ω-Conotoxin reduces facilitation of transmitter release at the frog neuromuscular junction

Zengel, J E; Sosa, María A.; Poage, Robert E.

doi:10.1016/0006-8993(93)91772-k

Cited by 19 publications

(20 citation statements)

References 27 publications

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“…This suggests that 739 results of Zengel et al [32], facilitation was depressed in 1 µM or in 0.2 µM ω-CgTx GVIA. Facilitation was apparent in 0.04 µM ω-CgTx GVIA, where it did not differ significantly from that in the controls.…”

Section: ω-Cgtx Gviamentioning

confidence: 67%

“…We initiated the ω-CgTx GVIA studies because of the discovery by Zengel et al [32] that this toxin depresses the magnitude of facilitation. Our results confirm their observations and add the following points.…”

Section: Discussionmentioning

confidence: 99%

“…ω-conotoxin (ω-CgTx) GVIA decreases the effectiveness of nicotinic agonists in producing autoinhibition. ω-CgTx GVIA has previously been shown to diminish facilitation at the frog neuromuscular junction [32]. Facilitation describes the observation that more quanta are released by a second stimulus following the first by some 10-50 ms. We confirm the diminution of facilitation by ω-CgTx GVIA and suggest that the target of the nicotinic agonists and of facilitation is a type of Ca 2+ channel blocked by ω-CgTx GVIA.…”

Section: Introductionmentioning

confidence: 99%

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Cholinergic agonists decrease quantal output at the frog neuromuscular junction by targeting a calcium channel blocked by ω-conotoxin

Kloot

Molgó

Naves

1997

Pfl�gers Archiv European Journal of Physiology

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Nicotinic cholinergic agonists are known to decrease synchronous evoked quantal output at the frog neuromuscular junction [Van der Kloot 1993, J Physiol (Lond) 468:567-589]. Here we also show that carbachol decreases the frequency of miniature endplate potentials (FMEPP) in solutions containing elevated levels of K+ and Ca2+. Carbachol did not decrease FMEPP in hypertonic solutions or in solutions containing the Ca2+ ionophore ionomycin and Ca2+. We conclude that the nicotinic agonists decrease Ca2+ influx through voltage-gated Ca2+ channels. Carbachol did not alter two-pulse facilitation. A blocker of N-type Ca2+ channels, omega-conotoxin GVIA, antagonized the nicotinic agonist-induced decrease in evoked quantal output. The effect of carbachol was not altered by omega-conotoxin MVIIC, a blocker of P-type and certain other Ca2+channels. The Ca2+ channel targeted by the nicotinic agonists appears to be of the N-type.

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Section: ω-Cgtx Gviamentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cholinergic agonists decrease quantal output at the frog neuromuscular junction by targeting a calcium channel blocked by ω-conotoxin

Kloot

Molgó

Naves

1997

Pfl�gers Archiv European Journal of Physiology

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“…It has been demonstrated that the elevation of [Ca2+]0 to 10 mm reverses the blockade wa-CgTX exerts on transmitter release (Kerr & Yoshikami, 1984). However, Zengel et al (1993) (Sano et al 1987) but to decrease MEPP frequency if used at a concentration of 10 /M (Grinnell & Pawson, 1989). Given that MEPP frequency in this system depends mainly on the resting [Ca]i (e.g.…”

Section: Discussionmentioning

confidence: 99%

“…At the frog neuromuscular junction, the N-type channel blocker w-conotoxin GVIA (w-CgTX), a venom peptide isolated from the marine snail Conus geographus (Olivera, McIntosh, Cruz, Luque & Gray, 1984), was shown, by electrophysiological studies, to block transmitter release (Kerr & Yoshikami, 1984;Sano, Enomoto & Maeno, 1987;Koyano, Abe, Nishiuch & Sakakibara, 1987), to reduce the process of facilitation (Zengel, Sosa & Poage, 1993) and to suppress Ca2P presynaptic currents (Silinsky & Solsona, 1992). It has also been demonstrated that c-CgTX binding sites are in close proximity to the presynaptic release active zones in register with the a-bungarotoxin binding sites at the postsynapsis (Robitaille, Adler & Charlton, 1990).…”

mentioning

confidence: 99%

Effects of Ca2+ channel blockers on transmitter release and presynaptic currents at the frog neuromuscular junction.

Katz

Ferro

Cherksey

et al. 1995

The Journal of Physiology

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1. The effects of the calcium channel blockers, funnel‐web spider toxin (FTX), omega‐agatoxin IVA (omega‐Aga IVA) and omega‐conotoxin GVIA (omega‐CgTX), were tested on transmitter release and presynaptic currents in frog motor nerve endings. 2. Evoked transmitter release was blocked by FTX (IC50 = 0.02 microliter ml‐1) and omega‐CgTX (1 microM) but was not affected by omega‐Aga IVA (0.5 microM). When FTX (0.1 microliter ml‐1) was assayed on spontaneous release either in normal Ringer solution or in low Ca(2+)‐high Mg2+ solution, it was found not to affect miniature endplate potential (MEPP) amplitude but to increase MEPP frequency by approximately 2‐fold in both conditions. 3. Presynaptic calcium currents (ICa), measured by the perineurial technique in the presence of 10 mM tetraethylammonium chloride (TEA) and 200 microM BaCl2 to block K+ currents, were blocked by omega‐CgTX (5 microM), partially blocked by FTX (1 microliter ml‐1) and not affected by omega‐Aga IVA (0.5 microM). 4. The presynaptic calcium‐activated potassium current (IK(Ca)) measured by the perineurial technique in the presence of 0.5 microM 3,4‐aminopyridine (DAP) to block voltage‐dependent K+ currents, was strongly affected by charybdotoxin (ChTX) (300 nM) and completely abolished by BaCl2 (200 microM). This current was also blocked by omega‐CgTX (5 microM) and by CdCl2 (200 microM) but was not affected by FTX (1 microliter ml‐1). The blockade by omega‐CgTX could not be reversed by elevating [Ca]o to 10 mM. 5. The results suggest that in frog synaptic terminals two omega‐CgTX‐sensitive populations might coexist. The transmitter release process seems to be mediated by calcium influx through a omega‐CgTX‐ and FTX‐sensitive population.

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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

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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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ω-Conotoxin reduces facilitation of transmitter release at the frog neuromuscular junction

Cited by 19 publications

References 27 publications

Cholinergic agonists decrease quantal output at the frog neuromuscular junction by targeting a calcium channel blocked by ω-conotoxin

Cholinergic agonists decrease quantal output at the frog neuromuscular junction by targeting a calcium channel blocked by ω-conotoxin

Effects of Ca2+ channel blockers on transmitter release and presynaptic currents 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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