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Publication : An essential role for vesicular glutamate transporter 1 (VGLUT1) in postnatal development and control of quantal size.

First Author  Wojcik SM Year  2004
Journal  Proc Natl Acad Sci U S A Volume  101
Issue  18 Pages  7158-63
PubMed ID  15103023 Mgi Jnum  J:89958
Mgi Id  MGI:3042058 Doi  10.1073/pnas.0401764101
Citation  Wojcik SM, et al. (2004) An essential role for vesicular glutamate transporter 1 (VGLUT1) in postnatal development and control of quantal size. Proc Natl Acad Sci U S A 101(18):7158-63
abstractText  Quantal neurotransmitter release at excitatory synapses depends on glutamate import into synaptic vesicles by vesicular glutamate transporters (VGLUTs). Of the three known transporters, VGLUT1 and VGLUT2 are expressed prominently in the adult brain, but during the first two weeks of postnatal development, VGLUT2 expression predominates. Targeted deletion of VGLUT1 in mice causes lethality in the third postnatal week. Glutamatergic neurotransmission is drastically reduced in neurons from VGLUT1-deficient mice, with a specific reduction in quantal size. The remaining activity correlates with the expression of VGLUT2. This reduction in glutamatergic neurotransmission can be rescued and enhanced with overexpression of VGLUT1. These results show that the expression level of VGLUTs determines the amount of glutamate that is loaded into vesicles and released and thereby regulates the efficacy of neurotransmission.
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