Modulation of Quantal Synaptic Release by Serotonin and Forskolin in Crayfish Motor Nerve Terminals

  • J. Dudel
Part of the NATO ASI Series book series (volume 19)


In crustacea, serotonin is released into the haemolymph and acts as a neurohormone and modulator at central and peripheral neurons (see Kravitz et al. 1983, Harris-Warrick and Kravitz 1984). Serotonin applied to neuromuscular junctions increases excitatory postsynaptic potentials (Grundfest and Reuben 1961, Dudel 1965, Wheal and Kerkut 1976, Enyeart 1981, Glusman and Kravitz 1982, Fischer and Florey 1983, Dixon and Atwood 1985). The increased synaptic potentials are due to enhanced release of transmitter quanta from motor nerve terminals (Dudel 1965, Glusman and Kravitz 1982, Dixon and Atwood 1985). These presynaptic effects of serotonin were suggested to reflect improvement of the action potential in the terminal nerve branch (Dudel 1965), or increases of the Ca concentration in the terminal (Glusman and Kravitz 1982, Dixon and Atwood 1985). These investigations have elicited release by action potentials and employed bath application of serotonin. Effects on the action potential and its conduction could not be distinguished from changes in the coupling between depolarization and release. In the present study excitation of the nerve terminals could be blocked depolarizing them with graded pulses, and serotonin was applied only to the terminal under investigation.


Magnesium Adenosine Serotonin Acetylcholine Forskolin 


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Copyright information

© Springer-Verlag Berlin Heidelberg 1988

Authors and Affiliations

  • J. Dudel
    • 1
  1. 1.Physiologisches InstitutTechnische Universität MünchenMünchen 40Federal Republic of Germany

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