Phosphorylated Upstream Frameshift 1 –dependent Nonsense-mediated μ-Opioid Receptor mRNA Decay in the Spinal Cord Contributes to the Development of Neuropathic Allodynia–like Behavior in Rats

ConclusionsThis study suggests that phosphorylated UPF1 –dependent nonsense-mediated μ-opioid receptor mRNA decay is involved in the pathogenesis of neuropathic pain.Editor ’s PerspectiveWhat We Already Know about This TopicMaladaptive neuroplasticity in the spinal cord contributes to the development of allodyniaNonsense-mediated messenger RNA (mRNA) decay regulates protein expression and plays an important role in synaptic plasticityThe role of nonsense-mediated mRNA decay in the development of allodynia is incompletely understoodWhat This Article Tells Us That Is NewIn adult rats, spinal nerve ligation triggered the development of allodynia-like behaviorThe underlying molecular mechanisms involve the phosphorylation of upstream frameshift 1 (UPF1) protein, which,via its interaction with the nonsense-mediated messenger RNA (mRNA) decay factor SMG7, triggers μ-opioid receptor mRNA decay in the spinal cordThese laboratory observations suggest that phosphorylated UPF1 protein –dependent nonsense-mediated μ-opioid receptor mRNA decay is involved in the pathogenesis of neuropathic pain
Source: Anesthesiology - Category: Anesthesiology Source Type: research