DESIGN AND DEVELOPMENT OF MEDICAL ELECTRONIC ...

STIMULATION OF EXCITABLE TISSUES 307Figure 7.2 Simulation results from the stimulation of a giant squid axon with weak (1 µA/cm 2 ) and strong (10 µA/cm 2 ) depolarizing (positiveelectrode inside the cell) and hyperpolarizing (negative electrode inside the cell) stimuli. (a) and (b) The change in membrane voltageevoked by the weak stimuli is related primarily to the change in charge across the membrane’s capacitance. (c) A strong depolarizing stimulus(10 µA/cm 2 ) takes the membrane voltage over the threshold, causing action potentials for the duration of the stimulus. (d) A stronghyperpolarizing stimulus (10 µA/cm 2 ) yields an action potential at the trailing edge of the pulse through rebound excitation.capacitance. However, the strong depolarizing stimulus (10 µA/cm 2 ) takes the membranevoltage over threshold, causing action potentials for the duration of the stimulus.The strong hyperpolarizing stimulus (10 µA/cm 2 ) also yields an action potential, butonly at the trailing edge of the hyperpolarizing pulse. This is what Hodgkin and Huxleyreferred to as anode break excitation or rebound excitation. The hyperpolarizing pulsedecreases the potassium conductance and removes sodium inactivation. The former leadsto less hyperpolarizing current and the latter to more depolarizing current. Since the kineticsof the potassium channels are slower than that for the sodium channel gate, a transientdepolarization takes place after a prolonged hyperpolarizing voltage, which if largeenough can generate an action potential.What we would like you to remember as we move to discuss the clinical uses of electricalstimulation is that anodic currents are usually responsible for the activation ofexcitable tissue when the current is delivered through an intracellular electrode. In addition,we would ask you to remember that hyperpolarizing currents can also lead to activationof excitable tissue via the rebound excitation mechanism.