We have a hypothesis that a drug may block the voltage-gated calcium channels (VGCC) in annelid worms. We are wondering whether there are any correlations between VGCCs and neuron conduction velocities. If there are fluctuations in calcium ion contents, would there be any changes in conduction velocities? Or if the channel is blocked, would it block the entire action potential along the worm's giant axon?
Most of the time, calcium is not the most important ion in terms of active propagation of an action potential along an axon. It is usually sodium and potassium which play the key roles here. In most living things the concentrations of ions for the intracellular and extracellular solutions are similar. For an action potential, you usually have an influx of sodium followed by an efflux of potassium. The sodium influx depolarizes the membrane and the potassium efflux re-polarizes it. The speed of conduction is determined by the membrane resistance and its "leakage". That is to say, how easily can a single travel along an axon? This is determined by the diameter of the axon, the greater the diameter, the faster the conduction. The leakage refers to ease with which ions leak out of the axon as the signal is propagating. Insulation via myelin sheaths help in preventing this, and, less leakage, the greater the signal at the next propagation site.
Calcium is the most important ion for the transmission of a signal from a pre to post synaptic cell. Without calcium, you have no neurotransmitter release. This is because the influx of calcium triggers a series of events involving the snare complex which eventually leads to vesicular release of neurotransmitter in quantal units. If you remove calcium from the extracellular solution, you will have no neurotransmitter release. If you block the calcium channels, you will have no neurotransmitter release.