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Mouse (Murine) Polyclonal SLC32A1 Primary Antibody für ELISA, MA - ABIN258394
Gruol, Vo, Bray, Roberts: CCL2-ethanol interactions and hippocampal synaptic protein expression in a transgenic mouse model. in Frontiers in integrative neuroscience 2014
Show all 3 Pubmed References
Rat (Rattus) Polyclonal SLC32A1 Primary Antibody für WB - ABIN361418
Korn, Koppel, Li, Mehta, Mehta, Seidl, Cramer: Astrocyte-secreted factors modulate the developmental distribution of inhibitory synapses in nucleus laminaris of the avian auditory brainstem. in The Journal of comparative neurology 2011
Show all 5 Pubmed References
The spatial and temporal expression patterns of xVIAAT during early developmental stages of Xenopus laevis.
Data indicate that GABAergic axons were labeled with vesicular inhibitory aa transporter (VIAAT) antibodies, whereas glutamatergic axons were detected with antisera against the major vesicular glutamate transporter (VGLUT) isoforms, VGLUT1 and VGLUT2.
We examined the ratio of excitatory to inhibitory vesicular neurotransmitter transporter (zeige SLC6A2 Antikörper) mRNAs (VGluT1 to VGAT) and their ratio in the dorsolateral prefrontal cortex during normal human development and in people with schizophrenia
VIATT has been identified in horizontal cells of the adult outer retina in culture, either at their terminals or throughout the entire cell.
The observed changes in gene and protein expression of vesicular GABA transporter, regional architecture, and morphology of mouse auditory forebrain may relate to-and to some extent enable-the emergence of mature sound-evoked activity patterns.
the AD-like tau accumulation induces anxiety through disrupting miR92a-vGAT-GABA signaling, which reveals molecular mechanisms underlying the anxiety behavior in AD patients and potentially leads to the development of new therapeutics for tauopathies.
This study demonstrated that Alterations in hypoglossal motor neurons due to VGAT deficiency in mice.
the deletion of VIAAT in GlyT2 (zeige SLC6A5 Antikörper)-Cre expressing neurons also strongly affects GABAergic transmission
This study showed that Conditional Knock-Out of Vesicular GABA Transporter Gene from Starburst Amacrine Cells Reveals the Contributions of Multiple Synaptic Mechanisms Underlying Direction Selectivity in the Retina.
Results indicate the significant contribution of not only GAD65 (zeige GAD2 Antikörper), GAD67 (zeige GAD1 Antikörper) and VGAT-mediated GABAergic but also glycinergic transmissions to both palate and abdominal wall formations
This study demonstrated that Genetic absence of the vesicular inhibitory amino acid transporter differentially regulates respiratory and locomotor motor neuron development.
results provide genetic, behavioral, and electrophysiological evidence that VGAT-mediated inhibitory drive alters very specific forms of sensory processing: those related to pain processing
Results suggest that the vesicular GABA transporter VGAT is fundamental for the GABA- and/or glycine-mediated transmission that supports embryonic development.
Cleft palate is caused by CNS dysfunction in Gad1 (zeige GAD1 Antikörper) and Viaat knockout mice
The protein encoded by this gene is an integral membrane protein involved in gamma-aminobutyric acid (GABA) and glycine uptake into synaptic vesicles. The encoded protein is a member of amino acid/polyamine transporter family II.
vesicular GABA transporter
, hypothetical protein LOC379652
, GABA and glycine transporter
, solute carrier family 32 member 1
, vesicular inhibitory amino acid transporter
, Vesicular inhibitory amino acid transporter
, vasicular inhibitory amino acid transporter 10D
, Betaine/GABA transporter 1
, GABA transporter 1
, Na(+)/Cl(-) betaine/GABA transporter
, sodium- and chloride-dependent betaine transporter
, solute carrier family 6 (neurotransmitter transporter, betaine/GABA), member 12
, solute carrier family 6 member 12