Injury-Induced Inhibition of Bystander Neurons Requires dSarm and Signaling from Glia.

ABSTRACT: Nervous system injury and disease have broad effects on the functional connectivity of the nervous system, but how injury signals are spread across neural circuits remains unclear. We explored how axotomy changes the physiology of severed axons and adjacent uninjured "bystander" neurons in a simple in vivo nerve preparation. Within hours after injury, we observed suppression of axon transport in all axons, whether injured or not, and decreased mechano- and chemosensory signal transduction in uninjured bystander neurons. Unexpectedly, we found the axon death molecule dSarm, but not its NAD⁺ hydrolase activity, was required cell autonomously for these early changes in neuronal cell biology in bystander neurons, as were the voltage-gated calcium channel Cacophony (Cac) and the mito

SUBMITTER: Hsu JM 

PROVIDER: S-EPMC7864878 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature