Inhibitory action of nicotinic antagonists on transmitter release at the neuromuscular junction of the rat

Wilson, David F.; West, Andrew E.; Lin, Yeong-Jer

doi:10.1016/0304-3940(95)11274-z

Cited by 12 publications

(11 citation statements)

References 17 publications

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“…In neither synapse is there a change in the rate of spontaneous mEPCs (Frank et al, 2006; our study), such that it appears unlikely that there is an increase in resting presynaptic Ca 2ϩ level. In addition, in both systems the increase in QC is due to an increase in the RRP (Wang et al, 2010b;Müller et al, 2012Müller et al, , 2015 our study) and is not sustained during repetitive stimulation, suggesting a special dependence on rapid vesicle replenishment (Wilson, 1982;Tian et al, 1994;Frank et al, 2006; our study). These findings suggest that the homeostatic regulation of QC is a similar process in the mouse and Drosophila.…”

Section: Discussionmentioning

confidence: 87%

“…In Drosophila, there is a several minute lag between the block of receptors and the upregulation of QC (Frank et al, 2006). (2) When external Ca 2ϩ concentration is reduced, there is no increase in QC following either short-term block (Tian et al, 1994;Wilson et al, 1995; our study) or long-term block (Gallant, 1982;Plomp et al, 1994) of AChRs at the mammalian NMJ. In Drosophila, the increase in QC occurs at both low and normal extracellular Ca 2ϩ levels (Frank et al, 2006;Müller et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

“…The majority of studies suggest that the induction of homeostatic regulation of QC occurs within 5-10 min at both the mammalian and Drosophila NMJ (Wilson, 1982;Tian et al, 1994;Frank et al, 2006;Weyhersmüller et al, 2011), while one study suggested it takes hours (Plomp et al, 1992). No study has been performed to determine the time course of the reversibility of homeostatic regulation of QC.…”

Section: Significance Statementmentioning

confidence: 99%

“…It has been proposed that homeostatic upregulation of QC in Drosophila may be due to the broadening of presynaptic action potentials such that there is prolongation of presynaptic Ca 2ϩ entry (Younger et al, 2013). We examined the effect of broadening the presynaptic action potential on release using 10 M 3,4-DAP to block presynaptic K channels (Thomsen and Wilson, 1983) and found that late release was increased to a greater degree than peak release (Fig.…”

Section: Deconvolution Of Epcs Reveals An Increase In Synchronized Rementioning

confidence: 99%

“…of acetylcholine receptors (AChRs) triggers a compensatory increase in QC (Katz and Miledi, 1978;Cull-Candy et al, 1980;Wilson, 1982;Plomp et al, 1992;Tian et al, 1994;Wang et al, 2010b).…”

Section: Significance Statementmentioning

confidence: 99%

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Reversible Recruitment of a Homeostatic Reserve Pool of Synaptic Vesicles Underlies Rapid Homeostatic Plasticity of Quantal Content

2016

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Homeostatic regulation is essential for the maintenance of synaptic strength within the physiological range. The current study is the first to demonstrate that both induction and reversal of homeostatic upregulation of synaptic vesicle release can occur within seconds of blocking or unblocking acetylcholine receptors at the mouse neuromuscular junction. Our data suggest that the homeostatic upregulation of release is due to Ca 2ϩ -dependent increase in the size of the readily releasable pool (RRP). Blocking vesicle refilling prevented upregulation of quantal content (QC), while leaving baseline release relatively unaffected. This suggested that the upregulation of QC was due to mobilization of a distinct pool of vesicles that were rapidly recycled and thus were dependent on continued vesicle refilling. We term this pool the "homeostatic reserve pool." A detailed analysis of the time course of vesicle release triggered by a presynaptic action potential suggests that the homeostatic reserve pool of vesicles is normally released more slowly than other vesicles, but the rate of their release becomes similar to that of the major pool during homeostatic upregulation of QC. Remarkably, instead of finding a generalized increase in the recruitment of vesicles into RRP, we identified a distinct homeostatic reserve pool of vesicles that appear to only participate in synchronized release following homeostatic upregulation of QC. Once this small pool of vesicles is depleted by the block of vesicle refilling, homeostatic upregulation of QC is no longer observed. This is the first identification of the population of vesicles responsible for the blockade-induced upregulation of release previously described.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Significance Statementmentioning

confidence: 99%

Section: Deconvolution Of Epcs Reveals An Increase In Synchronized Rementioning

confidence: 99%

“…of acetylcholine receptors (AChRs) triggers a compensatory increase in QC (Katz and Miledi, 1978;Cull-Candy et al, 1980;Wilson, 1982;Plomp et al, 1992;Tian et al, 1994;Wang et al, 2010b).…”

Section: Significance Statementmentioning

confidence: 99%

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Reversible Recruitment of a Homeostatic Reserve Pool of Synaptic Vesicles Underlies Rapid Homeostatic Plasticity of Quantal Content

2016

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Blockade of neuronal facilitatory nicotinic receptors containing α3β2 subunits contribute to tetanic fade in the rat isolated diaphragm

Faria

Oliveira

Timóteo

et al. 2003

Synapse

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Nicotinic receptor (nAChR) subtypes involved in pre- and postjunctional actions underlying tetanic fade were studied in rat phrenic-nerve hemidiaphragms. We investigated the ability of subtype-specific nAChR antagonists to depress nerve-evoked contractions and [(3)H]-acetylcholine ([(3)H]-ACh) release. Muscle tension was transiently increased during brief high frequency trains (50 Hz for 5 sec). The rank potency order of nAChR antagonists to reduce tetanic peak tension was alpha-bungarotoxin > d-tubocurarine >> mecamylamine > hexamethonium. Reduction of maximal tetanic tension produced by dihydro-beta-erythroidine (0.03-10 microM), methyllycaconitine (0.003-3 microM), and alpha-conotoxin MII (0.001-0.3 microM) did not exceed 30%. Besides reduction of peak tension d-tubocurarine (0.1-0.7 microM), mecamylamine (0.1-300 microM), and hexamethonium (30-3,000 microM) also caused tetanic fading. With alpha-conotoxin MII (0.001-0.3 microM) and dihydro-beta-erythroidine (0.03-10 microM), tetanic fade was evident only after decreasing the safety factor of neuromuscular transmission (with high magnesium ions, 6-7 mM). The antagonist rank potency order to reduce evoked (50 Hz for 5 sec) [(3)H]-ACh release from motor nerve terminals was alpha-conotoxin MII (0.1 microM) > dihydro-beta-erythroidine (1 microM) approximately d-tubocurarine (1 microM) > mecamylamine (100 microM) > hexamethonium (1,000 microM). When applied in a concentration (0.3 microM) above that producing tetanic paralysis, alpha-bungarotoxin failed to affect [(3)H]-ACh release. Data obtained suggest that postjunctional neuromuscular relaxants interact with alpha-bungarotoxin-sensitive nicotinic receptors containing alpha1-subunits, whereas blockade of neuronal alpha3beta2-containing receptors produce tetanic fade by breaking nicotinic autofacilitation of acetylcholine release.

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Homeostatic Plasticity of the Mammalian Neuromuscular Junction

Engisch

Wang

Rich

2022

Advances in Neurobiology

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Inhibitory action of nicotinic antagonists on transmitter release at the neuromuscular junction of the rat

Cited by 12 publications

References 17 publications

Reversible Recruitment of a Homeostatic Reserve Pool of Synaptic Vesicles Underlies Rapid Homeostatic Plasticity of Quantal Content

Reversible Recruitment of a Homeostatic Reserve Pool of Synaptic Vesicles Underlies Rapid Homeostatic Plasticity of Quantal Content

Blockade of neuronal facilitatory nicotinic receptors containing α3β2 subunits contribute to tetanic fade in the rat isolated diaphragm

Homeostatic Plasticity of the Mammalian Neuromuscular Junction

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