Identification of a vesicular glutamate transporter that defines a glutamatergic phenotype in neurons

Shigeo Takamori, Jeong Seop Rhee, Christian Rosenmund and Reinhard Jahn ()
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Shigeo Takamori: Max-Planck-Institute for Biophysical Chemistry
Jeong Seop Rhee: Max-Planck-Institute for Biophysical Chemistry
Christian Rosenmund: Max-Planck-Institute for Biophysical Chemistry
Reinhard Jahn: Max-Planck-Institute for Biophysical Chemistry

Nature, 2000, vol. 407, issue 6801, 189-194

Abstract: Abstract Glutamate is the major excitatory neurotransmitter in the mammalian central nervous system. Synaptic vesicles are loaded with neurotransmitter by means of specific vesicular transporters. Here we show that expression of BNPI, a vesicle-bound transporter associated with sodium-dependent phosphate transport1,2,3, results in glutamate uptake by intracellular vesicles. Substrate specificity and energy dependence are very similar to glutamate uptake by synaptic vesicles. Stimulation of exocytosis—fusion of the vesicles with the cell membrane and release of their contents—resulted in quantal release of glutamate from BNPI-expressing cells. Furthermore, we expressed BNPI in neurons containing GABA (γ-aminobutyric acid) and maintained them as cultures of single, isolated neurons that form synapses to themselves. After stimulation of these neurons, a component of the postsynaptic current is mediated by glutamate as it is blocked by a combination of the glutamate receptor antagonists, but is insensitive to a GABAA receptor antagonist. We conclude that BNPI functions as vesicular glutamate transporter and that expression of BNPI suffices to define a glutamatergic phenotype in neurons.

Date: 2000
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DOI: 10.1038/35025070

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