Analysis of the mechanism underlying the pathway formation using mutant animals.

使用突变动物分析通路形成的机制。

• 批准号: 13680832
• 负责人: KAWANO Hitoshi
• 金额: $ 2.24万
• 依托单位: Tokyo Metropolitan Organization for Medical Research
• 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
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-13680832/
• 关键词: mutant; Calbindin; N-syndecan; Brn-2; Nkx2.1; Pax-6; NB3; Pathway formation; 突然変異; ノックアウトマウス; 脳; 形態形成; Nxk2.1; TAG-1

We have examined the brain development in both normal and mutant animals by chiefly using the morphological technique. Recent findings obtained are as follows.1) Calbindin D-28k, a calsium-binding protein, is localized in neurons migrating from the nascent vomeronasal organ to the brain in rats (Toba et al., 2001). N-syndecan, a heparansulfate proteoglycan, is expressed in the migratory route from the rat olfactory placode (Toba et al., 2002).2) Defects of the development and pathway formation of hypothalamic neurosecretory neurons were found in animals lacking transcription factors Brn-2, Nkx2.1 and Pax-6 (Kawano et al., 2002).3) The abnormal development of cerebral neocortex is observed in double-knockout mice lacking both Brn-1 and Brn-2 (Sugitani et al., 2002).4) InPax-6 mutant rats, precerebellar neurons of the medulla oblongata exhibit a delayed migration and aberrant migratory route (Horie et al., 2003).5) Ascending dopaminergic axons of the mesencephalon abnormally cross the midline in knochout mice lacking Nkx2.1 (Kawano et al., 2003).6) The motor function of mice lackingNB3, a cell recognition molecule, is abnormal (Takeda et al., 2003).

我们已经主要使用形态学技术检查了正常动物和突变动物的大脑发育。最近获得的发现如下。1）Calbindin D-28K是一种CALSIUM结合蛋白，位于从新生的Vomeronasal器官迁移到大鼠大脑的神经元中（Toba等，2001）。 N-syndecan是一种肝硫酸盐蛋白聚糖，在从大鼠嗅觉上的迁移途径中表达出来（Toba等，2002）。 2，NKX2.1和PAX-6（Kawano等，2002）.3）在缺乏BRN-1和BRN-2的双敲除小鼠中观察到脑新皮质的异常发育（Sugitani等人，2002年） .4）内帕克斯-6突变大鼠，延髓的延迟迁移和异常的迁移途径（Horie等，2003）.5）上升的多巴胺能轴突升高的​​脑脑中多巴胺能轴突，异常在缺乏NKX2的NKX2中，在Midline中跨越了Midline。 1（Kawano等，2003）.6）缺乏细胞识别分子的小鼠的运动功能是异常的（Takeda等，2003）。

项目成果

Kawano, H: "Neuroplasticity Development & Hormone Action"CRC Press LLC. (2002)

Kawano, H：“神经可塑性发展

Horie, M: "Subpial neuronal migration in the fetal rat medulla oblongata with Pax-6 deficiency"Eur. J. neurosci.. 17(1). 49-57 (2003)

Horie, M：“Pax-6 缺陷的胎鼠延髓中的软膜下神经元迁移”Eur。

Sango K: "Phosphacan and neurocan are repulsive substrates for adhesion and neurite extension of adult rat dorsal root ganglion neurons in vitro"J. Neurobiol.. in press. (2003)

Sango K：“磷酸聚糖和神经聚糖是体外成年大鼠背根神经节神经元粘附和神经突延伸的排斥底物”J.

Toba, Y.: "Expression and immunohistochemical localization of heparan sulfate proteoglycan N-syndecan in the migratory pathway from the rat olfactory placode"Eur.J.Neurosci.. 15. 1461-1473 (2002)

Toba, Y.：“硫酸乙酰肝素蛋白聚糖 N-syndecan 在大鼠嗅觉基板迁移途径中的表达和免疫组织化学定位”Eur.J.Neurosci.. 15. 1461-1473 (2002)

Kawano H: "Aberrant trajectory of ascending dopaminergic pathway in mice lacking Nkx2.1"Exp. Neurol.. in press. (2003)

Kawano H：“缺乏 Nkx2.1 的小鼠上行多巴胺能通路的异常轨迹”实验。