POSTSYNAPTIC CALCIUM IS SUFFICIENT FOR POTENTIATION OF HIPPOCAMPAL SYNAPTIC TRANSMISSION
POSTSYNAPTIC CALCIUM IS SUFFICIENT FOR POTENTIATION OF HIPPOCAMPAL SYNAPTIC TRANSMISSION
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DOI：
10.1126/science.2845577
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发表时间：
1988-10-07
期刊：
影响因子：
56.9
通讯作者：
NICOLL, RA
中科院分区：
文献类型：
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作者：
MALENKA, RC;KAUER, JA;NICOLL, RA
海马体中兴奋性突触的短暂重复激活导致突触强度的增加，持续数小时。这种突触传递的长时程增强（LTP）是脊椎动物大脑中最引人注目的学习和记忆细胞模型。突触后钙在触发LTP中的关键作用已直接使用三种类型的实验检查。首先，使用nitr-5，一种对光不稳定的硝基二苯甲醇四羧酸钙螯合剂，其响应于紫外光释放钙。光解nitr-5注入海马CA 1区锥体细胞导致突触传递的大幅度增强。其次，与以前的结果一致，在低浓度缓冲细胞内钙阻断LTP。第三，突触后膜的去极化使得钙离子进入被抑制，从而阻止LTP。总之，这些结果表明，突触后钙的增加是必要的诱导LTP和足以加强突触传递。
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.