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001009116 1001_ $$0P:(DE-Juel1)169471$$aKolen, Bettina$$b0
001009116 245__ $$aVesicular glutamate transporters are H+-anion exchangers that operate at variable stoichiometry
001009116 260__ $$a[London]$$bNature Publishing Group UK$$c2023
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001009116 500__ $$aThis workwas supported by the Deutsche Forschungsgemeinschaft (GermanResearch Foundation) to Ch.F. (FA 301/15–2) as part of Research UnitFOR 2518, DynIon; to Ch.F. and G.U. as part of the Research Unit FOR2795, to REG (GU 2042/2-1), and by the NIH to G.U. (R01 AG053988).
001009116 520__ $$aVesicular glutamate transporters accumulate glutamate in synaptic vesicles, where they also function as a major Cl- efflux pathway. Here we combine heterologous expression and cellular electrophysiology with mathematical modeling to understand the mechanisms underlying this dual function of rat VGLUT1. When glutamate is the main cytoplasmic anion, VGLUT1 functions as H+-glutamate exchanger, with a transport rate of around 600 s−1 at −160 mV. Transport of other large anions, including aspartate, is not stoichiometrically coupled to H+ transport, and Cl- permeates VGLUT1 through an aqueous anion channel with unitary transport rates of 1.5 × 105 s−1 at −160 mV. Mathematical modeling reveals that H+ coupling is sufficient for selective glutamate accumulation in model vesicles and that VGLUT Cl- channel function increases the transport efficiency by accelerating glutamate accumulation and reducing ATP-driven H+ transport. In summary, we provide evidence that VGLUT1 functions as H+-glutamate exchanger that is partially or fully uncoupled by other anions.
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001009116 7001_ $$0P:(DE-Juel1)176659$$aBorghans, Bart$$b1$$ufzj
001009116 7001_ $$0P:(DE-Juel1)157846$$aKortzak, Daniel$$b2
001009116 7001_ $$0P:(DE-HGF)0$$aLugo, Victor$$b3
001009116 7001_ $$aHannack, Cora$$b4
001009116 7001_ $$0P:(DE-Juel1)156375$$aGuzman, Raul$$b5$$ufzj
001009116 7001_ $$00000-0002-3716-8742$$aUllah, Ghanim$$b6
001009116 7001_ $$0P:(DE-Juel1)136837$$aFahlke, Christoph$$b7$$eCorresponding author
001009116 773__ $$0PERI:(DE-600)2553671-0$$a10.1038/s41467-023-38340-9$$gVol. 14, no. 1, p. 2723$$n1$$p2723$$tNature Communications$$v14$$x2041-1723$$y2023
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