Abstract

Residual Ca2+ can accumulate in the nerve terminal during repetitive stimulation; thus, the basis for short-term facilitation (STF). The plasmalemmal Na+/Ca2+ exchanger [NCX], the Ca2+-ATPase (PMCA) and the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) on the endoplasmic reticulum are three important Ca2+ regulatory processes in controlling [Ca2+]i. The role of these [Ca2+]i regulators in the development and maintenance of STF was addressed at the neuromuscular junction. When the NCX is compromised by reduced [Na+]o, the EPSP amplitudes decrease, but with KB-R7943 (a reverse blocker of NCX) the amplitude increases. Compromising the PMCA with pH 8.8 produces an increase in EPSP amplitudes, but treatments with carboxyeosin (a blocker of PMCA) produced mixed results. Blocking the SERCA increases EPSP amplitudes. Facilitation was only slighted altered in some conditions with these manipulations. The results support the view that release is not saturated during a plateau phase of STF since the terminal is able to reach a new plateau with higher stimulation frequency or an altered [Ca2+]i. Multiple approaches in compromising the NCX and PMCA are presented. These findings are significant because there is a rapid alteration in transmission when compromising Ca2+ extrusion mechanisms during STF.

Document Type

Article

Publication Date

2010

Notes/Citation Information

Published in The Open Physiology Journal, v. 3, p. 37-50.

© Desai-Shah and Cooper; Licensee Bentham Open.

This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

Digital Object Identifier (DOI)

http://dx.doi.org/10.2174/1874360901003010037

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