The mechanism of<unk>  is not well understood, and it may have multiple mechanisms of action. In 1984, Squires et al. published a report analyzing<unk>  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. Many GABA-A ligands are effective anticonvulsants, such as the sedatives diazepam and phenobarbital, but presumably<unk>  has the opposite effect when it binds to the GABA-A receptor. Several studies have focused on the way<unk>  influences neuronal ion channels. A 1987 study found that<unk>  increases calcium influx and sodium influx, both of which depolarize the neuron. Because these effects were antagonized by calcium channel blockers,<unk>  apparently acts at calcium channels, and it causes them to lose selectivity and conduct sodium ions, as well.
Pentylenetetrazol
Glysobuzole
Glybuzole
Retigabine
Phenylpiracetam
Phenobarbital
Galantamine
Difebarbamate