|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Over the last 50 years, mechanisms controlling the release of neurotransmitter have been studied intensively (see reviews by Parnas et al. 1994, 1997; Zucker, 1996). Despite these efforts, the molecular mechanisms that transduce the physiological signal, the action potential, into release of neurotransmitter remain a mystery. To understand these mechanisms, it is useful to study two variables: the amount of release (quantal content) and the time course of release (reflected by the synaptic delay histogram; Katz & Miledi, 1965), especially if (as argued below) different mechanisms control these two variables.
It is widely accepted that entry of Ca2+ and its accumulation to high levels near release sites triggers the initiation of release. Furthermore, the rapid removal of Ca2+ from the release sites has been hypothesized to be responsible for cessation of release (the Ca2+ microdomain hypothesis; see review by Zucker, 1996). Accordingly, a change in the kinetics of entry and removal of Ca2+ is expected to affect both the quantal content and the time course of release. For example, a smaller quantal content should be associated with a shorter period of release. However, this straightforward prediction is not met experimentally. For example, Andreu & Barret (1980) showed that in the frog neuromuscular junction (NMJ), the time at which release starts and stops - the time course of release - remained the same even with a many-fold change in the quantal content. In other studies, synaptic delay histograms were found to be independent of experimental manipulations known to affect Ca2+ entry or removal. For example, when a fast Ca2+ buffer was injected into presynaptic terminals (Hochner et al. 1991), the quantal content declined markedly, indicating a faster removal of Ca2+, but the reduction in quantal content was not accompanied by a change in the time course of release. Taken together, these findings suggest that different processes control quantal content and the time course of release.
This article has been cited by other articles:
![]() |
E. E Nikolsky, F. Vyskocil, E. A Bukharaeva, D. Samigullin, and L. G Magazanik Cholinergic regulation of the evoked quantal release at frog neuromuscular junction J. Physiol., October 1, 2004; 560(1): 77 - 88. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. Slutsky, J. Wess, J. Gomeza, J. Dudel, I. Parnas, and H. Parnas Use of Knockout Mice Reveals Involvement of M2-Muscarinic Receptors in Control of the Kinetics of Acetylcholine Release J Neurophysiol, April 1, 2003; 89(4): 1954 - 1967. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. A. Bukharaeva, D. Samigullin, E. Nikolsky, and F. Vyskocil Protein kinase A cascade regulates quantal release dispersion at frog muscle endplate J. Physiol., February 1, 2002; 538(3): 837 - 848. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |