Malenka R C, Kauer J A, Zucker R S, Nicoll R A
Department of Pharmacology, School of Medicine, University of California, San Francisco 94143.
Science. 1988 Oct 7;242(4875):81-4. doi: 10.1126/science.2845577.
Brief repetitive activation of excitatory synapses in the hippocampus leads to an increase in synaptic strength that lasts for many hours. This long-term potentiation (LTP) of synaptic transmission is the most compelling cellular model in the vertebrate brain for learning and memory. The critical role of postsynaptic calcium in triggering LTP has been directly examined using three types of experiment. First, nitr-5, a photolabile nitrobenzhydrol tetracarboxylate calcium chelator, which releases calcium in response to ultraviolet light, was used. Photolysis of nitr-5 injected into hippocampal CA1 pyramidal cells resulted in a large enhancement of synaptic transmission. Second, in agreement with previous results, buffering intracellular calcium at low concentrations blocked LTP. Third, depolarization of the postsynaptic membrane so that calcium entry is suppressed prevented LTP. Taken together, these results demonstrate that an increase in postsynaptic calcium is necessary to induce LTP and sufficient to potentiate synaptic transmission.
海马体中兴奋性突触的短暂重复激活会导致突触强度增加，并持续数小时。这种突触传递的长期增强（LTP）是脊椎动物大脑中关于学习和记忆最有说服力的细胞模型。已经通过三种类型的实验直接研究了突触后钙在触发LTP中的关键作用。首先，使用了硝氮唑5（nitr - 5），一种对光不稳定的硝基苯氢醇四羧酸钙螯合剂，它在受到紫外线照射时会释放钙。注入海马体CA1锥体细胞的硝氮唑5发生光解会导致突触传递大幅增强。其次，与先前的结果一致，将细胞内钙缓冲在低浓度会阻断LTP。第三，突触后膜去极化从而抑制钙内流可阻止LTP。综上所述，这些结果表明突触后钙的增加是诱导LTP所必需的，并且足以增强突触传递。
