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FGF22 缺陷型小鼠对癫痫发作的反应中癫痫发生相关变化的抑制。

Suppression of epileptogenesis-associated changes in response to seizures in FGF22-deficient mice.

机构信息

Molecular and Behavioral Neuroscience Institute, University of Michigan Medical School Ann Arbor, MI, USA.

出版信息

Front Cell Neurosci. 2013 Apr 18;7:43. doi: 10.3389/fncel.2013.00043. eCollection 2013.

Abstract

In the developing hippocampus, fibroblast growth factor (FGF) 22 promotes the formation of excitatory presynaptic terminals. Remarkably, FGF22 knockout (KO) mice show resistance to generalized seizures in adults as assessed by chemical kindling, a model that is widely used to study epileptogenesis (Terauchi et al., 2010). Repeated injections of low dose pentylenetetrazol (PTZ) induce generalized seizures ("kindled") in wild type (WT) mice. With additional PTZ injections, FGF22KO mice do show moderate seizures, but they do not kindle. Thus, analyses of how FGF22 impacts seizure susceptibility will contribute to the better understanding of the molecular and cellular mechanisms of epileptogenesis. To decipher the roles of FGF22 in the seizure phenotype, we examine four pathophysiological changes in the hippocampus associated with epileptogenesis: enhancement of dentate neurogenesis, hilar ectopic dentate granule cells (DGCs), increase in hilar cell death, and formation of mossy fiber sprouting (MFS). Dentate neurogenesis is enhanced, hilar ectopic DGCs appeared, and hilar cell death is increased in PTZ-kindled WT mice relative to PBS-injected WT mice. Even in WT mice with fewer PTZ injections, which showed only mild seizures (so were not kindled), neurogenesis, hilar ectopic DGCs, and hilar cell death are increased, suggesting that mild seizures are enough to induce these changes in WT mice. In contrast, PTZ-injected FGF22KO mice do not show these changes despite having moderate seizures: neurogenesis is rather suppressed, hilar ectopic DGCs do not appear, and hilar cell death is unchanged in PTZ-injected FGF22KO mice relative to PBS-injected FGF22KO mice. These results indicate that FGF22 plays important roles in controlling neurogenesis, ectopic migration of DGCs, and hilar cell death after seizures, which may contribute to the generalized seizure-resistant phenotype of FGF22KO mice and suggests a possibility that inhibition of FGF22 may alleviate epileptogenesis.

摘要

在发育中的海马体中,成纤维细胞生长因子 22(fibroblast growth factor 22,FGF22)促进兴奋性突触前末梢的形成。值得注意的是,成纤维细胞生长因子 22 敲除(knockout,KO)小鼠在成年期对全身性癫痫发作表现出抗性,这可以通过化学点燃来评估,化学点燃是一种广泛用于研究癫痫发生(epileptogenesis)的模型(Terauchi 等人,2010 年)。反复给予低剂量戊四氮(pentylenetetrazol,PTZ)可诱导野生型(wild type,WT)小鼠发生全身性癫痫发作(“点燃”)。用额外的 PTZ 注射,FGF22KO 小鼠确实会出现中度癫痫发作,但它们不会点燃。因此,分析 FGF22 如何影响癫痫易感性将有助于更好地理解癫痫发生的分子和细胞机制。为了解 FGF22 在癫痫表型中的作用,我们研究了与癫痫发生相关的海马体的四个病理生理变化:齿状神经发生增强、齿状回异位颗粒细胞(dentate granule cells,DGCs)、颗粒细胞死亡增加和苔藓纤维发芽(mossy fiber sprouting,MFS)形成。与 PBS 注射的 WT 小鼠相比,PTZ 点燃的 WT 小鼠的齿状神经发生增强、出现齿状回异位 DGCs 和颗粒细胞死亡增加。甚至在 WT 小鼠中,即使注射的 PTZ 较少,只有轻度癫痫发作(因此没有点燃),神经发生、齿状回异位 DGCs 和颗粒细胞死亡也会增加,这表明轻度癫痫发作足以在 WT 小鼠中引起这些变化。相比之下,尽管 FGF22KO 小鼠有中度癫痫发作,但 PTZ 注射的 FGF22KO 小鼠不会出现这些变化:神经发生受到抑制,PTZ 注射的 FGF22KO 小鼠的齿状回异位 DGCs 不出现,颗粒细胞死亡与 PBS 注射的 FGF22KO 小鼠相比没有变化。这些结果表明,FGF22 在控制癫痫发作后的神经发生、DGC 异位迁移和颗粒细胞死亡中发挥重要作用,这可能有助于 FGF22KO 小鼠的全身性癫痫发作抗性表型,并表明抑制 FGF22 可能减轻癫痫发生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/23b2/3629311/301fca287bff/fncel-07-00043-g0001.jpg

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