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本文引用的文献

1
Chronic temporal lobe epilepsy: a neurodevelopmental or progressively dementing disease?慢性颞叶癫痫:神经发育性疾病还是进行性痴呆性疾病?
Brain. 2009 Oct;132(Pt 10):2822-30. doi: 10.1093/brain/awp182. Epub 2009 Jul 27.
2
Enhanced synaptic vesicle traffic in hippocampus of phenytoin-resistant kindled rats.苯妥英耐药点燃大鼠海马中突触小泡运输增强。
Neurochem Res. 2009 May;34(5):899-904. doi: 10.1007/s11064-008-9856-9. Epub 2008 Oct 8.
3
Altered expression of synaptotagmin I in temporal lobe tissue of patients with refractory epilepsy.难治性癫痫患者颞叶组织中突触结合蛋白I的表达改变。
J Mol Neurosci. 2009 Jun;38(2):193-200. doi: 10.1007/s12031-008-9143-x. Epub 2008 Sep 9.
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A beta 25-35 induces presynaptic changes in organotypic hippocampal slice cultures.β25 - 35在海马脑片器官型培养物中诱导突触前变化。
Neurotoxicology. 2008 Jul;29(4):691-9. doi: 10.1016/j.neuro.2008.04.001. Epub 2008 May 27.
5
Associations of SNAP-25 polymorphisms with cognitive dysfunctions in Caucasian patients with schizophrenia during a brief trail of treatment with atypical antipsychotics.在非典型抗精神病药物短期治疗期间,白种人精神分裂症患者中SNAP-25基因多态性与认知功能障碍的关联。
Eur Arch Psychiatry Clin Neurosci. 2008 Sep;258(6):335-44. doi: 10.1007/s00406-007-0800-9. Epub 2008 Mar 17.
6
Cochlear ablation in adult ferrets results in changes in insulin-like growth factor-1 and synaptophysin immunostaining in the cochlear nucleus.成年雪貂的耳蜗切除会导致耳蜗核中胰岛素样生长因子-1和突触素免疫染色的变化。
Neuroscience. 2007 Sep 21;148(4):1033-47. doi: 10.1016/j.neuroscience.2007.07.026. Epub 2007 Jul 21.
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Impaired single cell firing and long-term potentiation parallels memory impairment following recurrent seizures.反复癫痫发作后,单细胞放电受损和长时程增强与记忆障碍平行出现。
Eur J Neurosci. 2007 Jun;25(12):3667-77. doi: 10.1111/j.1460-9568.2007.05598.x.
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Posterior parahippocampal place learning in H.M.H.M.患者海马旁回后部的位置学习
Hippocampus. 2007;17(9):863-72. doi: 10.1002/hipo.20313.
9
Dissociation of the immunoreactivity of synaptophysin and GAP-43 during the acute and latent phases of the lithium-pilocarpine model in the immature and adult rat.在未成熟和成年大鼠的锂-匹罗卡品模型急性和潜伏期阶段,突触素和GAP-43免疫反应性的解离
Exp Neurol. 2007 Apr;204(2):720-32. doi: 10.1016/j.expneurol.2007.01.002. Epub 2007 Jan 13.
10
Cognitive outcomes in patients with chronic temporal lobe epilepsy.慢性颞叶癫痫患者的认知结果。
Epilepsia. 2006;47 Suppl 2:96-8. doi: 10.1111/j.1528-1167.2006.00702.x.

海人酸诱导的行为缺陷大鼠海马中突触素、SNAP-25和突触结合蛋白1的异常表达。

Abnormal expression of synaptophysin, SNAP-25, and synaptotagmin 1 in the hippocampus of kainic acid-exposed rats with behavioral deficits.

作者信息

Zhang Feng-Xia, Sun Qin-Jian, Zheng Xing-Yue, Lin You-Ting, Shang Wei, Wang Ai-Hua, Duan Rui-Sheng, Chi Zhao-Fu

机构信息

Department of Neurology, Shandong Provincial Hospital Affiliated to Shandong University, No. 324 jingwuweiqi Road, Jinan, 250021, China.

出版信息

Cell Mol Neurobiol. 2014 Aug;34(6):813-24. doi: 10.1007/s10571-014-0068-3. Epub 2014 May 16.

DOI:10.1007/s10571-014-0068-3
PMID:24832394
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11488916/
Abstract

Temporal lobe epilepsy is characterized by spontaneous recurrent seizures (SRS) and associated with behavioral problems. However, the molecular mechanisms underlying these problems are not yet clear. In this study, kainic acid (KA) was systemically administered to immature male Wistar rats to induce SRS. The behavior of the immature rats was evaluated with a water maze, elevated-plus mazes, and open field tests. The expression patterns of synaptophysin, SNAP-25, and synaptotagmin 1 (Syt 1) were examined by reverse-transcriptase polymerase chain reaction (RT-PCR) and Western blot analysis. KA-treated rats with SRS demonstrated learning and memory deficits, reduced anxiety, and increased locomotor activity, compared with placebo-treated rats and KA-treated rats without SRS. No neuronal cell loss was observed in the hippocampus 6 weeks after exposure to KA. However, RT-PCR and Western blot analyses revealed decreased synaptophysin, SNAP-25, and Syt 1 expression in KA-treated rats with SRS. Synaptophysin, SNAP-25, and Syt1 expression levels were found to be positively correlated with learning and memory but negatively correlated with anxiety and locomotor activity. These data suggested that SRS may induce changes in synaptophysin, SNAP-25, and Syt1 expression and may be functionally related to SRS-induced behavioral deficits.

摘要

颞叶癫痫的特征是自发性反复癫痫发作(SRS),并伴有行为问题。然而,这些问题背后的分子机制尚不清楚。在本研究中,将 kainic 酸(KA)全身注射给未成熟雄性 Wistar 大鼠以诱导 SRS。通过水迷宫、高架十字迷宫和旷场试验评估未成熟大鼠的行为。通过逆转录聚合酶链反应(RT-PCR)和蛋白质免疫印迹分析检测突触素、SNAP-25 和突触结合蛋白 1(Syt 1)的表达模式。与安慰剂处理的大鼠和未发生 SRS 的 KA 处理大鼠相比,发生 SRS 的 KA 处理大鼠表现出学习和记忆缺陷、焦虑减轻和运动活动增加。暴露于 KA 后 6 周,在海马体中未观察到神经元细胞丢失。然而,RT-PCR 和蛋白质免疫印迹分析显示,发生 SRS 的 KA 处理大鼠的突触素、SNAP-25 和 Syt 1 表达降低。发现突触素、SNAP-25 和 Syt1 的表达水平与学习和记忆呈正相关,但与焦虑和运动活动呈负相关。这些数据表明,SRS 可能诱导突触素、SNAP-25 和 Syt1 的表达变化,并且可能在功能上与 SRS 诱导的行为缺陷相关。