Neurons in Frog's Sciatic Nerve

ABSTRACT LAB 4

Neurons in frog's sciatic nerve utilize voltage and ligand ion channels to generate action potentials from depolarization and then undergoes either relative or absolute refractory period before generating new action potentials. There are fiber A, B, C which has conduction velocities 30-150 m/s, 3-15m/s, 2m/s respectively. The series of experiments is to distinguish each fiber by manipulating different parameters based on refractory periods and conduction.

Varying different settings and observing their effects on CAP characterize nerve action potential. Increasing in amplitude and duration increases the height of the CAP. High frequency draws multiple CAPs closer as action potentials are generated in shorter sequence. Polarity change does not affect the CAP. The lowest intensity with increasing duration provides a rheobase voltage and subsequently, chronaxie time. The lower chronaxie times, the greater nerve excitability. Fiber A has the lowest chronaxie time and C has the highest. In the refractory period test, the changes of two CAP are observed with increasing frequency. The frequency at which both action potentials disappear marks the end of absolute refractory period and beginning of the relative refractory period while the frequency at which the second potential is smaller marks the end of refractory period. The conduction velocity experiment can distinguish between three types of fibers. When the distance between stimulating electrodes and recording electrode is far apart, the conduction velocity can be determined and subsequently, the identification of the fiber based on the velocity. Another experiment is to place the recording electrode far apart from each other. Fiber A reaches the last electrodes before other fibers, so the lowest bump in the CAP represents the percentage of fiber A in the nerve. However, this cannot determine fiber B and C apart. The last experiment is to determine a neurotoxic (procaine) on nerve. The result points out the mechanisms of the toxic by blocking both sodium channels and prevent action potential.