![]() ![]() Complete deletion of the VMAT2 gene causes developmental defect and embryonic lethality in mice ( 4- 6).īecause of the exclusive expression of each transporter in the corresponding neurons, these transporters are often used as markers of specific neurons. For instance, two loss-of-function DAT mutants, 元68Q and P395L, cause infantile parkinsonism-dystonia in humans ( 3). Loss of a transporter could cause severe disease or lethality. Therefore, the overall function of these four transporters is to regulate tempo-spatial components of monoamine transmission. In the membrane of intracellular synaptic vesicles is the vesicular monoamine transporters 1 and 2 (VMAT1 and VMAT2), which use a proton gradient as the energy source to sequester cytosolic monoamines into the vesicles and then release the monoamines into synaptic cleft by exocytosis. ![]() The major function of these transporters is to terminate monoamine transmission by inward transport of substrates away from the synaptic cleft. These proteins use ion (Na +, Cl −) gradients as energy sources to move monoamines into or out of neurons. Monoamine transporters are transmembrane proteins located in plasma membranes of monoaminergic neurons, including the dopamine transporter (DAT), serotonin transporter (SERT, also expressed in platelets), and norepinephrine transporter (NET) ( 1, 2).
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