Prevention of the action of RGS4, a multifunctional protein in the brain circuit that processes pathological pain, mood and motivation can disrupt the maintenance of chronic pain states, researchers found in a study conducted in male and female mice.
Researchers from Mount Sinai in a study observed that RGS4 (Regulator of G protein signaling 4) plays a prominent role in maintaining pain states regardless of whether the cause of pain is nerve injury or inflammation.
The study published in The Journal of Neuroscience found the downregulation of RGS4 in the adult ventral posterolateral thalamic nuclei (VPL-THL) promoted recovery from mechanical and cold allodynia.
The discovery may help doctors stop acute pain from progressing into chronic pain, a condition in which patients experience a number of debilitating symptoms ranging from sensory deficits to depression and loss of motivation.
"RGS4 actions contribute to the transition from acute and sub-acute pain to pathological pain states and to the maintenance of pain," said Professor Venetia Zachariou from the Department of Pharmacological Sciences and The Friedman Brain Institute at the Icahn School of Medicine at Mount Sinai.
The researchers said that genetic inactivation of RGS4 did not affect acute pain or the induction of chronic pain but promoted recovery from sensory hypersensitivity symptoms in preclinical models of peripheral nerve injury, chemotherapy-induced neuropathy and peripheral inflammation.
Treatments for chronic pain conditions currently have limited results as well as problematic side effects or addictive properties that can lead to dependence.
Dr Zachariou said that his laboratory was further probing the actions of RGS4 in the spinal cord and mood-regulating areas of the brain to better understand the mechanism by which the protein affected sensory and affective pain symptoms.
