Seizure susceptibility of the pregnant mouse

The effect of pregnancy on chemically-induced seizures in mice was studied. Latencies to myoclonic and clonic seizures induced by inhalation of flurothyl were significantly reduced at days 12 through 18 of gestation. Parturition resulted in a return of seizure susceptibility to control levels. The possibility that this effect might be mediated by decreased neurotransmitter levels subsequent to the decreased vitamin B6 levels which are known to occur during pregnancy was suggested. A pregnancy-associated liver cytosolic aldehyde dehydrogenase (pi-AlDH) utilized pyridoxal as a substrate, and the peak of pi-AlDH activity was shown to coincide with the peak of seizure susceptibility. The activity of aldehyde oxidase, the major enzyme normally responsible for the metabolism of pyridoxal, was reduced in pregnant animals. The pyridoxal 5'-phosphate synthesizing enzymes, pyridoxal kinase and pyridoxamine phosphate oxidase, were marginally increased in activity during pregnancy. It was suggested that the increased activity of pi-AlDH was indirectly responsible for the increased seizure susceptibility due to increased metabolism of pyridoxal.