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

Bain, Allen I.; Quastel, D. M. J.

doi:10.1113/jphysiol.1992.sp019116

Cited by 31 publications

(52 citation statements)

References 31 publications

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“…A suitable candidate is the Ca¥-binding protein synaptotagmin III which, in contrast to synaptotagmin I, has high Ca¥ affinity and functions in the presence of Sr¥ as well as Ca¥ (for review see Geppert & S udhof, 1998). A more traditional explanation is the 'residual ion' model (Dodge et al 1969;Bain & Quastel, 1992;van der Kloot & Molg o, 1993) in which the asynchronous phase is due to Sr¥ accumulating temporarily in the presynaptic terminal (for review see van der Kloot & Molg o, 1994). A mainstay of this hypothesis regarding late release mediated by Sr¥ influx was that, as shown here for central inhibitory synapses, BAPTA AM curtailed Sr¥-induced late release.…”

Section: Discussionmentioning

confidence: 99%

“…BAPTA is known as a rapid, high-affinity chelator for Ca¥, and has been used to buffer Sr¥ (Bain & Quastel, 1992). However, information about its Sr¥-binding properties is not available.…”

Section: Effects Of Exogenous Chelatorsmentioning

confidence: 99%

“…after a presynaptic impulse (Bain & Quastel, 1992;Abdhul-Ghani et al 1996;Behrends & ten Bruggencate, 1998). Since the work of Goda & Stevens, reports have focused on the use of Sr¥ substitution as a tool to determine quantal size and its variation at CNS synapses (Abdhul-Ghani et al 1996;Oliet et al 1996;Morishita & Alger, 1997;Behrends & ten Bruggencate, 1998).…”

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confidence: 99%

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Sr²⁺‐dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro

Rumpel

Behrends

1999

The Journal of Physiology

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In all preparations studied, a characteristic distinction of Sr¥versus Ca¥-mediated synaptic transmission is a reduced early (or phasic) component and an augmented late (or asynchronous) tail of individual miniature-like events called 'late release'. Thus, transmission in Sr¥ is desynchronized with respect to the normal situation. Understanding this non-physiological phenomenon may entail important insights into the mechanisms which under physiological conditions control the kinetics of evoked transmitter release. Thus, have proposed that preferential activation by Sr¥ of late, asynchronous release is due to binding at a secondary, highaffinity divalent cation binding site, where the action of Sr¥ is stronger than that of Ca¥. A high-affinity site in addition to the putative low-affinity receptor involved in synchronous release (cf. Heidelberger et al. 1994) has also been postulated in order to account for use-dependent synaptic facilitation (Yamada & Zucker, 1992). The twobinding-site hypothesis has gained indirect support from experiments on excitatory synapses lacking the presynaptic Ca¥-binding protein synaptotagmin I, where phasic release was suppressed and asynchronous release was intact or increased (Geppert et al. 1994). Alternatively, it has been suggested that a single releaseinducing binding site may suffice to explain Sr¥-induced late release if buffering, extrusion or sequestration are assumed to be less efficient for Sr¥ than for Ca¥ so that free Sr¥ concentration remains elevated for longer times

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Section: Discussionmentioning

confidence: 99%

Section: Effects Of Exogenous Chelatorsmentioning

confidence: 99%

mentioning

confidence: 99%

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Sr²⁺‐dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro

Rumpel

Behrends

1999

The Journal of Physiology

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“…These mPSPs or mPSCs, together with ultrastructural evidence of the existence of synaptic vesicles, provide important support for the quantal nature of chemical synaptic neurotransmission (Fatt & Katz, 1952;Heuser & Reese, 1981;Redman, 1990;Stevens, 1993). Indeed, at many synapses the evoked PSPs or PSCs can be shown to result from a transient (<1 ms duration) enhancement of the probability of occurrence of postsynaptic quantal events (del Castillo & Katz, 1954;Bain & Quastel, 1992;Stevens, 1993). This enhancement of the release rate of quanta of neurotransmitter is related to the entry of calcium (Ca2+) through voltage-activated CaP+ channels in the presynaptic membrane.…”

Section: A Abdul-chani T a Valiante And P S Pennefathermentioning

confidence: 99%

Sr2+ and quantal events at excitatory synapses between mouse hippocampal neurons in culture.

Abdul‐Ghani

Valiante

Pennefather

1996

The Journal of Physiology

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1. Whole-cell for Papp (apparent probability of releasing a quantum at one of those synapses). These parameters predicted the number of observed failures. The observed coefficient of variation for quantal content predicted the observed coefficient of variation of the EPSC amplitude when the coefficient of variability of quantal amplitude of after-discharge mEPSCs was taken into account.6. In six pairs of neurons, where more than 250 evoked events were recorded, the observed amplitude histogram for EPSCs could be approximated by a predicted amplitude distribution generated from the estimated binomial parameters and an empirical function describing the amplitude distribution of after-discharge mEPSCs. 7. The observation that parameters derived from mEPSCs that contribute to the Sr2+-generated after-discharge can predict the shape of the EPSC amplitude distribution and a quantal content consistent with the observed failure rate and EPSC amplitude variance, suggests that this subset of mEPSCs has the same properties as the quantal events released around the time

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“…Other divalent cations such as Ba 2ϩ and Sr 2ϩ are able to move through Ca 2ϩ channels and mimic Ca 2ϩ action (1)(2)(3)(4)(5). The divalent charge carriers affect transmitter release at the neuromuscular junction (1,(5)(6)(7) and the squid giant synapse (3) as well as the neuronal (8)(9)(10)(11)(12)(13) and neuroendocrine cells (14).…”

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Ionic dependence of Ca ²⁺ channel modulation by syntaxin 1A

Wiser

Cohen²,

Atlas³

2002

Proc. Natl. Acad. Sci. U.S.A.

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Alteration of the kinetic properties of voltage-gated2 in all permeating ions tested. The Syn1A-channel interaction, unlike the synaptotagmin-channel interaction, proved significantly more sensitive to the type of permeating ion. It is well established that exocytosis is affected by switching the charge carriers. Based on the present results, we suggest that the channel-Syn1A interaction could respond to the conformational changes induced within the channel during membrane depolarization and divalent ion binding. These changes could partially account for the charge specificity of synaptic transmission as well as for the fast signaling between the Ca 2؉ source and the fusion apparatus of channel-associatedvesicles (CAV). Furthermore, propagation of conformational changes induced by the divalent ions appear to affect the concerted interaction of the channel with the fusion͞docking machinery upstream to free Ca 2؉ buildup and͞or binding to a cytosolic Ca 2؉ sensor. These results raise the intriguing possibility that the channel is the Ca 2؉ sensor in the process of fast neurotransmitter release.exocytosis ͉ synaptotagmin ͉ Ca 2ϩ sensor ͉ strontium ͉ transmitter release

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

Cited by 31 publications

References 31 publications

Sr²⁺‐dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro

Sr²⁺‐dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro

Sr2+ and quantal events at excitatory synapses between mouse hippocampal neurons in culture.

Ionic dependence of Ca ²⁺ channel modulation by syntaxin 1A

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

Cited by 31 publications

References 31 publications

Sr2+‐dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro

Sr2+‐dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro

Sr2+ and quantal events at excitatory synapses between mouse hippocampal neurons in culture.

Ionic dependence of Ca 2+ channel modulation by syntaxin 1A

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Sr²⁺‐dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro

Sr²⁺‐dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro

Ionic dependence of Ca ²⁺ channel modulation by syntaxin 1A