Changes in MEPP frequency during depression of evoked release at the frog neuromuscular junction.

Abstract

1. Endplate potentials (EPPs) and miniature endplate potentials (MEPPs) were recorded from frog neuromuscular junctions bathed in Ringer solutions containing normal (1P8 mM) or high (3-6 mM) Ca2". The peptide toxin /s-conotoxin GIIIA was added to the Ringer solution to prevent muscle action potentials and contraction. 2. The nerve was stimulated with conditioning trains of 200-4800 impulses applied at 20 impulses s' to characterize the effects of repetitive stimulation on changes in EPP amplitude and MEPP frequency under high quantal conditions. 3. MEPP frequency was dramatically increased during and immediately following repetitive stimulation under high quantal conditions, whereas EPP amplitude was greatly depressed. There was no effect of repetitive stimulation on MEPP amplitude. 4. Following the conditioning stimulation the increase in MEPP frequency decayed back to the control level with a time course that could be described by four exponentials. The time constants of these exponentials were very similar to those that describe the components of stimulation-induced increases in EPP amplitude and MEPP frequency observed under low quantal conditions when depression is absent. 5. The results of this study indicate that depression and the components of stimulationinduced increases in release (facilitation, augmentation and potentiation) can be present at the same time, suggesting that the mechanism of depression involves different underlying factors from the mechanism(s) responsible for increases in release. They also indicate either that depression selectively affects only those quanta destined to be released in direct response to the nerve action potential, which would suggest that EPPs and MEPPs arise from different pools of transmitter, or that depression in some way affects a step in the release process involved only in evoked release, and not asynchronous (spontaneous) release.

Calcium-Dependent Paired-Pulse Facilitation of Miniature EPSC Frequency Accompanies Depression of EPSCs at Hippocampal Synapses in Culture

“…Thus, it seemed that there could be a differential plasticity between synchronous and asynchronous release during tetanic stimuli. This increase in mEPSC frequency accompanying tetanic stimulation was consistent with the results of experiments at the frog neuromuscular junction (Zengel and Sosa, 1994) and at the avian nucleus magnocellularis synapse (Zhang and Trussell, 1994) showing a tetanic increase in mEPSC frequency.…”

Adaptive Depression in Synaptic Transmission in the Nucleus of the Solitary Tract afterIn VivoChronic Intermittent Hypoxia: Evidence for Homeostatic Plasticity

“…However, miniature and asynchronous release was greater in CIH rather than reduced. Directionally different results have been observed previously in which a decrease in evoked EPSP/EPSCs or endplate potentials is accompanied by increases or unaltered miniature events (Eliot et al, 1994;Zengel and Sosa, 1994;Cummings et al, 1996;Pan et al, 1996). We propose that the effects of CIH on the frequency of mEPSCs and aEPSCs versus the eEPSCs reflect differential regulation of release of two vesicular pools.…”

The Number of Components of Enhancement Contributing to Short-Term Synaptic Plasticity at the Neuromuscular Synapse during Patterned Nerve Stimulation Progressively Decreases As Basal Release Probability Is Increased from Low to Normal Levels by Changing Extracellular Ca2+

“…That F1, F2, A, and P components of miniature EPP frequency (Zengel and Magleby, 1981) are still observed in the presence of depression (Zengel and Sosa, 1994) suggests that the presumed Ca 2ϩ -dependent driving processes for the enhancement components (Kamiya and Zucker, 1994;Tank and Zucker, 1997;Suzuki et al, 2000;Zucker and Regehr, 2002;Kalkstein and Magleby, 2004;García-Chacó n et al, 2006) are still present during marked rundown, but uncoupled from evoked release so that F2, A, and P of evoked release are not detected. The reason for this uncoupling during marked depression is not known but may be related to the fact that spontaneous and evoked release may have differences in location and/or molecular components (Washbourne et al, 2002;Zucker and Regehr, 2002;Maximov and Südhof, 2005;Wadel et al, 2007;Young and Neher, 2009;Yoshihara et al, 2010).…”

“…Such surface recording gives a good measure of average intracellular response (Magleby, 1973a). Under the conditions of our experiments, where EPP amplitudes are typically a few millivolts or less because of low quantal content or the presence of curare, nonlinear summation of EPP amplitudes (McLachlan and Martin, 1981) is minimal and quantal size (miniature EPP amplitude) and postsynaptic sensitivity remain constant during a stimulation train (Magleby and Pallotta, 1981;Zengel and Sosa, 1994). Hence, observed changes in EPP amplitudes (synaptic strength) and STP in our experiments are presynaptic in origin, arising from a change in the number of vesicles whose contents are released by each nerve impulse.…”

“…End plate potential (EPP) amplitude is used to track STP, as under the conditions of our experiments EPP amplitude is proportional to the number of synaptic vesicles releasing their transmitter after each nerve impulse (Zengel and Sosa, 1994;Zengel and Magleby, 1981). EPP amplitudes were recorded from the sartorius nerve-muscle preparation of northern grass frogs (Rana pipiens) of either sex with a surface electrode, as described previously (Magleby, 1973a).…”