[PTZ-induced paroxysmal depolarization shift on Helix p. neurons: mechanism of plateau and pacemaker potentials (author's transl)]

Abstract

The convulsant pentylenetetrazol (PTZ), 1% induces paroxysmal depolarization shifts (PDS) on regularly firing neurones of Helix. Synaptic or antidromic stimulation or transmembrane current produces PDSs followed by a refractory period. For 5% of PTZ-treated neurons the membrane depolarizes up to -15 mV and PDS can be obtained by injected inward current. In voltage clamp experiments the steady i equals f(V) characteristic of PTZ-treated neurons is N-shaped with a current flowing inwardly between -45 and -15 mV. The negative conductance is enhanced by warming and disappears at temperatures lower than 15 degrees C. Besides, a slow triangular function (less than or equal to 10 mV/sec) applied to the voltage clamp system indicates an important hysteresis in the i equals f(V) curves according to the direction of sweeping: depolarization or repolarization. From a hyperpolarized state (-70 mV) the stable point of the N-shaped i equals f(V) characteristic is at -15 mV bringing the membrane potential to this level. From a depolarized state congruent to 10 mV) the i equals f(V) characteristic shows no local negative slope and the stable point is at -45 mV bringing the membrane potential down to this level. PDSs correspond to the voltage transition between these two stable points. The amplitude of PDSs is directly related to the amplitude of hysteresis and their frequency to the kinetics of the i equals f(V) characteristics. The different modes of activity under PTZ are explained by the position of the i equals 0 axis in relation with the region of negative resistance. It is suggested that increase of K+ -inactivation by PTZ is the main phenomenon leading to a N-shaped characteristic.