Related Experiment Video
Updated: Sep 18, 2026

Historical View and Physiology Demonstration at the NMJ of the Crayfish Opener Muscle
Published on: November 9, 2009
omega-Conotoxin reduces facilitation of transmitter release at the frog neuromuscular junction
J E Zengel1, M A Sosa, R E Poage
1Department of Veterans Affairs Medical Center, Gainesville, FL.
Abstract:
We have examined the effects of the peptide toxin omega-conotoxin GVIA (omega-CgTx), a known calcium channel blocker, on stimulation-induced changes in end-plate potential (EPP) amplitude at the frog neuromuscular junction. We found that the addition of this toxin in submicromolar concentrations 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 omega-CgTx developed slowly following its addition to the bathing solution, were concentration-dependent and were essentially irreversible. The effects of omega-CgTx appeared to result from reductions in the facilitation and augmentation components of stimulation-induced increases in release. While the effects of omega-CgTx on EPP amplitude could be reversed by increasing the extracellular concentration of Ca2+, we were unable to reverse the effects of the toxin on stimulation-induced increases in EPP amplitude. Thus it appears that omega-CgTx has a dual effect on neuromuscular transmission, perhaps by acting at two different presynaptic sites.
More Related Videos
17:05Loading a Calcium Dye into Frog Nerve Endings Through the Nerve Stump: Calcium Transient Registration in the Frog Neuromuscular Junction
Published on: July 8, 2017
10:45Levator Auris Longus Preparation for Examination of Mammalian Neuromuscular Transmission Under Voltage Clamp Conditions
Published on: May 5, 2018
Related Concept Videos
Excitatory and Inhibitory Effects of Neurotransmitters
Neuromuscular Junction And Blockade
Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action
Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...
Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin
The binding of dantrolene to the RYR1...
Relaxation of Skeletal Muscles
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.
Botulism