Open AccessUncoupling of electrotonic synapses by calcium.
Author(s) -
Gérard Baux,
Michel Simonneau,
L Tauc,
J. P. Segundo
Publication year - 1978
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.75.9.4577
Subject(s) - calcium , biophysics , intracellular , ionophore , gap junction , chemistry , coupling (piping) , endogeny , calcium in biology , free nerve ending , biochemistry , biology , anatomy , materials science , organic chemistry , metallurgy
The degree of axo-axonal synaptic coupling between nerve cells in the buccal ganglion of Navanax was investigated in relation to intracellular ionic calcium. Increasing intracellular Ca2+ by injection of Ca2+, injection of Na+, or application of ionophore X537A produced uncoupling after at least 90 min, if metabolic inhibitor was present in the medium. Subsequent removal of the metabolic inhibitor reestablished the coupling in less than 30 min. Injected Sr2+ also mimicked the uncoupling action of Ca2+. The presence of a metabolic inhibitor alone had no effect on the coupling. These results lead to the following conclusions: (i) Uncoupling is due to an increased free Ca2+ concentration at the junctions. (ii) The liberation of endogenous sequestered Ca2+ is not sufficient to produce uncoupling except if an excess Ca2+ had been previously sequestered. The electrical synapses in the buccal ganglion of Navanax thus appear to be affected by Ca2+ in a similar way as gap junctions studied in non-neural tissues.