HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Naves, L. A. Articles by Kloot, W. V. d. Search for Related Content PubMed PubMed Citation Articles by Naves, L. A. Articles by Kloot, W. V. d.

Repetitive nerve stimulation decreases the acetylcholine content of quanta at the frog neuromuscular junction

Ligia A. Naves and William Van der Kloot

1. We investigated how elevated quantal release produced by motor nerve stimulation affects the size of the quanta. The motor nerve was stimulated at 10 Hz in preparations in which excitation-contraction coupling was disrupted. Two hundred stimuli reduced the size of the time integrals of the miniature endplate currents (MEPCs), measured at the same junction immediately after stimulation, by 16 %. Three thousand stimuli reduced size by 23 %. When the solution contained 10 µM neostigmine (NEO) 3000 stimuli reduced MEPCs by 60 %, because with acetylcholinesterase (AChE) inhibited, MEPC size is more sensitive to changes in acetylcholine (ACh) content. Similar decreases in miniature endplate potential size (MEPP) followed repetitive stimulation of contracting preparations.
2. The depolarization produced by iontophoretic pulses of ACh was scarcely changed by 3000 nerve stimuli at 10 Hz, suggesting that the decreases in miniature sizes are largely due to less ACh released per quantum.
3. Following 3000 stimuli at 10 Hz the sizes of the MEPCs increased back to pre-stimulus values with a half-time of 8-10 min. Recovery was blocked by (-)-vesamicol (VES), by hemicholinium-3 (HC3) and by nicotinic cholinergic agonists - all of which inhibit ACh loading into synaptic vesicles.
4. The number of quanta in the total store was estimated by releasing them with carbonyl cyanide m-chlorophenylhydrazone (CCCP). CCCP releases fewer quanta after stimulation than from unstimulated controls. After resting for hours following stimulation, the releasable number increased, even when ACh loading inhibitors were present.
5. We conclude that the inhibitors do not block a significant fraction of the ACh loading into reformed reserve vesicles and propose that ACh can be loaded in a series of steps.

This article has been cited by other articles:

				X. Wang, Y. Li, K. L. Engisch, S. T. Nakanishi, S. E. Dodson, G. W. Miller, T. C. Cope, M. J. Pinter, and M. M. Rich Activity-Dependent Presynaptic Regulation of Quantal Size at the Mammalian Neuromuscular Junction In Vivo J. Neurosci., January 12, 2005; 25(2): 343 - 351. [Abstract] [Full Text] [PDF]

				N. Axmacher, M. Stemmler, D. Engel, A. Draguhn, and R. Ritz Transmitter Metabolism as a Mechanism of Synaptic Plasticity: A Modeling Study J Neurophysiol, January 1, 2004; 91(1): 25 - 39. [Abstract] [Full Text]

				J. D. Talbot, G. David, and E. F. Barrett Inhibition of Mitochondrial Ca2+ Uptake Affects Phasic Release From Motor Terminals Differently Depending on External [Ca2+] J Neurophysiol, July 1, 2003; 90(1): 491 - 502. [Abstract] [Full Text] [PDF]

				S. O. Rizzoli and W. J. Betz Effects of 2-(4-Morpholinyl)-8-Phenyl-4H-1-Benzopyran-4-One on Synaptic Vesicle Cycling at the Frog Neuromuscular Junction J. Neurosci., December 15, 2002; 22(24): 10680 - 10689. [Abstract] [Full Text] [PDF]