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CA1区无棘中间神经元兴奋性突触的长期可塑性缺乏突触特异性。

Long-term plasticity at excitatory synapses on aspinous interneurons in area CA1 lacks synaptic specificity.

作者信息

Cowan A I, Stricker C, Reece L J, Redman S J

机构信息

Division of Neuroscience, John Curtin School of Medical Research, Australian National University, Canberra 0200, ACT, Australia.

出版信息

J Neurophysiol. 1998 Jan;79(1):13-20. doi: 10.1152/jn.1998.79.1.13.

Abstract

The synaptic specificity of long-term potentiation (LTP) was examined at synapses formed on aspinous dendrites of interneurons whose somata were located in the pyramidal cell layer of hippocampal area CA1. Intracellular recordings from slices prepared from rats were used to monitor excitatory postsynaptic potentials (EPSPs) elicited by extracellular stimulation in stratum radiatum. Two synaptic inputs were evoked at 0.5 Hz by stimulating axons adjacent to stratum pyramidale and s. lacunosum-moleculare. After obtaining baseline recordings (>/=10 min), one of the EPSPs was conditioned. The protocol involved tetanic stimulation, sometimes combined with somatic depolarization. Low-frequency stimulation of the two pathways was then resumed and EPSPs were recorded for <30 min. We observed both homosynaptic and heterosynaptic changes in synaptic strength. LTP and long-term depression (LTD) were seen in both pathways and all possible combinations of changes in the two EPSPs were observed, including heterosynaptic LTP associated with either homosynaptic LTP or LTD. Intracellular 1,2-bis (2-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (10 mM) abolished alterations in synaptic strength. When axons in s. radiatum synapse onto a spiny pyramidal cell, synaptic specificity of LTP is preserved. However the results obtained from aspinous interneurons show that synaptic specificity of LTP is lost. These results are consistent with the hypothesis that spines provide postsynaptic mechanism(s) for conferring specificity to LTP.

摘要

在位于海马体CA1区锥体细胞层的中间神经元无棘树突上形成的突触处,研究了长时程增强(LTP)的突触特异性。使用从大鼠制备的脑片进行细胞内记录,以监测辐射层中细胞外刺激引发的兴奋性突触后电位(EPSP)。通过刺激与锥体层和腔隙-分子层相邻的轴突,以0.5 Hz的频率诱发两个突触输入。在获得基线记录(≥10分钟)后,对其中一个EPSP进行条件刺激。该方案包括强直刺激,有时结合体细胞去极化。然后恢复对两条通路的低频刺激,并记录<30分钟的EPSP。我们观察到了突触强度的同突触和异突触变化。在两条通路中均观察到了LTP和长时程抑制(LTD),并且观察到了两个EPSP变化的所有可能组合,包括与同突触LTP或LTD相关的异突触LTP。细胞内注射1,2-双(2-氨基苯氧基)乙烷-N,N,N',N'-四乙酸(10 mM)消除了突触强度的改变。当辐射层中的轴突与有棘锥体细胞形成突触时,LTP的突触特异性得以保留。然而,从无棘中间神经元获得的结果表明,LTP的突触特异性丧失。这些结果与以下假设一致,即棘突为赋予LTP特异性提供了突触后机制。

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