Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.
Skip to main content

Autophagy is a mechanism whereby cells digest themselves from within and so may be used in lieu of apoptosis to execute cell death. Little is known about its role in neurons. In newly isolated sympathetic neurons, two independent apoptotic stimuli, NGF-deprivation or cytosine arabinoside added in the presence of NGF, caused a 30-fold increase in autophagic particle numbers, many autophagosomes appearing before any signs of DNA-fragmentation. The anti-autophagic drug 3-methyladenine also delayed apoptosis, its neuroprotection correlating with inhibition of cytochrome c release from mitochondria and prevention of caspase activation. In contrast, autophagic activity remained elevated in neurons treated with the pan-caspase inhibitor Boc-Asp(OMe)fmk, which inhibited morphological apoptosis but did not inhibit cytochrome c release nor prevent cell death. We propose that the same apoptotic signals that cause mitochondrial dysfunction also activate autophagy. Once activated, autophagy may mediate caspase-independent neuronal death.

Original publication

DOI

10.1006/mcne.1999.0780

Type

Journal article

Journal

Mol Cell Neurosci

Publication Date

09/1999

Volume

14

Pages

180 - 198

Keywords

Adenine, Animals, Animals, Newborn, Apoptosis, Autophagy, Caspase Inhibitors, Cells, Cultured, Cysteine Proteinase Inhibitors, DNA Fragmentation, Mitochondria, Neurons, Rats, Rats, Wistar, Signal Transduction, Superior Cervical Ganglion