The effect of pentylenetetrazol on inward currents of non-bursting neurons and its role in plateau formation.
The epileptogenic drug, pentylenetetrazol (PTZ) produces paroxysmal depolarization shifts in molluscan neurons that are similar to PDSs seen at a mammalian epileptic focus. Most research on molluscan neurons indicates that PTZ acts by altering ionic somatic conductances. This study was carried out to investigate the effect of PTZ on inward currents in isolated neurons of the pond snail, Lymnaea stagnalis, and to investigate how these altered currents might lead to the production of PDSs. In concentrations from 10 to 60 mM, PTZ decreased maximum inward current conductance and shifted the inactivation and activation curves to the left with the former shift being consistently greater. There was no change in reversal potential or time constants for activation and inactivation of inward currents. The effects of the PTZ-induced alterations in the inward currents were studied by incorporating them along with alterations of outward currents seen in this and other studies in a computer model for molluscan neuronal firing. The composite model reproduced in large part the intermediate changes in electrical activity seen before the development of the PDS as well as the PDS.
D000818:Animals; D005724:Ganglia / Q000187:drug effects*; D007473:Ion Channels / Q000187:drug effects*; D008195:Lymnaea; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000187:drug effects; D010433:Pentylenetetrazole / Q000494:pharmacology*; D012964:Sodium / Q000378:metabolism; D013569:Synapses / Q000187:drug effects; D009435:Synaptic Transmission / Q000187:drug effects*
D007473:Ion Channels; D012964:Sodium; D010433:Pentylenetetrazole