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

对癫痫易感小鼠大脑皮层、白质、间脑、中脑、海马和小脑等不同脑区的Poly(A)~+聚合酶活性进行了测定。与其他脑区相比，海马区表现出较高的该酶活性。癫痫发作时，该酶活性降至发作间期水平的65%，但在癫痫发作后30min恢复至正常值。这些结果表明，海马区的聚(A)~+聚合酶与癫痫易感性有关。全脑的Poly(A)~+聚合酶分为两种形式，分别位于核汁液中，命名为I型，结合染色质为II型，前者的活性是后者的5倍，而EL(+)组的活性低于ddy鼠。II型酶参与了染色质上合成的mRNA的多聚腺苷化反应。在EL小鼠脑组织中，hnRNA中多聚(A)^+片段的加入量不足，发作间期mRNAs合成不足。癫痫发作后即刻，形式II的活动降至发作间期的75%。而延长Poly(A)^+束链的I型酶在癫痫发作过程中和/或发作后没有明显变化。癫痫易感性与Poly(A)~+聚合酶亚单位改变之间的关系还需要进一步的实验来阐明。EL小鼠大脑转录后的调控机制将是显而易见的。

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.