Anti-VGLUT2-ATTO Fluor-594

Antibodies

ATTO-594. Maximum absorption 601 nm; Maximum fluorescence 627 nm. The fluorescence is excited most efficiently in the 580 - 615 nm range. This label belongs to the class of Rhodamine dyes and can be used with fluorescent equipment typically optimized to detect Texas Red and Alexa-594.

Shipped at room temperature. Product as supplied can be stored intact at room temperature for several weeks. For longer periods, it should be stored at -20°C

Lyophilized powder

Vesicular glutamate transporter 2, Differentiation-associated Na+-dependent inorganic phosphate cotransporter, DNPI, SLC17A6 - A Rabbit Polyclonal Antibody to Vesicular Glutamate Transporter 2 Conjugated to the Fluorescent Dye ATTO-594

Mouse - identical; human - 11/12 amino acid residues identical

Confirmed by amino acid analysis and mass spectrometry

1 mg/ml

Cytoplasmic, N-terminus

Rat

41116161

Central nervous system neurons have traditionally been thought to express exclusively membrane transporters and/or vesicular transporters for their transmitter. Three vesicular glutamate transporters (VGLUTs) have been cloned: BNPI/VGLUT1 (a brain-specific sodium dependent inorganic phosphate (Pi) transporter), and its homologs DNPI/VGLUT2 (differentiation-associated sodium-dependent Pi transporter) and VGLUT31. These transporters mediate glutamate uptake inside presynaptic vesicles and are anatomical and functional markers of glutamatergic excitatory transmission2.BNPI/DNPI encodes a membrane protein with 6-8 putative transmembrane domains which exhibits weak similarities to a kidney Na+-dependent inorganic phosphate co-transporter3. The transporters use a membrane potential gradient set by the vesicular H+-ATPase for glutamate uptake4. VGLUT1-3 are very similar in structure and function, but are used by different neuronal populations. VGLUT1 and VGLUT2 are expressed by the cortical and subcortical neurons respectively. VGLUT3 is expressed by non-glutamatergic neurons5. VGLUT2 is expressed in the thalamus, brainstem, and deep cerebellar nuclei2. A Recent study has shown that targeted deletion of VGLUT2 in mice causes perinatal lethality and a 95% reduction in evoked glutamatergic responses in thalamic neurons, although hippocampal synapses function normally. Behavioral analysis of heterozygous VGLUT2 mice showed discrete behavioral phenotypes that suggest a deficit in thalamic processing6.