SPECIFIC LONG-LASTING POTENTIATION OF SYNAPTIC TRANSMISSION IN HIPPOCAMPAL SLICES

SPECIFIC LONG-LASTING POTENTIATION OF SYNAPTIC TRANSMISSION IN HIPPOCAMPAL SLICES
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DOI:
10.1038/266736a0
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发表时间:
1977-01-01
期刊:
影响因子:
64.8
通讯作者:
WIGSTROM, H
WIGSTROM, H
中科院分区:
综合性期刊1区
文献类型:
--
作者:
ANDERSEN, P;SUNDBERG, SH;WIGSTROM, H

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短时间的强直刺激(10-50赫兹,10-15 S)可在完整的海马区1和脑片中引起突触传递的长时程增强。这种增强可能会持续几个小时。由于时间进程和所需的条件冲动数量很少,这一过程可能会引起人们对作为神经系统长期可塑性模型的普遍兴趣。然而,由于缺乏对输入截击的大小和参与细胞膜电位变化的数据的控制,LLP潜在机制的研究一直受到阻碍。此外,不知道该增强是否是特制输入所特有的。Schwartzkroin和West2发现了一个不变的逆向场电位,并得出结论,突触后没有普遍的变化。然而,Lynchet al.3发现谷氨酸敏感度在增强阶段降低,并暗示兴奋性已经降低。我们在此报告了在豚鼠海马片上的实验,在该实验中,我们监测了两个独立传入输入的大小,其中一个被破伤风处理以产生LLP,另一个作为控制线来检查兴奋性的非特异性变化。此外,细胞内的记录支持我们的假设,即LLP是由递质释放的特定增强引起的。
SHORT bursts of tetanic stimulation (10–50 Hz for 10–15 s) give rise to long-lasting potentiation (LLP) of synaptic transmission in the intact hippocampal formation1and in hippocampal slices2. The potentiation may last several hours. Because of the time course and the small number of conditioning impulses required, the process may have general interest as a model for long-term plasticity in the nervous system. Studies of the mechanisms underlying LLP have been hampered, however, by lack of control with the size of the input volley and of data on membrane potential changes of the participating cells. Further, it is not known whether the potentiation is specific for the tetanised input. Schwartzkroin and Wester2found an unchanged antidromic field potential, and concluded that there were no general postsynaptic changes. Lynchet al.3, however, found a reduction in glutamate sensitivity during the potentiated stage, and suggested that a reduction in excitability had taken place. We report here experiments on transverse hippocampal slices4of guinea pigs in which we have monitored the size of two independent afferent inputs, one of which is tetanised to produce LLP, leaving the other as a control line to check for non-specific changes in excitability. Furthermore, intracellular recordings support our suggestion that LLP is caused by a specific augmentation of transmitter release.