DeLorenzo R J
Brain Res. 1977 Sep 23;134(1):125-38. doi: 10.1016/0006-8993(77)90930-1.
The opposing actions of diphenylhydantoin (DPH) and calcium on the level of [32P]phosphate incorporation into particular rat and human brain proteins have been demonstrated in this study by employing the techniques of acrylamide gel electrophoresis and autoradiography. In the presence of calcium several brain proteins showed a marked increase in the incorporation of [32P]phosphate from [gamma-32P]ATP. The calcium-induced increase in phosphorylation of two proteins, designated proteins DPH-L and DPH-M, was significantly inhibited by DPH. DPH inhibited both the calcium-stimulated initial rate and net level of [32P]phosphate incorporated into proteins DPH-L and DPH-M in homogenate and synaptosomal preparations. The data presented in this study are compatible with the hypothesis that the effect of DPH on protein phosphorylation may play an important role in mediating the stabilizing actions of this anticonvulsant on neuronal tissue and seizure discharge.
在本研究中，通过使用丙烯酰胺凝胶电泳和放射自显影技术，已证明二苯妥英（DPH）和钙对特定大鼠和人类脑蛋白中[32P]磷酸盐掺入水平具有相反作用。在钙存在的情况下，几种脑蛋白显示出从[γ-32P]ATP掺入[32P]磷酸盐的显著增加。两种被命名为DPH-L和DPH-M的蛋白的钙诱导磷酸化增加被DPH显著抑制。在匀浆和突触体制剂中，DPH抑制了钙刺激的[32P]磷酸盐掺入DPH-L和DPH-M蛋白的初始速率和净水平。本研究中呈现的数据与以下假设一致，即DPH对蛋白磷酸化的作用可能在介导这种抗惊厥药对神经元组织和癫痫放电的稳定作用中起重要作用。
