Abstract
The calcium binding protein calmodulin (CaM) appears to mediate a number of Ca2+ activated cellular processes(1), included among which are the secretary activities of a variety of cell types (2). Of particular interest is the fact that CaM has been implicated in the release of transmitters from synaptosomes. Using this preparation De Lorenzo and his group have shown that CaM is present in the presynaptic cytoplasm and in synaptic vesicle preparations and that it has a variety of effects on synaptosomal componenents that are suggestive of an involvement of CaM in exocytotic transmitter release (3). These workers have also shown that transmitter release from synaptosomes is inhibited by CaM-interacting drugs, their hypothesis being that in the intact synaptosome interaction of Ca2+ with CaM activates a kinase resulting in phosphorylation of specific proteins (possibly tubulin) and that this phosphorylation is an important step in excitation secretion coupling (3).
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Cheung WY: Calmodulin plays a pivotal role in cellular regulation. Science 207: 19–27, 1980.
Publicover SJ: Presynaptic action of trifluoperazine at the frog neuromuscular junction. Naunyn-Schmiedeberg’s Arch Pharmacol 322: 83–88, 1983.
De Lorenzo RJ: Calmodulin in neurotransmitter release and synaptic function. Fed Proc 41: 2265–2272,1982.
Landry Y, Amellal M, Ruckstuhl M: Can calmodulin inhibitors be used to probe calmodulin effects? Biochem Pharmacol 30: 2031–2032, 1981.
Cheng K-C, Lambert JJ, Henderson EG, Smilowitz H, Epstein P: Postsynaptic inhibition of neuromuscular transmission by trifluoperazine. J.Pharm Exp Ther 217: 44–50, 1981.
Lev-Tov A, Rahamimoff R: A study of tetanic and post-tetanic poten-tiation of miniature end-plate potentials at the frog neuromuscular junction. J Physiol Lond 309: 247–273, 1980.
Douglas WW, Nemeth EF: On the calcium receptor activating exocytosis: inhibitory effect of calmodulin-interacting drugs on rat mast cells. J Physiol Lond 323: 229–244, 1982.
Leung MTK, Collard KJ: The effect of trifluoperazine and R24571 on the K+-evoked release of 5-hydroxytryptamine from super-fused synapt-osomes. Neuropharmacol 22: 1095–1099, 1983.
Van Belle H: R24571: a potent inhibitor of calmodulin activated enzymes. Cell Calcium 2:483–494 (1981).
Statham HE, Duncan CJ, Publicover SJ: Dual effect of 2, 4-dinitrophinol on the spontaneous release of transmitter at the frog neuromuscular junction. Biochem Pharmacol 27: 2199–2022. 1978.
Argov Z, Yaari Y: The action of chlorpromazine at an isolated cholinergic synapse. Brain Res 164: 227–236, 1979.
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1986 Martinus Nijhoff Publishing, Boston
About this chapter
Cite this chapter
Publicover, S.J., Sahaf, Z.Y. (1986). Calmodulin Inhibitors and Transmitter Release at the Frog Neuromuscular Junction. In: Rahamimoff, R., Katz, B. (eds) Calcium, Neuronal Function and Transmitter Release. Topics in the Neurosciences, vol 1. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2307-5_36
Download citation
DOI: https://doi.org/10.1007/978-1-4613-2307-5_36
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4612-9420-7
Online ISBN: 978-1-4613-2307-5
eBook Packages: Springer Book Archive