编码低亲和度NGF受体p75的基因的向突变导致外周感官神经系统的缺陷
1Whitehead Institute for Biomedical Research, Nine Cambridge Center, Massachusetts 02142.
Cell
|May 29, 1992
概括
缺乏低亲和度NGF受体p75神经受体 (p75NGFR) 的小鼠显示感觉神经纤维减少,导致热敏度下降和. 恢复p75NGFR可以挽救这些感官缺陷.
科学领域:
- 神经科学是一个神经科学.
- 遗传学 是一个遗传学.
- 发育生物学 发展生物学
背景情况:
- 低亲和度的神经受体,p75神经受体 (p75NGFR),与神经元的发育和功能有关.
- 它在感官神经元发育和维护中的确切作用仍然不完全理解.
研究的目的:
- 用小鼠模型研究p75NGFR在感觉神经元发育和功能中的功能.
- 确定p75NGFR缺陷对感官内接,热敏度和皮肤完整性的影响.
主要方法:
- 在编码p75NGFR的基因中产生具有向突变的小鼠.
- 在突变和野生类型小鼠的感觉和交感内置的免疫组织化学分析.
- 评估热敏度和观察远端肢体的皮肤完整性.
- 通过引入人类p75NGFR转基因来补充突变.
主要成果:
- 对于p75NGFR突变具有同位素的小鼠在脚皮肤中表现出显著减少的感觉内置,其特征是与素基因相关的和物质P-免疫活性纤维的减少.
- 这种有缺陷的内化与热敏度的丧失和远端肢体严重皮肤的发展相关,由细菌感染复杂化.
- 引入人类的p75NGFR转基因挽救了热敏度,防止了的形成,并恢复了感官内置密度.
- 没有观察到对同情性质的大小或对虹膜或唾液腺的同情性内化密度的显著变化.
结论:
- p75神经质受体 (p75NGFR) 在感官神经元内置的发展和维持中发挥着关键作用.
- 缺乏p75NGFR会导致感官缺陷,包括受损的热感和易受皮肤.
- 针对p75NGFR可能为涉及感官神经病变的疾病提供治疗潜力.
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