An essential role for vesicular glutamate transporter 1 (VGLUT1) in postnatal development and control of quantal size.
Proceedings of the National Academy of Sciences. 2004-04-21; 101(18): 7158-7163
DOI: 10.1073/pnas.0401764101
Lire sur PubMed
1. Proc Natl Acad Sci U S A. 2004 May 4;101(18):7158-63. Epub 2004 Apr 21.
An essential role for vesicular glutamate transporter 1 (VGLUT1) in postnatal
development and control of quantal size.
Wojcik SM(1), Rhee JS, Herzog E, Sigler A, Jahn R, Takamori S, Brose N, Rosenmund
C.
Author information:
(1)Department of Molecular Neurobiology, Max Planck Institute for Experimental
Medicine, Hermann-Rein Strasse 3, D-37075 Göttingen, Germany.
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.
DOI: 10.1073/pnas.0401764101
PMCID: PMC406482
PMID: 15103023 [Indexed for MEDLINE]