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

从易患癫痫的El小鼠的大脑皮层、白色物质、间脑、中脑、海马和小脑等不同区域的脑核中估计聚（A）^+聚合酶活性。海马显示这种酶的活性高于其他脑区。该酶活性在癫痫发作时下降至发作间期的65%，但在癫痫发作后30分钟恢复至正常值。这些结果表明海马的poly（A）^+聚合酶是导致癫痫发作的原因。全脑Poly（A）^+聚合酶分为两种形式，Ⅰ型定位于核细胞液中，Ⅱ型与染色质结合。前者的活性比后者高5倍，而El（+）小鼠的活性低于ddY小鼠。II型酶参与启动在染色质上合成的mRNA的多腺苷酸化。E1小鼠脑内poly（A）^+片段的添加不足，发作间期mRNA合成不足。发作后立即，II型的活性下降到发作间期值的75%。而延长poly（A）^+束链的I型酶在癫痫发作期间和/或之后没有显著变化。还需要进一步的实验来阐明多聚腺苷酸^+聚合酶亚基改变与细菌易感性之间的关系。E1小鼠脑内转录后调控机制将更加明显。

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.