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高频刺激颞前铵通路可诱导内嗅皮层爆发细胞的输入特异性长时程增强。

High-frequency stimulation of the temporoammonic pathway induces input-specific long-term potentiation in subicular bursting cells.

机构信息

Department of Psychiatry and Psychotherapy, Charité Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany.

出版信息

Brain Res. 2012 Jan 9;1430:1-7. doi: 10.1016/j.brainres.2011.10.040. Epub 2011 Oct 31.

Abstract

The subiculum (Sub) as a part of the hippocampal formation is thought to play a functional role in learning and memory. In addition to its major input from CA1 pyramidal cells, the subiculum receives input from the entorhinal cortex (EC) via the temporoammonic pathway. Thus far, synaptic plasticity in the subiculum was mainly investigated at CA1-Sub synapses. According to their spiking pattern, pyramidal cells in the subiculum were classified as bursting cells and non-bursting cells. In the present study, we demonstrate that subicular bursting cells show input-specific forms of long-term potentiation (LTP). At CA1-Sub synapses, bursting cells have been shown to express a presynaptic NMDA receptor-dependent LTP that depends on the activation of a cAMP-PKA cascade (Wozny et al., Journal of Physiology 2008). In contrast, at EC-Sub synapses the induction of LTP in bursting cells shows a high induction-threshold and relies on the activation of postsynaptic NMDA receptors, postsynaptic depolarization and postsynaptic Ca(2+) influx. Each form of LTP is input-specific and fails to induce heterosynaptic plasticity. Taken together, our data suggest that distinct, input-specific mechanisms govern high frequency-induced LTP at subicular bursting cells' synapses.

摘要

下托(Sub)作为海马结构的一部分,被认为在学习和记忆中发挥功能作用。除了来自 CA1 锥体神经元的主要输入外,Sub 还通过颞叶弓状纤维接收来自内嗅皮层(EC)的输入。到目前为止,Sub 中的突触可塑性主要在 CA1-Sub 突触上进行了研究。根据其尖峰模式,Sub 中的锥体神经元被分类为爆发细胞和非爆发细胞。在本研究中,我们证明了 Sub 中的爆发细胞表现出输入特异性的长时程增强(LTP)形式。在 CA1-Sub 突触上,已经表明爆发细胞表达依赖于 cAMP-PKA 级联激活的具有 presynaptic NMDA 受体依赖性的 LTP(Wozny 等人,《生理学杂志》2008)。相比之下,在 EC-Sub 突触上,爆发细胞中 LTP 的诱导表现出高诱导阈值,并依赖于 postsynaptic NMDA 受体、postsynaptic 去极化和 postsynaptic Ca(2+)内流的激活。每种形式的 LTP 都是输入特异性的,并且不能诱导异突触可塑性。总之,我们的数据表明,不同的输入特异性机制控制着 Sub 中爆发细胞突触的高频诱导 LTP。

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