Get access

The sodium-driven chloride/bicarbonate exchanger in presynaptic terminals

Authors

  • Alain C. Burette,

    Corresponding author
    1. Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, North Carolina 27599
    • Dept. of Cell & Developmental Biology, University of North Carolina, CB # 7090, Chapel Hill, NC 27599
    Search for more papers by this author
  • Richard J. Weinberg,

    1. Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, North Carolina 27599
    2. Neuroscience Center, University of North Carolina, Chapel Hill, North Carolina 27599
    Search for more papers by this author
  • Patrick Sassani,

    1. David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, California 90095
    Search for more papers by this author
  • Natalia Abuladze,

    1. David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, California 90095
    Search for more papers by this author
  • Liyo Kao,

    1. David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, California 90095
    Search for more papers by this author
  • Ira Kurtz

    1. David Geffen School of Medicine, University of California-Los Angeles, Los Angeles, California 90095
    2. Brain Research Institute, University of California-Los Angeles, Los Angeles, California 90095
    Search for more papers by this author

Abstract

The sodium-driven chloride/bicarbonate exchanger (NDCBE), a member of the SLC4 family of bicarbonate transporters, was recently found to modulate excitatory neurotransmission in hippocampus. By using light and electron microscopic immunohistochemistry, we demonstrate here that NDCBE is expressed throughout the adult rat brain, and selectively concentrates in presynaptic terminals, where it is closely associated with synaptic vesicles. NDCBE is in most glutamatergic axon terminals, and is also present in the terminals of parvalbumin-positive γ-aminobutyric acid (GABA)ergic cells. These findings suggest that NDCBE can regulate glutamatergic transmission throughout the brain, and point to a role for NDCBE as a possible regulator of GABAergic neurotransmission. J. Comp. Neurol. 520:1481–1492, 2012. © 2011 Wiley Periodicals, Inc.

Ancillary