Neurogenesis and aberrant neuronal reorganization in the hippocampus of the animal models of epilepsy

癫痫动物模型海马的神经发生和异常神经元重组

基本信息

  • 批准号:
    13670984
  • 负责人:
  • 金额:
    $ 2.37万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2001
  • 资助国家:
    日本
  • 起止时间:
    2001 至 2002
  • 项目状态:
    已结题

项目摘要

We investigated the changes in hippocampal neurogenesis after the epileptic seizures using several models of epilepsy ; trimethyltin (TMT)-induced seizure model and spontaneous epileptic strain (Noda epileptic rat : NER). After TMT administration, neurogenesis was significantly decreased in the dentate gyrus at 5-7 d after treatment, and subsequently returned to basal level at 14-28 d. In comparison, the number of newly generated neurons was significantly decreased in the hippocampus of young (7W) NERs compared with their controls, while no significant differences in immunostaining of neurogenic markers were observed between adult (12W) NERs and their controls. Further, we evaluated the effect of neuropeptides and neural immune system on neurogenesis in these models. TMT-administered rats were treated with metyrapone in order to transiently suppress circulating corticosterone. The pathologically low levels of corticosterone induced by metyrapone did not alter the hippocampal damage of TMT at 3-5 d after treatment, however, subsequently increased hippocampal neurogenesis at 14 d after TMT administration. NPY-immunoreactivity increased at 4 d after TMT treatment in the hilus, and progressively decreased to a level below controls at 16 d after treatment. NPY mRNA signals increased in the hilus for 2 days after TMT treatment. In NER, NPY immunoreactivity in the dentate gyrus was continuously elevated, while NPY mRNA increased transiently (within 24 h) after a seizure. These results suggest that both neural immune system and neuropeptides may play a crucial role for the control of neurogenesis after epileptic seizures with different pathogenesis.
我们用几种癫痫模型研究了癫痫发作后海马神经发生的变化;三甲基锡(TMT)诱导的癫痫模型和自发性癫痫毒株(野田癫痫大鼠:NER)。TMT给药后5-7天齿状回神经发生明显减少,14-28天恢复到基础水平。相比之下,幼龄(7W)神经元海马新生神经元数量与对照组相比显著减少,而成年(12W)神经元海马神经发生标记物免疫染色与对照组无显著差异。进一步,我们评估了神经肽和神经免疫系统对这些模型中神经发生的影响。给予tmt的大鼠用美替拉酮治疗,以短暂抑制循环皮质酮。在治疗后3-5天,美替拉酮诱导的病理性低水平皮质酮并没有改变TMT的海马损伤,然而,随后在TMT给药后14天,海马神经发生增加。在TMT治疗后第4天,肺门npy免疫反应性增加,并在治疗后第16天逐渐下降到低于对照组的水平。TMT治疗后2天,大鼠门部NPY mRNA信号升高。在NER中,齿状回NPY免疫反应性持续升高,而NPY mRNA在癫痫发作后短暂性升高(24小时内)。这些结果提示,神经免疫系统和神经肽可能在不同发病机制的癫痫发作后神经发生的控制中起重要作用。

项目成果

期刊论文数量(15)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Tsutsumi S, Akaike M, Arimitsu H, Imai H, Kato N.: "Circulating corticosterone alters the rate of neuropathological and behavioral changes induced by trimethyltin in rats"Exp.Neurol.. 173(1). 86-94 (2002)
Tsutsumi S、Akaike M、Arimitsu H、Imai H、Kato N.:“循环皮质酮改变大鼠三甲基锡诱导的神经病理学和行为变化的速率”Exp.Neurol.. 173(1)。
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    0
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Tsutsumi S, Akaike M, Arimitsu H, Imai H, Kato N.: "Circulating corticosterone alters the rate of neuropathological and behavioral changes induced by trimethyltin in rats"Exp. Neurol.. 173. 86-94 (2002)
Tsutsumi S、Akaike M、Arimitsu H、Imai H、Kato N.:“循环皮质酮改变大鼠三甲基锡诱导的神经病理学和行为变化的速率”Exp。
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    0
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Jinde S, Masui A, Morinobu S, Noda A, Kato N.: "Differential changes in messenger RNA expressions and binding sites of neuropeptide Y Y(1),Y(2) and Y(5) receptors in the hippocampus of an epileptic mutant rat : Noda epileptic rat"Neuroscience. 115. 1035-1
Jinde S、Masui A、Morinobu S、Noda A、Kato N.:“癫痫突变体海马中信使 RNA 表达和神经肽 Y Y(1)、Y(2) 和 Y(5) 受体结合位点的差异变化
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    0
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Imai H, Nishimura T, Sadamatsu M, Liu Y, Kabuto M, Kato N.: "Type II glucocorticoid receptors are involved in neuronal death and astrocyte activation induced by trimethyltin in the ret hippocampus"Exp Neurol. 171(1). 22-28 (2001)
Imai H、Nishimura T、Sadamatsu M、Liu Y、Kabuto M、Kato N.:“II 型糖皮质激素受体参与视网膜海马三甲基锡诱导的神经元死亡和星形胶质细胞激活”Exp Neurol。
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    0
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Imai H, Nishimura T, Sadamatsu M, Liu Y, Kabuto M, Kato N.: "Type II glucocorticoid receptors are involved in neuronal death and astrocyte activation induced by trimethyltin in the rat hippocampus"Exp Neurol. 171(1). 22-28 (2001)
Imai H、Nishimura T、Sadamatsu M、Liu Y、Kabuto M、Kato N.:“II 型糖皮质激素受体参与大鼠海马三甲基锡诱导的神经元死亡和星形胶质细胞激活”Exp Neurol。
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KATO Nobumasa其他文献

KATO Nobumasa的其他文献

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{{ truncateString('KATO Nobumasa', 18)}}的其他基金

Developmental brain pathophysiology at an early prenatal period in autism spectrum disorder ? gene, molecule and neuroimaging studies
自闭症谱系障碍产前早期的发育性脑病理生理学?
  • 批准号:
    18209037
  • 财政年份:
    2006
  • 资助金额:
    $ 2.37万
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
Research for Creutzfeldt-Jakob Disease : vCJD
克雅氏病研究:vCJD
  • 批准号:
    13800006
  • 财政年份:
    2001
  • 资助金额:
    $ 2.37万
  • 项目类别:
    Grant-in-Aid for Special Purposes
Molecular mechanisms in hippocampal impairment induced by endocrine disrupters
内分泌干​​扰物引起海马损伤的分子机制
  • 批准号:
    11839011
  • 财政年份:
    1999
  • 资助金额:
    $ 2.37万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Molecular biological study on the mechanisms underlying seizure susceptibility and seizure development
癫痫易感性和癫痫发展机制的分子生物学研究
  • 批准号:
    08671084
  • 财政年份:
    1996
  • 资助金额:
    $ 2.37万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Basic and Clinical Studies on Humoral Control of Sleep
睡眠体液控制的基础与临床研究
  • 批准号:
    01480279
  • 财政年份:
    1989
  • 资助金额:
    $ 2.37万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)
Changes of neuropeptide contents in rat brain after chronic interruption of dopaminergic transmission by administrations with haloperidol and 6-hydroxydopamine.
给予氟哌啶醇和 6-羟基多巴胺慢性阻断多巴胺能传递后大鼠脑中神经肽含量的变化。
  • 批准号:
    60570510
  • 财政年份:
    1985
  • 资助金额:
    $ 2.37万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)

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Abeta Oligomers and Mechanisms of Neuronal Cell Death in Alzheimer's Disease
Abeta 寡聚物和阿尔茨海默病神经细胞死亡机制
  • 批准号:
    8968683
  • 财政年份:
    2015
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    8644005
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    2002
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Liberation of Intracellular Zinc and Neuronal Cell Death
细胞内锌的释放和神经元细胞死亡
  • 批准号:
    9313936
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    2002
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    $ 2.37万
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Liberation of Intracellular Zinc and Neuronal Cell Death
细胞内锌的释放和神经元细胞死亡
  • 批准号:
    9097809
  • 财政年份:
    2002
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The role of phosphorylation reaction of tau factor in ischemic neuronal cell death
tau因子磷酸化反应在缺血性神经细胞死亡中的作用
  • 批准号:
    13671445
  • 财政年份:
    2001
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钙蛋白酶和 CASPASE-3 在神经细胞死亡中的作用
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    6186735
  • 财政年份:
    2000
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CALPAINS AND CASPASE-3 IN NEURONAL CELL DEATH
钙蛋白酶和 CASPASE-3 在神经细胞死亡中的作用
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    6192714
  • 财政年份:
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L-DOPA Plays a role as a neurotransmitter regulating blood pressure in the lower brain stem, and endogenously evoked L-DOPA is a casual factor for glutamate release and resultant delayed neuronal cell death by transient ischemia in rats
L-DOPA 作为调节下脑干血压的神经递质发挥作用,内源性诱发的 L-DOPA 是大鼠短暂性缺血导致谷氨酸释放和由此导致的延迟性神经元细胞死亡的偶然因素
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    10470026
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    1998
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Mechanism of Neuronal Cell Death following Cerebral Ischemia
脑缺血后神经细胞死亡的机制
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    1993
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