In a study examining the effects of a spider venom on neuromuscular transmission, blockade of which channel explains decreased end-plate potential amplitude?

The decrease in end-plate potential amplitude can be explained by the blockade of presynaptic, voltage-gated calcium channels. In the context of neuromuscular transmission, the arrival of an action potential at the nerve terminal leads to the opening of these calcium channels. Calcium ions then enter the nerve terminal, facilitating the release of acetylcholine (ACh) from vesicles into the synaptic cleft.

If the function of presynaptic, voltage-gated calcium channels is inhibited, there would be a reduced influx of calcium ions, leading to diminished release of ACh. Since the end-plate potential is directly dependent on the amount of ACh that binds to the postsynaptic receptors at the neuromuscular junction, a lower release of ACh results in a smaller end-plate potential amplitude. This ultimately impairs the ability of the muscle to generate an action potential strong enough to initiate contraction.

Therefore, the blockade of presynaptic, voltage-gated calcium channels crucially impacts the overall process of neuromuscular transmission by reducing the amount of neurotransmitter released, which directly correlates with the observed decrease in end-plate potential amplitude.