PBL 2: Toxin/drug that modulates action potentials
Analysis of toxin induced changes in action potential shape for drug development
Authors: Nesar Akanda, MD, PhD, Peter Molnar, PhD, Maria Stancescu, MS, and James J.
Hickman, PhD
Akanda, Nesar et al. “Analysis of toxin-induced changes in action potential shape for drug
development.” Journal of biomolecular screening vol. 14,10 (2009): 1228-35.
doi:10.1177/1087057109348378
An action potential occurs when a neuron transmits information or sends signals to other
neurons. Ion channels in the membrane generate this action potential and the shape of the action
potential can vary if toxins or drugs interfere with the ion channels. In this article, the
researchers clamp specialized cells to study the effects of selected toxins on the recorded action
potential. The researchers used the toxins Veratridine, TEA, and quinine to analyze how the
action potential would change and how the ion channels were affected. Veratridine is a
neurotoxin derived from plants of the lily family, quinine is a medication used to treat malaria
and the TEA toxin is a quaternary ammonium cation molecule. The researchers are monitoring
the physiological changes in the cell due to the drugs or toxins introduced. They record the
action potential before and after introducing the toxins by using voltage-clamp and current-clamp
protocols. Veratridine modified the voltage-gated sodium channels and prevented their
inactivation which prolongs the action potential by delaying hyperpolarization. Veratridine does
not interact with a closed sodium channel but if the channel is open then this toxin will modify it.
This toxin had no effect on depolarization, but it prevented hyperpolarization and affected
intracellular calcium levels. TEA toxin has a similar effect to the Veratridine toxin because it
does not affect the depolarization of the action potential but influences the time by slowing the
