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Sodium‐dependent vitamin C transporter‐2 mediates vitamin C transport at the cortical nerve terminal
Author(s) -
Pierce Marquicia R.,
Raj Amita,
Betke Katherine M.,
Zeidan L. Nora,
Matthies Heinrich J.G.,
May James M.
Publication year - 2015
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.23669
Subject(s) - reuptake , transporter , monoamine neurotransmitter , vesicular monoamine transporter 2 , efflux , biology , synaptic vesicle , synaptosome , sodium , chemistry , microbiology and biotechnology , biophysics , biochemistry , pharmacology , dopamine transporter , in vitro , vesicle , serotonin , receptor , organic chemistry , membrane , gene
It has been shown that vitamin C (VC) is transported at synaptic boutons, but how this occurs has not been elucidated. This study investigates the role of the sodium‐dependent vitamin C transporter‐2 (SVCT2) in transporting VC at the cortical nerve terminal. Immunostaining of cultured mouse superior cervical ganglion cells showed the SVCT2 to be expressed in presynaptic boutons, colocalizing with the vesicular monoamine transporter‐2 and the norepinephrine transporter. Immunoblotting of enriched cortical synaptosomes demonstrated that the SVCT2 was enriched in presynaptic fractions, confirming a predominantly presynaptic location. In crude synaptosomes, known inhibitors of SVCT2 inhibited uptake of VC. Furthermore, the kinetic features of VC uptake were consistent with SVCT2‐mediated function. VC was also found to efflux from synaptosomes by a mechanism not involving the SVCT2. Indeed, VC efflux was substantially offset by reuptake of VC on the SVCT2. The presence and function of the SVCT2 at the presynaptic nerve terminal suggest that it is the transporter responsible for recovery of VC released into the synaptic cleft. © 2015 Wiley Periodicals, Inc.