Inhibited mechanism during the post-transcription in nuclei of El mouse brain.

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The poly(A)^+ polymerase activity was estimated with respect to brain nuclei of various areas such as cerebral cortex, white matter, diencephalon, mesencephalon, hippocampus and cerebellum from seizure-susceptible El mice. Hippocampus showed a higher activity of this enzyme as compared with other brain regions. This enzyme activity was decreased to 65% of interictal level by the seizures, but restored to a normal value at 30 min after the seizures. These results suggest that poly(A)^+ polymerase of hippocampus is responsible for seizure-susceptibitity. Poly(A)^+ polymerase of whole brain was divided into two forms, which are located in nuclear cell sap designating as Form I, and bind chromatin as Form II. The former activity was 5 times higher than the latter one, which was lower in El(+) as compared with ddY mice. Form II enzyme was involved in initiating the polyadenylation of mRNA synthesized on the chromatin. The addition of poly(A)^+ segment to hnRNA is insufficient in El mouse brain, and mRNAs did not enough synthesize during interictal period. Immediately after the seizures, the activity of Form II decreased to 75% of interictal value. While Form I enzyme which lengths the chain of poly(A)^+ tracts did not alter significantly during and/or after the seizures. Further experiments are needed to elucidate the relationship between seizure-susceptibility and alteration of subunits of poly(A)^+ polymerase. The regulatory mechanism of posttranscription in El mouse brain will be obvious.