We then used a model of long-lasting vulnerability for chronic pain that is determined by the balance between latent central sensitization (LCS) and mu opioid receptor constitutive activity (MOR<sub>CA</sub>).
Of note, descending inhibitory pain pathways are often disrupted in chronic OA pain, and pharmacotherapies targeting those pathways - eg, those that block norepinephrine reuptake may be more appropriate for managing chronic pain than pure μ-opioid receptor (MOR) agonists.
A single-nucleotide polymorphism, at nucleotide 118 for opioid receptor mu 1 (OPRM1), has been reported to alter the opioid effects to relieve acute or chronic pain.