Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2000 Jul 10;150(1):131–144. doi: 10.1083/jcb.150.1.131

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2000 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

PMC Copyright notice

Sympathetic neuronal death induced by NGF deprivation. Sequence of events occurring after NGF deprivation in sympathetic neurons. Cycloheximide (CHX) inhibits an upstream event that leads to the translocation of BAX to the mitochondria and the subsequent release of cytochrome c (Cyt c) from the mitochondria. Cytosolic cytochrome c presumably activates caspase-9 and induces cell death. Cytochrome c–mediated activation of caspases also requires the NGF deprivation–induced development of competence. Loss of mitochondrial membrane potential (Δψ_m) occurs subsequent to loss of cytochrome c. If caspases are inhibited, rescue of the NGF-deprived, caspase-inhibited neurons is possible with NGF readdition even after the point of cytochrome c release, but not beyond the point of loss of mitochondrial membrane potential.