Quantal transmitter release mediated by strontium at the mouse motor nerve terminal.

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Abstract
1. In isolated mouse diaphragm, nerve stimulation in the presence of Sr2+ evokes phasic quantal transmitter release (endplate potentials, EPPs) with the same time course as in the presence of Ca2+. 2. Brief tetanic trains of nerve stimuli in the presence of Sr2+ cause an increase in quantal content of EPPs accompanied by an increase in the frequency of miniature EPPs (MEPPs); the latter persists as a 'tail' that subsides within about a second. Pseudo-random stimulation sequences were used to characterize these changes. 3. The fourth root of MEPP frequency during or after stimulation rose and fell in accordance with first order kinetics with the same time constants for rising and falling phases, in agreement with a 'residual ion' model in which (a) each nerve impulse causes the same entry of Sr2+ into the nerve terminal, (b) transmitter release (MEPP frequency) is proportional to the fourth power of [Sr2+] at release sites, and (c) Sr2+ removal is a first order process with a time constant of about 250 ms. 4. After exposure to bis (O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, acetoxymethyl ester form (BAPTA AM), 'Sr2+ tails' of MEPP frequency were reduced in magnitude and prolonged. 5. During stimulation trains, growth of phasic transmitter release rates (and quantal content of EPPs) were related to growth of MEPP frequency in almost exact agreement with a residual ion model, in which 'phasic' release (EPPs) and MEPP frequency are governed by the same equation, with the same parameters, and without any effect of depolarization per se to affect phasic release. 6. Prolonged (1 s) nerve terminal depolarizations in the presence of Sr2+ produce increased MEPP frequency with a time course corresponding to a model in which depolarization per se has little or no effect to increase transmitter release. 7. It was concluded that in the presence of Sr2+ the intense 'phasic' acceleration of quantal release induced by nerve impulse manifest in an EPP can be attributed to a transient rise of intracellular [Sr2+] in the vicinity of release sites, while the modulation of 'phasic' release by antecedent nerve impulses can be attributed to residual Sr2+ which is also manifest in a rise in MEPP frequency.