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

Loss of mitochondrial membrane potential during sympathetic neuronal death requires upstream events that are dependent on macromolecular synthesis and Bax expression. Shown are representative photomicrographs of sympathetic neurons either maintained in NGF (+NGF) or deprived of NGF for 72 h either in the presence of 1 μg/ml cycloheximide (−NGF/+CHX) or 50 μM BAF (−NGF/+BAF). Also shown are Bax-deficient sympathetic neurons that were deprived of NGF for 72 h (−NGF/ Bax^−/−). Neurons were loaded with 1 μM Mitotracker orange for 1 h and processed for cytochrome c immunostaining. Cytochrome c immunostaining and Mitotracker signal for the same cells, and the corresponding nuclei labeled with Hoechst 33258, are shown. Bar, 15 μm.