Research
Education
Sign In
EN
EN - English
CN - 中文
DE - Deutsch
ES - Español
KR - 한국어
IT - Italiano
FR - Français
PT - Português
TR - Turkish
JA - Japanese
Please note that all translations are automatically generated. Click here for the English version.
843 Views
•
10:50 min
April 24th, 2021
DOI :
10.3791/61974-v
Chapters
0:05
Introduction
0:50
Primary Rat Cortical Neuron Cultures
2:25
Lentivirus Production
4:41
Lentivirus Infection
6:23
Primary Neuron Cultures Stressed with Ganglioside GM2 Accumulation and Immunocytochemistry
7:43
Neurite Atrophy Analysis
8:38
Results: GM2 Accumulation-Induced Neuritic Atrophy Modulated by CN-Aα and CHOP Knock-Down in an Opposite Manner
10:07
Conclusion
Transcript
这种方法可以通过操纵下游对组分的分子表达来用于内质网应力的细胞系统模型。该技术的主要优点是通过神经通路的可视化和测量来消除配对信号传导的影响。该方法有助于了解除GM2神经节苷脂增多症以外的各种神经退行性疾病模型中ER应激急性期和慢性期之间过渡的分子基础首先,在20X放大镜下解剖组织,用两个细尖五号镊子,将额叶皮层与脑膜分开。
将额叶皮层转移到15毫升锥形管中,并在37摄氏度下用3至4毫升胰蛋白酶EDTA孵育组织15分钟以进行化学消化。之后,用不含钙镁离子的Hank平衡盐溶液和0
Sign in or start your free trial to access this content
Summary
在本研究中,通过使用特定的shRNA敲低PERK途径的两个下游信号成分,即细胞保护性钙调磷酸酶和促凋亡CHOP的表达。相反,这些调节原代皮质神经元在诱导内质网应激后对神经突萎缩的易感性。
Explore More Videos
Privacy
Terms of Use
Policies
Contact Us
Recommend to library
JoVE NEWSLETTERS
JoVE Journal
Methods Collections
JoVE Encyclopedia of Experiments
Archive
JoVE Core
JoVE Business
JoVE Science Education
JoVE Lab Manual
Faculty Resource Center
Authors
Librarians
Access
ABOUT JoVE
Copyright © 2024 MyJoVE Corporation. All rights reserved