Inhibitory action of Ca2+ on spontaneous transmitter release at motor nerve terminals in a high K+ solution

Ohta, Y.; Kuba, Kenji

doi:10.1007/bf00584183

Cited by 17 publications

(6 citation statements)

References 40 publications

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“…In contrast, when Ψ m was depolarized (filled circles), asynchronous release rose to much higher levels during stimulation, reaching a peak and then declining somewhat towards the end of the train. Such reductions in asynchronous release under conditions expected to elevate cytosolic [Ca 2+ ] to very high levels have also been reported by Ohta & Kuba (1980) and Calupca et al . (2001).…”

Section: Resultssupporting

confidence: 82%

Mitochondrial Ca2+ uptake prevents desynchronization of quantal release and minimizes depletion during repetitive stimulation of mouse motor nerve terminals

David¹,

Barrett²

2003

J Physiology

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Section: Resultssupporting

confidence: 82%

Mitochondrial Ca2+ uptake prevents desynchronization of quantal release and minimizes depletion during repetitive stimulation of mouse motor nerve terminals

David¹,

Barrett²

2003

J Physiology

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“…The same sort of question hangs over the idea that hypertonic and hypotonic solutions act by changing [Ca2+], (Shimoni, Alnaes & Rahamimoff, 1977). Moreover there is some evidence that an over-all rise in [Ca2+], can decrease the probability of release (Ohta & Kuba, 1980; Van der Kloot & Latta, in preparation), and that release at the squid synapse falls when [Ca2+], is still high (Miledi & Parker, 1981). Perhaps these uncertainties can be resolved by the use of intracellular Ca2+ buffers (Tsien, 1981 …”

Section: Methodsmentioning

confidence: 99%

The relation between tonicity and impulse‐evoked transmitter release in the frog

Kita

Narita

Kloot

1982

The Journal of Physiology

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SUMMARY1. The increase in miniature end-plate potential (m.e.p.p.) frequency in response to tetanic stimulation ofthe motor nerve at frog neuromuscular junctions in Ca2+-free, Mg2+ EGTA-containing (0 Ca2+-Mg2+ EGTA) solutions of varying tonicity has been studied. The response to stimulation is markedly increased in hypertonic solutions and is decreased in hypotonic solutions. Under these conditions changes in tonicity have comparable effects on stimulated and spontaneous quantal release.2. The tonicity was raised by adding sucrose, NaCl or glycine to the extracellular solution. The effects of the addition depended primarily on the increase in osmolarity of the solution, not on the chemical species producing it.3. The tonicity was decreased by lowering [NaCl]0. The hypotonic solution decreased the response to tetanic stimulation. When the tonicity of the solution with the low [NaCl]. was restored to normal by adding sucrose, the response was restored to its usual level. These results suggest that in 0 Ca2+-Mg2+ EGTA solutions stimulation does not enhance the probability of quantal release by raising [Na+]i.4. Repeated bouts of tetanic stimulation produced almost identical responses. In some instances the frequency continued to rise after the end ofthe tetanic stimulation, as reported by . This suggests that the stimulation of the nerve leads to the elevation within the terminal of a substance that in turn liberates an activator for quantal release.5. The Q10 for the increase in probability of quantal release is as high as 7. High Q10 values have also been reported for spontaneous m.e.p.p. frequencies. Tonicity and temperature appear to affect spontaneous and stimulated quantal release similarly.

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“…The evidence, however, for the involvement of CICR in exocytosis at presynaptic terminals is rather indirect. Caffeine and theophylline, activators of ryanodine receptor, have been known to enhance both the evoked and spontaneous release of transmitters in several types of terminals, including frog motor nerve terminals ( Elmqvist and Feldman, 1965 ; Onodera, 1973 ; Ohta and Kuba, 1980 ; Lockerbie and Gordon-Weeks, 1986 ; Tóth et al, 1990 ). Recent studies suggested ryanodine-sensitive components of tetanus-induced rise in [Ca 2+ ] i and transmitter release in autonomic nerve terminals ( Peng, 1996 ; Smith and Cunnane, 1996 ).…”

Section: Introductionmentioning

confidence: 99%

A Ca2+-induced Ca2+ Release Mechanism Involved in Asynchronous Exocytosis at Frog Motor Nerve Terminals

Narita

Akita

Osanai

et al. 1998

The Journal of General Physiology

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The extent to which Ca2+-induced Ca2+ release (CICR) affects transmitter release is unknown. Continuous nerve stimulation (20–50 Hz) caused slow transient increases in miniature end-plate potential (MEPP) frequency (MEPP-hump) and intracellular free Ca2+ ([Ca2+]i) in presynaptic terminals (Ca2+-hump) in frog skeletal muscles over a period of minutes in a low Ca2+, high Mg2+ solution. Mn2+ quenched Indo-1 and Fura-2 fluorescence, thus indicating that stimulation was accompanied by opening of voltage-dependent Ca2+ channels. MEPP-hump depended on extracellular Ca2+ (0.05–0.2 mM) and stimulation frequency. Both the Ca2+- and MEPP-humps were blocked by 8-(N,N-diethylamino)octyl3,4,5-trimethoxybenzoate hydrochloride (TMB-8), ryanodine, and thapsigargin, but enhanced by CN−. Thus, Ca2+-hump is generated by the activation of CICR via ryanodine receptors by Ca2+ entry, producing MEPP-hump. A short interruption of tetanus (<1 min) during MEPP-hump quickly reduced MEPP frequency to a level attained under the effect of TMB-8 or thapsigargin, while resuming tetanus swiftly raised MEPP frequency to the previous or higher level. Thus, the steady/equilibrium condition balancing CICR and Ca2+ clearance occurs in nerve terminals with slow changes toward a greater activation of CICR (priming) during the rising phase of MEPP-hump and toward a smaller activation during the decay phase. A short pause applied after the end of MEPP- or Ca2+-hump affected little MEPP frequency or [Ca2+]i, but caused a quick increase (faster than MEPP- or Ca2+-hump) after the pause, whose magnitude increased with an increase in pause duration (<1 min), suggesting that Ca2+ entry-dependent inactivation, but not depriming process, explains the decay of the humps. The depriming process was seen by giving a much longer pause (>1 min). Thus, ryanodine receptors in frog motor nerve terminals are endowed with Ca2+ entry-dependent slow priming and fast inactivation mechanisms, as well as Ca2+ entry-dependent activation, and involved in asynchronous exocytosis. Physiological significance of CICR in presynaptic terminals was discussed.

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Inhibitory action of Ca2+ on spontaneous transmitter release at motor nerve terminals in a high K+ solution

Cited by 17 publications

References 40 publications

Mitochondrial Ca2+ uptake prevents desynchronization of quantal release and minimizes depletion during repetitive stimulation of mouse motor nerve terminals

Mitochondrial Ca2+ uptake prevents desynchronization of quantal release and minimizes depletion during repetitive stimulation of mouse motor nerve terminals

The relation between tonicity and impulse‐evoked transmitter release in the frog

A Ca2+-induced Ca2+ Release Mechanism Involved in Asynchronous Exocytosis at Frog Motor Nerve Terminals

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