MPA induces two types of generalised epileptic seizures in rodents: the minimal clonic seizure and the major tonic-clonic seizure. The compound is a convulsive agent with very rapid action. The convulsive dose and seizure latency does not differ in the individual species.

After systemic MPA administration, GABA concentration in most brain regions decreases, which is considered to be the cause of the seizure by most authors. It is raised by inhibition of GAD in the nerve tissue. In vitro MPA was found to be a competitive inhibitor of this enzyme.

Several authors consider it unprobable that such a rapid development of seizures could be caused solely by mere inhibition of synthesis of one inhibitory neurotransmitter. Direct inhibitory effect of MPA on GABA release, which was observed in in vitro experiments with tissue slices, may participate in the rapid onset of seizures, too. On the other hand, no influence of MPA on synaptosomal GABA transport has been observed. According to some authors, also excitatory amino acids take part in the development of convulsions after MPA.