Abstract
Residual Ca 2+ can accumulate in the nerve terminal during repetitive stimulation; thus, the basis for short-term facilitation (STF). The plasmalemmal Na + /Ca 2+ exchanger (NCX), the Ca 2+ -ATPase (PMCA) and the sarcoplasmic/endoplasmic reticulum Ca 2+ -ATPase (SERCA) on the endoplasmic reticulum are three important Ca 2+ regulatory processes in controlling (Ca 2+ )i. The role of these (Ca 2+ )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 (Ca 2+ )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 Ca 2+ extrusion mechanisms during STF.
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