The toxins released from Conus catus contain neuroexcitatory peptides that cause the motor neurons in zebrafish spinal cords to fire repetitively. With their neurons firing repetitively, the zebrafish go into a paralysis as their neurons can no longer function properly due to the repetitive activation. C4a/c4e, a prominent neuroexcitatory peptide of C. catus , stimulates the motor neurons in zebrafish spines and causes them to swim in a circle. The actual molecular target for these peptide is not yet confirmed, but recent studies have pointed to the sodium channels as the primary target in zebrafish motor neurons. In effect, these neuroexcitatory peptides may have the ability to affect persistent sodium channels, which have many medical applications, including treating various cardiovascular diseases. Thus, it becomes important to create a physiological approach in order to affirm the suspected molecular target of these neuroexcitatory C. catus peptides in zebrafish motor neurons. It is not (yet) possible to actually see the ion channels of the motor neurons be directly affected by the c4a/c4e peptide, but a physiological approach allows one to prove this using previously known physiological knowledge. Thus, the method described here attempts to provide a protocol for the isolation of zebrafish motor neurons, thus allowing for direct study of motor neuron ion channel activity.