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Neurochemical Research

, Volume 9, Issue 6, pp 815–821 | Cite as

Role of synaptosomal Na-accumulation in transmitter release

  • Edwin M. Meyer
  • Jack R. Cooper
Original Articles

Abstract

The mechanism whereby Na+, K+-ATPase inhibitors such as ouabain trigger transmitter release in a calcium-independent manner remains obscure. We have examined the possible role of intra-synaptosomal sodium ion accumulation in ouabain-induced acetylcholine (ACh) release by: 1) Measuring22Na accumulation in cat cortical synaptosomes in the presence of ouabain, A23187, veratridine, or strophanthidin over the same time course in which we previously determined their effects on ACh release; and 2) measuring synaptosomal22Na accumulation and ACh-release in the presence of ouabain plus tetrodotoxin in normal or calcium-free buffer. Our results indicate that tetrodotoxin-dependent22Na accumulation is at least partially responsible for ouabain-induced ACh release in normal and calcium-free media, but that this ion-accumulation per se is not sufficient to elicit release with other secretogogues.

Keywords

Sodium Acetylcholine Ouabain A23187 Transmitter Release 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Publishing Corporation 1984

Authors and Affiliations

  • Edwin M. Meyer
    • 1
  • Jack R. Cooper
    • 1
  1. 1.Department of PharmacologyYale University School of MedicineNew Haven

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