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体内脑源性神经营养因子对高频刺激诱导的海马苔藓纤维可塑性的调节。

In vivo BDNF modulation of hippocampal mossy fiber plasticity induced by high frequency stimulation.

机构信息

División de Investigación y Estudios de Posgrado, Facultad de Psicología, Universidad Nacional Autónoma de México, 04360 México, DF, México.

出版信息

Hippocampus. 2012 Jan;22(1):1-8. doi: 10.1002/hipo.20866. Epub 2010 Sep 16.

DOI:10.1002/hipo.20866
PMID:20848610
Abstract

Changes in synaptic efficacy and morphology have been proposed as mechanisms underlying learning and memory processes. In our previous studies, high frequency stimulation (HFS) sufficient to induce LTP at the hippocampal mossy fiber (MF) pathway, leads to MF synaptogenesis, in a prominent contralateral form, at the stratum oriens of hippocampal CA3 area. Recently we reported that acute intrahippocampal microinfusion of BDNF induces a lasting potentiation of synaptic efficacy at the MF projection accompanied by a structural reorganization at the CA3 area within the stratum oriens region in a prominent ipsilateral form. It is considered that the capacity of synapses to express plastic changes is itself subject to variation dependent on previous experience. Here we used intrahippocampal microinfusion of BDNF to analyze its effects on functional and structural synaptic plasticity induced by subsequent mossy fiber HFS sufficient to induce LTP in adult rats, in vivo. Our results show that BDNF modifies the ability of the MF pathway to present LTP by HFS. Moreover BDNF modified the structural reorganization pattern produced by HFS, presenting a balanced bilateral appearance. Microinfusion of K252a blocks the functional and morphological effects produced by BDNF, revealing that the BDNF modulation is dependent on its TrkB receptor activation. These findings support the idea that BDNF actions modify subsequent synaptic plasticity; a homeostatic mechanism thought to be essential for synaptic integration among prolonged temporal domains in the adult mammalian brain.

摘要

突触效能和形态的变化被认为是学习和记忆过程的基础机制。在我们之前的研究中,足够引起海马苔藓纤维(MF)通路长时程增强(LTP)的高频刺激(HFS)会导致 MF 突触发生,以明显的对侧形式出现在海马 CA3 区的层状。最近,我们报道了急性海马内微注射 BDNF 会引起 MF 投射的突触效能持久增强,并伴有 CA3 区层状内的结构重组,以明显的同侧形式出现。人们认为,突触表达可塑性变化的能力本身会受到先前经验的变化的影响。在这里,我们使用海马内微注射 BDNF 来分析其对随后的 MF HFS 诱导的成年大鼠体内功能和结构突触可塑性的影响,MF HFS 足以诱导 LTP。我们的结果表明,BDNF 改变了 MF 通路通过 HFS 呈现 LTP 的能力。此外,BDNF 改变了 HFS 产生的结构重组模式,呈现出平衡的双侧外观。K252a 的微注射阻断了 BDNF 产生的功能和形态效应,表明 BDNF 的调节依赖于其 TrkB 受体的激活。这些发现支持了 BDNF 作用可以修饰随后的突触可塑性的观点;这种内稳态机制被认为是成年哺乳动物大脑中长时间域内突触整合的关键。

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