Long-term potentiation of inhibitory circuits and synapses in the central nervous system.
Long-term potentiation of inhibitory circuits and synapses in the central nervous system.
复制标题
中枢神经系统抑制回路和突触的长期增强。
DOI：
10.1073/pnas.89.1.440
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发表时间：
1992
影响因子：
11.1
通讯作者：
D. Faber
中科院分区：
文献类型：
--
作者：
H. Korn;Y. Oda;D. Faber
甘氨酸能抑制诱发的双突触在硬骨鱼Mauthner细胞刺激对侧第八神经表现出长时程增强后，经典的强直的途径。这种增强发生在初级传入到二级中间神经元之间的突触以及这些抑制性细胞与Mauthner神经元之间的连接处。甘氨酸能传递改变的证据是，强直后突触前齐射和突触电导之间的关系的斜率可以更大。在用谷氨酸拮抗剂药理学阻断兴奋性突触的增强作用后，这种增益的增加仍然明显。抑制性长时程增强是由破伤风诱导的，弱于增强另一个（同侧）Mauthner细胞的单突触兴奋所需的破伤风。因此，体内学习可以通过修改其中一个或两个来改变网络内兴奋和抑制之间的平衡。
Glycinergic inhibition evoked disynaptically in the teleost Mauthner cell by stimulation of the contralateral eighth nerve exhibits long-term potentiation following classical tetanization of that pathway. This enhancement occurs at the synapses between primary afferents onto second-order interneurons and the connections between these inhibitory cells and the Mauthner neuron. The evidence for modifications of glycinergic transmission is that the slope of the relation between the presynaptic volley and the synaptic conductance can be greater after the tetanus. This increase in gain is still manifest after pharmacological block of potentiation at the excitatory synapse with glutamate antagonists. Inhibitory long-term potentiation is induced by tetani weaker than those required for enhancement of the monosynaptic excitation of the other (ipsilateral) Mauthner cell. Thus, in vivo learning can alter the balance between excitation and inhibition within a network by modifying one or both of them.