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Barium Evokes Glutamate Release from Rat Brain Synaptosomes by Membrane Depolarization: Involvement of K+, Na+, and Ca2+ Channels

  • Author(s): Sihra, TS
  • Piomelli, D
  • Nichols, RA
  • et al.
Abstract

Abstract: During K+ ‐induced depolarization of isolated rat brain nerve terminals (synaptosomes), 1 mM Ba2+ could substitute for 1 mM Ca2+ in evoking the release of endogenous glutamate. In addition, Ba2+ was found to evoke glutamate release in the absence of K+‐induced depolarization. Ba2+ (1–10 mM) depolarized synaptosomes, as measured by voltage‐sensitive dye fluorescence and [3H]‐tetraphenylphosphonium cation distribution. Ba2+ partially inhibited the increase in synaptosomal K+ efflux produced by depolarization, as reflected by the redistribution of radiolabeled 86Rb+. The release evoked by Ba2+ was inhibited by tetrodotoxin (TTX). Using the divalent cation indicator fura‐2, cytosolic [Ca2+] increased during stimulation by approximately 200 nM, but cytosolic [Ba2+] increased by more than 1 μM. Taken together, our results indicate that Ba2+ initially depolarizes synaptosomes most likely by blocking a K+ channel, which then activates TTX‐sensitive Na+ channels, causing further depolarization, and finally enters synaptosomes through voltage‐sensitive Ca2+channels to evoke neurotransmitter release directly. Though Ba2+‐evoked glutamate release was comparable in level to that obtained with K+‐induced depolarization in the presence of Ca2+, the apparent intrasynaptosomal level of Ba2+ required for a given amount of glutamate release was found to be several‐fold higher than that required of Ca2+. Copyright © 1993, Wiley Blackwell. All rights reserved

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