Stress regulation of neurotransmission

NIH RePORTER · NIH · R01 · $412,500 · view on reporter.nih.gov ↗

Abstract

Project Summary The long-term goal of the proposed research is to identify the mechanisms by which bidirectional communication between the nervous system and the intestine regulates organism-wide responses to oxidative stress through regulated neuropeptide release. Oxidative stress plays a critical role in cognitive dysfunction and neuronal death associated with neurodegenerative diseases, but little is known about the physiological roles that reactive oxygen species play as signaling molecules in the brain. My laboratory uses the model C. elegans to study new signaling pathways that modulate neurotransmitter release. We have identified a role for hydrogen peroxide as a signaling molecule that positively regulates the secretion of specific neuropeptide-like proteins from dense core vesicles through sulfenylation of dense core vesicle (DCV) release factors. We found that the regulated release of these neuropeptides activates the antioxidant transcription factor SKN-1/Nrf2 in the intestine. Here we seek to uncover the molecular mechanisms by which hydrogen peroxide regulates DCV release, and how, in turn, neuropeptide signaling activates the antioxidant response. This study will reveal novel mechanisms underlying ROS regulation of DCV secretion and it will provide fundamental insights into how redox homeostasis is achieved through gut-brain signaling, and may therefore have direct relevance for the development of strategies to treat neurodegenerative diseases whose progression is associated with unregulated ROS signaling.

Key facts

NIH application ID
10658235
Project number
2R01NS099414-05A1
Recipient
UNIVERSITY OF SOUTHERN CALIFORNIA
Principal Investigator
DEREK SIEBURTH
Activity code
R01
Funding institute
NIH
Fiscal year
2023
Award amount
$412,500
Award type
2
Project period
2017-04-01 → 2028-01-31