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.

Evidence suggests that nerve growth factor (NGF) may function as a mediator of some persistent pain states. We have used a synthetic protein, trkA-IgG, to sequester endogenous NGF and block the survival effects of NGF on cultured sensory neurons. We show that administration of trkA-IgG produces a sustained thermal and chemical hypoalgesia and leads to a downregulation of the sensory neuropeptide CGRP (calcitonin gene-related peptide) in treated sensory neurons. Acute administration of the molecule blocks the hyperalgesia that develops with carrageenan-induced inflammation. These data suggest that peripherally produced NGF normally acts to maintain the sensitivity of nociceptive sensory neurons and that, in some inflammatory states, an upregulation of NGF is responsible for alterations in pain-related behaviour. Antagonists of NGF may therefore be of clinical use in treating some chronic pain states.

Type

Journal article

Journal

Nat Med

Publication Date

08/1995

Volume

1

Pages

774 - 780

Keywords

Animals, Behavior, Animal, Calcitonin Gene-Related Peptide, Capsaicin, Carrageenan, Cells, Cultured, Dose-Response Relationship, Drug, Down-Regulation, Immunoglobulin G, Inflammation, Nerve Growth Factors, Neurons, Afferent, Nociceptors, Pain, Pain Measurement, Proto-Oncogene Proteins, Rats, Receptor Protein-Tyrosine Kinases, Receptor, trkA, Receptors, Nerve Growth Factor, Recombinant Fusion Proteins