Protein kinase C is required for long-lasting synaptic enhancement by the
neuropeptide DRNFLRFamide in crayfish.
Rainer W. Friedrich, Gregory F. Molnar, Michael Schiebe and A. Joffre Mercier.
Department of Biological Sciences, Brock University, St. Catharines, ON L2S
3A1, Canada. Abteilung fr angewandte Physiologie, Universitt Ulm,
Einsteinallee 11, D-89069 Ulm, Germany. Max-Planck-Institut fr
Entwicklungsbiologie, Abteilung Physikalische Biologie, Spemannstr. 35
D-72076 Tbingen, Germany.
APStracts 4:317N, 1997.
ABSTRACT
The FMRFamide-related neuropeptide DRNFLRFamide (DF2) induces a long-lasting
enhancement of synaptic transmission at neuromuscular junctions on the
crayfish deep abdominal extensor muscles. Here we investigated the function of
protein kinase C (PKC) in this effect because PKC has been implied in the
control of long-term synaptic modulation in other systems. The general kinase
antagonist staurosporine reduced both the initial increase in EPSP amplitude
and the duration of synaptic enhancement. Unlike staurosporine, the selective
PKC inhibitors, chelerythrine and bisindolylmaleimide, augmented the initial
EPSP increase. However, like staurosporine, they also reduced the duration of
synaptic enhancement. The PKC activator, phorbol-12-myristate 13-acetate,
induced a long-lasting synaptic enhancement that was blocked by chelerythrine.
These results show that synaptic enhancement by DF2 is mediated by different
intracellular signaling systems that act in temporal sequence. The initial
increase in EPSP amplitudes is negatively regulated by PKC and involves
another, staurosporine-sensitive, kinase, whereas the maintenance of synaptic
enhancement requires PKC.
Received 18 August 1997; accepted in final form 7 November 1997.
APS Manuscript Number J681-7.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 12 December 1997