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The stoichiometry for GABA Transporter 1 is 2 Na +: 1 Cl −: 1 GABA. [13] The presence of a Cl − /Cl − exchange is also proposed because the Cl − transported across the membrane does not affect the net charge. [14] GABA is also the primary inhibitory neurotransmitter in the cerebral cortex and has the highest level of expression within ...
The signal is terminated by removal of GABA from the synaptic cleft by transport of GABA back into the nerve terminal by the plasma membrane GABA transporter (GAT) 1. GABA transporters in the plasma membrane help in regulating the concentration of GABA in the extracellular matrix by reabsorbing the transmitter and clearing the synapse. They ...
Sodium- and chloride-dependent betaine transporter, also known as Na(+)/Cl(-) betaine/GABA transporter (BGT-1), is a protein that in humans is encoded by the SLC6A12 gene. BGT-1 is predominantly expressed in the liver (hepatocytes). [5] It is also expressed in the kidney [5] where it is regulated by NFAT5 during a response to osmotic stress. [6]
CI-966 (developmental code name) is a central nervous system depressant acting as a GABA reuptake inhibitor, specifically a highly potent and selective blocker of the GABA transporter 1 (GAT-1) (IC 50 = 0.26 μM), [1] and hence indirect and non-selective GABA receptor full agonist.
Vesicular inhibitory amino acid transporter is a protein that in humans is encoded by the SLC32A1 gene. [5] 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. [5]
The glutamate/GABA–glutamine cycle is a metabolic pathway that describes the release of either glutamate or GABA from neurons which is then taken up into astrocytes (non-neuronal glial cells). In return, astrocytes release glutamine to be taken up into neurons for use as a precursor to the synthesis of either glutamate or GABA.
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Moreover, GABA-bound GAD65 is intrinsically more flexible and exists as an ensemble of states, thus providing more opportunities for autoantigenicity as seen in Type 1 diabetes. [ 14 ] [ 15 ] GAD derived from Escherichia coli shows additional structural intricacies, including a pH-dependent conformational change.