Frey U, Krug M, Reymann K G, Matthies H
Institute of Neurobiology and Brain Research, Academy of Sciences G.D.R., Magdeburg.
Brain Res. 1988 Jun 14;452(1-2):57-65. doi: 10.1016/0006-8993(88)90008-x.
Long-term potentiation (LTP) with its extremely long duration has been frequently regarded as an elementary mechanism of information storage in the nervous system or at least as a suitable model for the study of mechanisms underlying functional plasticity and processes of learning and memory formation. Considering the necessity of an increased protein synthesis for memory consolidation and for the maintenance of LTP in granular synapses in vivo it was of interest to determine whether the LTP of the CA1 region of the hippocampus depends on protein synthesis as well. For the solution of this question anisomycin (ANI), a reversible blocker of protein synthesis, was used at a concentration of 20 microM, which blocked the [3H]leucine incorporation in hippocampal slices by at least 85%. It has been shown that in the CA1 region in vitro the maintenance of LTP (i.e. a late phase greater than 5 h) depends on an ongoing protein synthesis. A 3-h treatment with ANI immediately following multiple tetanization resulted in gradually developing loss of field excitatory postsynaptic potential (EPSP) and population spike (PS) potentiation (15 +/- 19% increase of the PS instead of the 96 +/- 14% increase in non-treated control experiments at the 8th h after tetanization). Furthermore, a late PS potentiation (greater than 6 h) of a second non-tetanized pathway to CA1 pyramidal cells has been observed (increase by 64 +/- 18% at the 8th h) for the first time. This potentiation was ANI-sensitive as well and suggests that the maintenance of LTP is dependent on a postsynaptic mechanism.
长期增强作用（LTP）因其持续时间极长，常被视为神经系统中信息存储的基本机制，或者至少是研究功能可塑性以及学习和记忆形成机制的合适模型。考虑到在体内颗粒突触中记忆巩固和LTP维持需要增加蛋白质合成，确定海马体CA1区的LTP是否也依赖蛋白质合成就很有意义。为了解决这个问题，使用了浓度为20微摩尔的茴香霉素（ANI），它是一种蛋白质合成的可逆阻滞剂，可使海马切片中[3H]亮氨酸的掺入至少减少85%。研究表明，在体外CA1区，LTP的维持（即大于5小时的晚期阶段）依赖于持续的蛋白质合成。在多次强直刺激后立即用ANI进行3小时处理，导致场兴奋性突触后电位（EPSP）和群体峰电位（PS）增强逐渐丧失（强直刺激后第8小时，PS增强为15±19%，而非未处理对照实验中的96±14%）。此外，首次观察到向CA1锥体细胞的第二条未强直刺激通路的晚期PS增强（大于6小时）（第8小时增加64±18%）。这种增强也对ANI敏感，表明LTP的维持依赖于一种突触后机制。
