Receptors in Endosomes Mediate Chronic Pain Associated with Trauma and Stress: Non-Opioid Targets for Pain
Abstract
The grant seeks to determine whether G protein-coupled receptors (GPCRs) in endosomes, rather than at the plasma membrane, are mediators and therapeutic targets for chronic pain. Aim 1 examines whether GPCRs in endosomes control activity of ion channels and expression of genes that induce sustained neuronal excitation. Aim 2 determines whether endosomally-targeted antagonists inhibit channel activity, gene expression and hyperexcitability of neurons. Aim 3 evaluates the therapeutic potential of endosomally-targeted GPCR antagonists in trauma- and stress-induced pain relevant to militarypersonnel. Progress has been made in all aims. Neuropeptides (substance P, calcitonin gene-related peptide) and proteases(trypsin) stimulated GPCR endocytosis and evoked sustained signals and hyperexcitability in pain-sensing neurons. Dynamin and clathrin inhibitors suppressed endocytosis, signaling and hyperexcitability.
Document Details
- Document Type
- Technical Report
- Publication Date
- Sep 01, 2020
- Accession Number
- AD1118513
Entities
People
- Nigel W Bunnett
Organizations
- New York University