Differential effects of pentylenetetrazole on ion currents of Aplysia neurones

Hartung, Klaus; Hermann, A.

doi:10.1016/0006-8993(87)90568-3

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Differential effects of pentylenetetrazole on ion currents of Aplysia neurones

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Hartung, Klaus
Transport Proteins Group, Max Planck Institute of Biophysics, Max Planck Society;

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Hartung, K., & Hermann, A. (1987). Differential effects of pentylenetetrazole on ion currents of Aplysia neurones. Brain Research, 419(1-2), 55-64. doi:10.1016/0006-8993(87)90568-3.

Cite as: https://hdl.handle.net/21.11116/0000-0007-ED41-5

Abstract

The effects of the convulsant drug pentylenetetrazole (PTZ) on separated membrane current components has been studied in identified voltage-clamped Aplysia neurones. External PTZ blocks the voltage-dependent Na,Ca²⁺ currents and the delayed rectifier current (IN_a, I_Ca and I_K,V, respectively). The amplitude of the Ca²⁺-activated K current (I_K,Ca) is increased. The amplitude of the fast inactivating K current (I_A) is transiently increased at low concentrations of PTZ but is depressed at higher concentrations or after long-lasting application of the drug. The effect of PTZ on leakage current (I_L) seems to depend on the cell type. In some cells (R-15, L-7, LP-1) I_L is decreased while it is increased in other cells (L-11, BL-1, BR-1). PTZ accelerates the inactivation of I_K,V and I_A and shifts the current—voltage relation of I_Ca to negative voltages by 5–8 mV. Pressure injection of PTZ into the neurone did not affect I_K,V or I_K,Ca. Thus PTZ seems to act on the outside of the plasma membrane. The effect of external PTZ on I_Na, I_Ca, I_K,V and IL is also observed if the internal Ca²⁺ activity is buffered with EGTA suggesting that an increase in the internal Ca²⁺ activity is not involved. At −40 mV PTZ induces a tetrodotoxin-insensitive inward current carried by Na ions. PTZ transforms the beating pacemaker cell L-11 into a bursting pacemaker and the bursting pacemaker cell R-15 exhibits ‘square-wave’-like oscillations of the membrane potential.