[1] In 1939, pentylenetetrazol was replaced by electroconvulsive therapy, which is easier to administer, as the preferred method for inducing seizures in England's mental hospitals.

In 1984, Squires et al. published a report analyzing pentylenetetrazol and several structurally related convulsant drugs.

They found that in vivo convulsant potency was strongly correlated to in vitro affinity to the picrotoxin binding site on the GABA-A receptor complex.

Pentylenetetrazol produces a reliable discriminative stimulus, which is largely mediated by the GABAA receptor.

Several classes of compounds can modulate the pentylenetetrazol discriminative stimulus, including 5-HT1A, 5-HT3, NMDA, glycine, and L-type calcium channel ligands.