High impact information on SLC32A1

• Our recent work shows that this includes alterations in the levels of expression of vesicular glutamate (VGLUT1 and VGLUT2) and GABA (VIAAT) transporters [1].
• We previously demonstrated that the GABA and glycine transporter vesicular inhibitory amino acid transporter (VIAAT also known as VGAT) is present in rat islets [2].
• Our results have indicated that islet content of V52, but not V57, is responsive to changes in glucose concentration and other extracellular conditions [2].
• V57 and V52 display different patterns of post-translational modification and cellular expression [2].
• Here we have also provided additional evidence for the presence of VIAAT in islet beta cells and show that the beta cell line INS-1 expresses V57 [2].

Anatomical context of SLC32A1

• In addition, GlyT2a shows a severe limitation for reverse uptake, which suggests an essential role of GlyT2a in maintaining a high intracellular glycine pool, thus facilitating the refilling of synaptic vesicles by the low affinity, low specificity vesicular transporter VGAT/VIAAT [3].
• V52 may be better adapted than V57 to the unique rat alpha cell GAD-GABA system, which lacks GAD65 and in which VIAAT traffics to secretory granules rather than just to synaptic microvesicles [2].
• In 3 h postictal group, the density of VGAT immunoreactivity was significantly increased in the hippocampus, as compared to pre-seizure group [4].
• Unlike VGAT, CLC-2 immunoreactivity was markedly reduced in the hippocampus during epileptogenic periods and was re-enhanced only in the dentate gyrus after recurrent seizure onset [5].

Associations of SLC32A1 with chemical compounds

• Bidirectional and opposite activity-dependent regulation of VGLUT1 and VIAAT expression would serve to adjust the balance of glutamate and GABA release and therefore the level of postsynaptic receptor saturation [1].
• In the phaclofen-treated SS gerbils, VGAT expression was dramatically elevated, compared to SS gerbil controls [6].
• In addition, VGAT immunoreactivity in the hippocampus was also increased by vigabatrin (GVG) administration [4].
• In the baclofen-treated seizure-resistant gerbils, VGAT expression was significantly reduced, as compared with the control animals, thus the VGAT immunoreactive pattern in these gerbils was similar to that in control seizure-sensitive (SS) gerbils [6].
• Chronic treatment with bumetanide decreased vesicular GABA transporter (VGAT)-immunopositive particles without affecting paired-pulse ratio of evoked IPSCs (eIPSCs), indicating decrease in the number of functional GABAergic synapses [7].

Analytical, diagnostic and therapeutic context of SLC32A1

• Changes in vesicular gamma-aminobutyric acid (GABA) transporter (VGAT) expression in the gerbil hippocampus after treatment with baclofen (GABA(B) receptor agonist) or phaclofen (GABA(B) receptor antagonist) were investigated to identify the GABA(B) receptor-mediated regulation of VGAT expression [6].

References