A new study published in SCIENCE from Dr. Taylor’s lab revealed that inflammation or injury causes μ-opioid receptors (MOR) to become constitutively active for months. This prevents chronic pain, but at the expense of cellular and physical dependence on endogenous MOR signaling. This cover of the September 20th, 2013 issue of SCIENCE is a microscopy image of a biomarker of endogenous withdrawal (phosphorylated extracellular regulated kinase, red) that increases in mouse spinal cord neurons (green) during opioid receptor blockade (image width: 250 micrometers). See Corder et al, Science, 2013, also in the news in Businessweek, Pain Research Forum, Nature Medicine, Nature Reviews Neuroscience, The Scientist, and Science Daily. The properties and functions of µ-opioid receptors have been studied intensively with respect to the binding of endogenous or exogenous ligands. However, much less is known about the constitutive, ligand-independent, activation of opioid receptors.

Months after an injury has healed, receptors involved in modulating pain remain active.