Both augmentation and potentiation occur independently of internal Ca2+ at the frog neuromuscular junction

Tanabe, Noriko; Kijima, Hiroshi

doi:10.1016/0304-3940(89)90280-2

Cited by 20 publications

(31 citation statements)

References 17 publications

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“…We have confirmed previous observations (Charlton & Iwanchyshyn, 1986;Tanabe & Kijima, 1989) that treatment with the permeant calcium chelator BAPTA/AM can reduce electrically evoked neurotransmitter release from an intact preparation. Quin-2/AM, another permeant intracellular Ca2" chelator (Tsien, 1981) When BAPTA is injected into the squid giant neurone to a concentration of 4mm, the postsynaptic response, and by inference the transmitter release, was reduced by 80% (Llinas, 1991).…”

Section: Discussionsupporting

confidence: 91%

“…BAPTA/AM (1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetomethylester) is such a compound (Tsien, 1980). BAPTA/AM has been used to study the role of intracellular calcium changes in the regulation of neurotransmitter release from the crayfish neuromuscular junction (Charlton & Iwanchyshyn, 1986) and the frog endplate (Tanabe & Kijima, 1989).…”

Section: Introductionmentioning

confidence: 99%

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Effect of an intracellular calcium chelator on the regulation of electrically evoked [³H]‐noradrenaline release from rat hippocampal slices

Fredholm

1993

British J Pharmacology

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1 The electrically (3 Hz, 5 min) evoked [3H]-noradrenaline ([3H]-NA) release from rat hippocampal slices was reduced by prior treatment of the slices with 1,2-bis(2-aminophenoxy)ethane-N,N,N'N'-tetraacetomethylester (BAPTA/AM) in a concentration-(10 to 500 JM) dependent manner (40% at 30 JM). Reduction of medium calcium from 1.3 to 0.5 mm caused a larger (70%) decrease. BAPTA free acid (100 mM), a non-permeable Ca2+-chelator had no significant effect.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Effect of an intracellular calcium chelator on the regulation of electrically evoked [³H]‐noradrenaline release from rat hippocampal slices

Fredholm

1993

British J Pharmacology

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“…This form of modulation occurs through either strengthening (referred to as facilitation, augmentation, or potentiation, depending on the duration) or weakening (depression) of the synaptic response during a train of action potential stimuli (Eccles et al 1941;Feng 1941;Fisher et al 1997;Magleby 1987;Zucker and Regehr 2002). In the frog NMJ, facilitation is a prominent form of short-term plasticity extending over tens to hundreds of milliseconds after an action potential (Mukhamedyarov et al 2006;Tanabe and Kijima 1992;present study). During a pair or train of stimuli, the magnitude of synaptic vesicle release in the frog NMJ can increase to several times the size of the initial response (Cho and Meriney 2006;Tanabe and Kijima 1989).…”

mentioning

confidence: 97%

“…In the frog NMJ, facilitation is a prominent form of short-term plasticity extending over tens to hundreds of milliseconds after an action potential (Mukhamedyarov et al 2006;Tanabe and Kijima 1992;present study). During a pair or train of stimuli, the magnitude of synaptic vesicle release in the frog NMJ can increase to several times the size of the initial response (Cho and Meriney 2006;Tanabe and Kijima 1989).…”

mentioning

confidence: 97%

“…Since the seminal studies of synaptic function at the frog neuromuscular junction (NMJ) by Katz and coworkers (Fatt and Katz 1953;Miledi 1965a, 1968), a large number of experimental and, more recently, computational studies have been conducted to investigate synaptic facilitation mechanisms (Magleby 1979;Matveev et al 2006;Tang et al 2000;Tank et al 1995;Yamada and Zucker 1992). In addition, integrative computer models have been developed to study synaptic vesicle priming, facilitation, and depression (Dittman et al 2000;Pan and Zucker 2009).…”

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confidence: 99%

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New insights into short-term synaptic facilitation at the frog neuromuscular junction

Kelly

Ingram

et al. 2015

Journal of Neurophysiology

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Short-term synaptic facilitation occurs during high-frequency stimulation, is known to be dependent on presynaptic calcium ions, and persists for tens of milliseconds after a presynaptic action potential. We have used the frog neuromuscular junction as a model synapse for both experimental and computer simulation studies aimed at testing various mechanistic hypotheses proposed to underlie short-term synaptic facilitation. Building off our recently reported excess-calcium-binding-site model of synaptic vesicle release at the frog neuromuscular junction (Dittrich M, Pattillo JM, King JD, Cho S, Stiles JR, Meriney SD. Biophys J 104: 2751–2763, 2013), we have investigated several mechanisms of short-term facilitation at the frog neuromuscular junction. Our studies place constraints on previously proposed facilitation mechanisms and conclude that the presence of a second class of calcium sensor proteins distinct from synaptotagmin can explain known properties of facilitation observed at the frog neuromuscular junction. We were further able to identify a novel facilitation mechanism, which relied on the persistent binding of calcium-bound synaptotagmin molecules to lipids of the presynaptic membrane. In a real physiological context, both mechanisms identified in our study (and perhaps others) may act simultaneously to cause the experimentally observed facilitation. In summary, using a combination of computer simulations and physiological recordings, we have developed a stochastic computer model of synaptic transmission at the frog neuromuscular junction, which sheds light on the facilitation mechanisms in this model synapse.

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Effects of calcium channel blockers on stimulation‐induced changes in transmitter release at the frog neuromuscular junction

Zengel

Lee

Sosa

et al. 1993

Synapse

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We have examined the effects of various calcium channel blockers on stimulation-induced changes in end-plate potential (EPP) amplitude at the frog neuromuscular junction. We found that the addition of small concentrations (1-10 microM) of Cd2+ to the low calcium bathing Ringer reduced both the control EPP amplitude and the increase in EPP amplitude that normally occurs during repetitive stimulation under low quantal conditions. These effects of Cd2+, which developed rapidly following its addition to the bathing solution and were equally rapidly reversed, resulted from changes in the amount of transmitter released from the nerve terminal. The major effect of Cd2+ appeared to be on the facilitation and augmentation components of increased release. Cd2+ had little or no effect on potentiation of release. The other divalent cations tested, Zn2+, Co2+, and Ni2+, also decreased both control EPP amplitude and the stimulation-induced increase in EPP amplitude, but higher concentrations (> 100 microM) of these cations were required. The order of effectiveness in reducing stimulation-induced increases in EPP amplitude was: Cd2+ >>> Co2+,Zn2+ > Ni2+. The organic calcium channel blockers verapamil (20-100 microM) and nimodipine (20-50 microM) had little effect on stimulation-induced increases in EPP amplitude. The results of this study are consistent with previous suggestions that the different components of increased release represent different mechanisms. Furthermore, if Cd2+ is acting by reducing Ca2+ entry into the nerve terminal, then these results suggest that facilitation and augmentation are dependent in some way on Ca2+ entry.

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Both augmentation and potentiation occur independently of internal Ca2+ at the frog neuromuscular junction

Cited by 20 publications

References 17 publications

Effect of an intracellular calcium chelator on the regulation of electrically evoked [³H]‐noradrenaline release from rat hippocampal slices

Effect of an intracellular calcium chelator on the regulation of electrically evoked [³H]‐noradrenaline release from rat hippocampal slices

New insights into short-term synaptic facilitation at the frog neuromuscular junction

Effects of calcium channel blockers on stimulation‐induced changes in transmitter release at the frog neuromuscular junction

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Both augmentation and potentiation occur independently of internal Ca2+ at the frog neuromuscular junction

Cited by 20 publications

References 17 publications

Effect of an intracellular calcium chelator on the regulation of electrically evoked [3H]‐noradrenaline release from rat hippocampal slices

Effect of an intracellular calcium chelator on the regulation of electrically evoked [3H]‐noradrenaline release from rat hippocampal slices

New insights into short-term synaptic facilitation at the frog neuromuscular junction

Effects of calcium channel blockers on stimulation‐induced changes in transmitter release at the frog neuromuscular junction

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Effect of an intracellular calcium chelator on the regulation of electrically evoked [³H]‐noradrenaline release from rat hippocampal slices

Effect of an intracellular calcium chelator on the regulation of electrically evoked [³H]‐noradrenaline release from rat hippocampal slices