Suppr超能文献

液体冲击伤后海马长时程增强选择性丧失,但长时程抑制未受影响。

Selective loss of hippocampal long-term potentiation, but not depression, following fluid percussion injury.

作者信息

D'Ambrosio R, Maris D O, Grady M S, Winn H R, Janigro D

机构信息

Department of Neurological Surgery, University of Washington, School of Medicine, Seattle, WA 98104, USA.

出版信息

Brain Res. 1998 Mar 9;786(1-2):64-79. doi: 10.1016/s0006-8993(97)01412-1.

Abstract

We investigated the early effects of in vivo fluid percussion injury (FPI) on hippocampal synaptic potentials and excitability. In vitro field potential recordings and immunocytochemistry were performed in the CA1 region in slices from naïve, post-FPI, or sham-operated rats. The following electrophysiological and morphological parameters were affected following FPI: (1) threshold for population spike generation was increased suggesting that post-FPI neurons were hypoexcitable; (2) long-term potentiation (LTP) could not be induced in injured hippocampi; (3) GFAP and inducible NO synthase (iNOS) immunoreactivity were enhanced post-FPI; and (4) following injury, synaptophysin immunoreactivity was enhanced in CA1 stratum radiatum. The effects of FPI on synaptic plasticity were LTP-specific, since long-term depression (LTD) could be equally induced and maintained in post-FPI, sham-operated and control slices. Sham-operated slices were characterized by synaptic excitability indistinguishable from naïve controls, but displayed decreased ability for LTP production and expressed high levels of iNOS. We conclude that FPI causes a selective loss of LTP, possibly due to a previous potentiation induced by trauma as reflected by the increased expression of synaptic proteins. Sham surgical procedures were, however, not without effects on long-term potentiation itself; the latter effects appear to be mediated by an increased production of NO. Our study demonstrates for the first time that hippocampal slices can be used to investigate the correlates of in vivo FPI. Furthermore, we describe LTP-specific deficits in post-traumatic brain injury, suggesting that FPI can selectively erase one of the two main NMDA-dependent forms of synaptic plasticity in the hippocampus.

摘要

我们研究了活体液压冲击伤(FPI)对海马突触电位和兴奋性的早期影响。对未受伤、FPI后或假手术大鼠的海马切片CA1区进行了体外场电位记录和免疫细胞化学检测。FPI后,以下电生理和形态学参数受到影响:(1)群体峰电位产生的阈值升高,表明FPI后神经元兴奋性降低;(2)受伤海马中无法诱导长时程增强(LTP);(3)FPI后胶质纤维酸性蛋白(GFAP)和诱导型一氧化氮合酶(iNOS)免疫反应性增强;(4)损伤后,CA1辐射层中突触素免疫反应性增强。FPI对突触可塑性的影响具有LTP特异性,因为在FPI后、假手术和对照切片中均可同等程度地诱导和维持长时程抑制(LTD)。假手术切片的特点是突触兴奋性与未受伤对照组无明显差异,但LTP产生能力下降且iNOS表达水平较高。我们得出结论,FPI导致LTP选择性丧失,可能是由于创伤诱导的先前增强作用,这可通过突触蛋白表达增加反映出来。然而,假手术操作对长时程增强本身并非没有影响;后者的影响似乎是由NO产生增加介导的。我们的研究首次证明海马切片可用于研究活体FPI的相关机制。此外,我们描述了创伤性脑损伤后LTP特异性缺陷,表明FPI可选择性消除海马中两种主要的NMDA依赖性突触可塑性形式之一。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验