcher, Erica L.; Pow, David V.

doi:10.1002/cne.10095

Cited by 63 publications

(73 citation statements)

References 17 publications

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“…The differential compartmentation of glutamate transporters within very small domains of sperm is comparable to the microcompartmentation of such proteins in the brain and retina. 21,38 Roles of glutamate and possible functional consequences of glutamate transporter expression It has previously been shown that mice which lack EAAC1 in the epididymis (due to the knockout of c-ros) 11 exhibit swollen spermatozoa. 12 This has been interpreted as an example of the role of glutamate as an osmolyte, which in this instance would be dys-regulated due to impaired epididymal supply of the osmolyte (glutamate) or its premature loss.…”

Section: Discussionmentioning

confidence: 99%

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Expression of multiple glutamate transporter splice variants in the rodent testis

Lee¹,

Anderson²,

Barnett³

et al. 2010

Asian J Androl

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Glutamate is a regulated molecule in the mammalian testis. Extracellular regulation of glutamate in the body is determined largely by the expression of plasmalemmal glutamate transporters. We have examined by PCR, western blotting and immunocytochemistry the expression of a panel of sodium-dependent plasmalemmal glutamate transporters in the rat testis. Proteins examined included: glutamate aspartate transporter (GLAST), glutamate transporter 1 (GLT1), excitatory amino acid carrier 1 (EAAC1), excitatory amino acid transporter 4 (EAAT4) and EAAT5. We demonstrate that many of the glutamate transporters in the testis are alternately spliced. GLAST is present as exon-3-and exon-9-skipping forms. GLT1 was similarly present as the alternately spliced forms GLT1b and GLT1c, whereas the abundant brain form (GLT1a) was detectable only at the mRNA level. EAAT5 was also strongly expressed, whereas EAAC1 and EAAT4 were absent. These patterns of expression were compared with the patterns of endogenous glutamate localization and with patterns of D-aspartate accumulation, as assessed by immunocytochemistry. The presence of multiple glutamate transporters in the testis, including unusually spliced forms, suggests that glutamate homeostasis may be critical in this organ. The apparent presence of many of these transporters in the testis and sperm may indicate a need for glutamate transport by such cells.

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Section: Discussionmentioning

confidence: 99%

“…[31][32][33][34][35][36][37][38] Figure 1 schematically illustrates the locations of antibody epitopes for normally spliced GLAST and the exon-skipping forms of GLAST (GLAST1a and GLAST1b). Multiple GLT1 antisera were used in this study (Figure 2).…”

Section: Primary Antibodies Against Transportersmentioning

confidence: 99%

Expression of multiple glutamate transporter splice variants in the rodent testis

Lee¹,

Anderson²,

Barnett³

et al. 2010

Asian J Androl

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show abstract

“…Given the complex mechanisms regulating GLT-1 expression (Anderson and Swanson, 2000;Gegelashvili and Schousboe, 1997;Plachez et al, 2000), its post-transcriptional regulation in neurons was invoked to explain the contrasting data (e.g., Danbolt et al, 1998). It subsequently became apparent that part of the uncertainty was because of the existence of three different isoforms, GLT-1a-c. (Berger et al, 2005;Chen et al, 2002Chen et al, , 2004Pines et al, 1992;Rauen et al, 2004;Reye et al, 2002;Schmitt et al, 2002;Sullivan et al, 2004). Despite regional variations of expression, GLT-1a (the protein originally called GLT-1), appears more abundant and more closely related to synapses than GLT-1b, presumably mediating most of the known synaptic effects of GLT-1 (Berger et al, 2005;Chen et al, 2004;Lauriat and McInnes, 2007;Sullivan et al, 2004); GLT-1c is expressed only in the retina.…”

Section: Introductionmentioning

confidence: 98%

Synaptic localization of GLT‐1a in the rat somatic sensory cortex

Melone

Bellesi

Conti

2008

Glia

106

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GLT-1a, the major glutamate transporter, plays an important role in both physiological and pathological conditions. Uncertainty regarding its localization in the cerebral cortex prompted us to re-examine its cellular and subcellular localization in the rat somatic sensory cortex. GLT-1a detection was sensitive to fixation; in optimal conditions approximately 25% of GLT-1a+ profiles were axon terminals. GLT-1a/VGLUT1 double-labeling and pre-embedding electron microscopy studies showed that approximately 50% of GLT-1a+ profiles were in the vicinity of asymmetric synapses. Using pre-embedding electron microscopy, we found that approximately 70% of GLT-1a located in the vicinity of asymmetric synapses was astrocytic and approximately 30% was neuronal. Post-embedding immunogold studies showed that the density of gold particles coding for GLT-1a was much higher in astrocytic processes than in axon terminals, and that in the latter they were never at the active zone. In both astrocytic processes and axon terminals most gold particles were localized in a membrane region extending for about 250 nm from active zone margin, with a peak at 140 nm for astrocytic processes and at 80 for axon terminals. We conclude that, although GLT-1a is expressed by both astrocytes and axon terminals, astrocytic GLT-1a predominates at asymmetric synapses, and that the perisynaptic localization of GLT-1a in cortex is well-suited to modulate Glu concentrations at the cleft and also to restrict Glu spillover.

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“…In order to maintain normal retinal function, glutamate must be removed rapidly from the synaptic cleft. At the molecular level, five glutamate transporters have been cloned: excitatory amino acid transporters (EAAT) 1-5, all of which have been identified in the retina [13,14,[18][19][20][21][22]. Although the function of specific transporter types is contentious, it is clear that GLAST (EAAT1) is the predominant transporter for removal of glutamate within the retina and defects in its function lead to major deleterious effects on vision [20,23,24].…”

Section: Introductionmentioning

confidence: 99%

Glutamate uptake in retinal glial cells during diabetes

et al. 2005

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Aims: Glutamate recycling is a major function of retinal Müller cells. The aim of this study was to evaluate the expression and function of glutamate transporters during diabetes. Methods: Sprague-Dawley rats were rendered diabetic by a single dose of streptozotocin (50 mg/kg). Following 12 weeks of diabetes, immunolocalisation and mRNA expression of the two glial cell transporters, GLAST and EAAT4 were evaluated using indirect immunofluorescence and real-time PCR. The function of glutamate transport was investigated at 1, 4 and 12 weeks following induction of diabetes by measuring the level of uptake of the non-metabolisable glutamate analogue, D-aspartate, into Müller cells. Results: There was no difference in the localisation of either GLAST or EAAT4 during diabetes. Although there was a small apparent increase in expression of both GLAST and EAAT4 in diabetic retinae compared with controls this was not statistically significant. At 1, 4 and 12 weeks following diabetes, D-aspartate immunoreactivity was significantly increased in Müller cells of diabetic rats compared to controls (p<0.001). The EC 50 was found to increase by 0.304 log units in diabetic Müller cells compared with controls, suggesting that glutamate uptake is twice as efficient. Conclusions: These data suggest that there are alterations in glutamate transport during diabetes. However, these changes are unlikely to play a significant role in glutamate-induced neuronal excitoxicity during diabetes. These results suggest that although Müller cells undergo gliosis at an early stage of diabetes, one of the most important functions for maintaining normal retinal function is preserved within the retina.

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Distribution of two splice variants of the glutamate transporter GLT1 in the retinas of humans, monkeys, rabbits, rats, cats, and chickens

Cited by 63 publications

References 17 publications

Expression of multiple glutamate transporter splice variants in the rodent testis

Expression of multiple glutamate transporter splice variants in the rodent testis

Synaptic localization of GLT‐1a in the rat somatic sensory cortex

Glutamate uptake in retinal glial cells during diabetes

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