GLAST1b, the exon-9 skipping form of the glutamate-aspartate transporter EAAT1 is a sensitive marker of neuronal dysfunction in the hypoxic brain

Sullivan, Susan M.; Macnab, L. T.; Björkman, S. T.; Colditz, Paul B.; Pow, David V.

doi:10.1016/j.neuroscience.2007.08.011

Cited by 30 publications

(40 citation statements)

References 41 publications

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“…Similarly, our previous studies have shown that the amino-terminal region of GLAST1b is typically absent. 23 We conclude that much of the GLAST in the testis is the exon-3-and exon-9-skipping forms, but with the additional caveat that these splice variants also lack the amino-terminal region, and mostly lack the carboxyl-terminal region.…”

Section: Discussionmentioning

confidence: 71%

“…9 It has been reported that GLAST1a is a functional transporter in bone, 49 and so, in accord with our prior comments, is probably also functional in the testis. The role of GLAST1b is unclear, since although it is abundant in the brain, especially after insults, 23 there are suggestions that it is not a functional glutamate transporter, but may interfere with trafficking of glutamate by normally spliced forms of GLAST. 50 Maturation of glutamate transporter expression An overt feature of our immunocytochemical studies was the presence of maturational differences in immunolabeling characteristics between sperm in different tubules, and a further maturation of this in more mature sperm isolated from the rete testis.…”

Section: Discussionmentioning

confidence: 99%

“…[21][22][23] To study the expression of GLAST1a, GLAST1b, GLT1b and GLT1c in testis, PCR primers specific for each splice variant were synthesized (Table 1).…”

Section: Reverse Transcription (Rt)-pcrmentioning

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: 71%

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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“…This theory is supported by Martin et al [23] who demonstrated a significant increase in GFAP immunoreactivity in the HI pig brain at 96h post-insult. Our previous studies have demonstrated that the post-HI brain undergoes significant changes in the expression of various astrocytic and neuronal proteins and the structure of grey and white matter astrocytes [6,[24][25][26][27][28][29]. We have demonstrated pre-gliotic astrocyte changes are evident from 1-8h after an HI insult, prior to histological evidence of neuronal damage [6,29].…”

Section: Introductionmentioning

confidence: 93%

Phosphorylation of GFAP is Associated with Injury in the Neonatal Pig Hypoxic-Ischemic Brain

Sullivan

Miller

et al. 2012

Neurochem Res

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Glial fibrillary acidic protein (GFAP) is an intermediate filament protein expressed in the astrocytecytoskeleton that plays an important role in the structure and function of the cell. GFAP can be phosphorylated at six serine (Ser) or threonine (Thr) residues but little is known about the role of GFAP phosphorylation in physiological and pathophysiological states. We have generated antibodies against two phosphorylated GFAP (pGFAP) proteins: p8GFAP, where GFAP is phosphorylated at Ser-8 and p13GFAP, where GFAP is phosphorylated at Ser-13. We examined p8GFAP and p13GFAP expression in the control neonatal pig brain and at 24h and 72h after an hypoxic-ischemic (HI) insult. Immunohistochemistry demonstrated pGFAP expression in astrocytes with an atypical cytoskeletal morphology, even in control brains. Semi-quantitative western blotting revealed that p8GFAP expression was significantly increased at 24h post-insult in HI animals with seizures in frontal, parietal, temporal and occipital cortices. At 72h post-insult, p8GFAP and p13GFAP expression were significantly increased in HI animals with seizures in brain regions that are vulnerable to cellular damage (cortex and basal ganglia), but no changes were observed in brain regions that are relatively spared following an HI insult (brain stem and cerebellum). Increased pGFAP expression was associated with poor neurological outcomes such as abnormal encephalography (EEG) and neurobehaviour, and increased histological brain damage.Phosphorylation of GFAP may play an important role in astrocyte remodelling during development and disease and could potentially contribute to the plasticity of the central nervous system. 3

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“…Recent evidence supports novel roles in brain for splice variants of EAAT1 and EAAT2 (Macnab and Pow, 2007;Sullivan et al, 2007). Enhanced expression of EAAT2 resulting from administration of ß-lactam antibiotics (e.g.…”

mentioning

confidence: 95%

Glutamate (excitatory amino acid) transporters

2009

British Journal of Pharmacology

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GLAST1b, the exon-9 skipping form of the glutamate-aspartate transporter EAAT1 is a sensitive marker of neuronal dysfunction in the hypoxic brain

Cited by 30 publications

References 41 publications

Expression of multiple glutamate transporter splice variants in the rodent testis

Expression of multiple glutamate transporter splice variants in the rodent testis

Phosphorylation of GFAP is Associated with Injury in the Neonatal Pig Hypoxic-Ischemic Brain

Glutamate (excitatory amino acid) transporters

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