Roisin M P, Leinekugel X, Tremblay E
Université René Descartes, Paris C, INSERM U 29, Hopital de Port-Royal, Paris, France.
Brain Res. 1997 Jan 16;745(1-2):222-30. doi: 10.1016/s0006-8993(96)01155-9.
The involvement of Ca2+/phospholipid-dependent (alpha, beta, gamma, PKCs) and Ca(2+)-independent PKC (epsilon and zeta isoforms) in mechanisms of long-term potentiation was investigated in CA1 hippocampal slices, using a brief high potassium pulse (50 mM, 40 s) to induce long-term potentiation (K+/LTP). The K+ pulse induced first, in 15 s a translocation of PKC activity to the membrane. This was rapidly followed, from 1 to 60 min after the pulse, by a selective activation of PKC in the cytosol. This activation, which could be blocked by the NMDA (N-methyl-D-aspartate) receptor antagonist 2-amino-5-phosphonovalerate (APV), was associated with a significant increase n immunoreactivity for gamma PKC in he cytosol, and also to a less degree for beta PKC. In contrast, application of the phorbol ester PMA (phorbol 12-mirystate 13 acetate) to other slices induced a rapid and persistent translocation to the membrane of alpha, beta, epsilon and zeta PKCs. A major role for the activation role for the activation of cytosolic gamma PKC in the maintenance of LTP is discussed.
利用短暂的高钾脉冲（50 mM，40秒）诱导长时程增强（K⁺/LTP），在海马CA1区脑片中研究了Ca²⁺/磷脂依赖性蛋白激酶C（α、β、γ、PKC）和Ca²⁺非依赖性蛋白激酶C（ε和ζ亚型）在长时程增强机制中的作用。K⁺脉冲首先在15秒内诱导PKC活性向膜的转位。随后，在脉冲后1至60分钟内，胞质中的PKC迅速被选择性激活。这种激活可被NMDA（N-甲基-D-天冬氨酸）受体拮抗剂2-氨基-5-磷酸戊酸（APV）阻断，与胞质中γ-PKC免疫反应性显著增加有关，β-PKC的免疫反应性也有一定程度增加。相比之下，将佛波酯PMA（佛波醇12-肉豆蔻酸酯13-乙酸酯）应用于其他脑片可诱导α、β、ε和ζ-PKC迅速且持续地转位至膜。文中讨论了胞质γ-PKC激活在维持LTP中的主要作用。
