New protein discovered to treat chronic pain

Will there be an improved treatment for chronic pain soon?

A special protein plays a prominent role in long-term pain and can serve as a promising new target for the treatment of chronic pain.

A study by the Icahn School of Medicine at Mount Sinai found that a protein called RGS4 (Regulator of G protein signaling 4) plays an important role in maintaining long-term pain. The results of the study were published in the English-language journal "Journal of Neuroscience".

Additional effects of chronic pain

The new discovery can help prevent the transition from acute pain to chronic pain. In the case of chronic pain, further effects are imminent and those affected also show symptoms ranging from sensory deficits to loss of motivation and depression.

Available medications have limited effectiveness and side effects

The transition from acute to chronic (pathological) pain is accompanied by numerous adjustments in immune, glial and neuron cells. Many of these cells have not been studied sufficiently to fully understand them. As a result, the currently available drugs for neuropathic or chronic inflammatory pain are of limited effectiveness and often have considerable side effects.

Risks when using opioids

The commonly administered opioids provide temporary relief from some pain symptoms, but also involve serious risks such as addiction when used as part of long-term treatment for chronic pain. Therefore, there is an urgent need for new approaches to the treatment of chronic pain and for the development of new drugs.

Protein could interfere with pain maintenance

The research shows that RGS4 contributes to the transition from acute and subacute pain to pathological pain states and to the maintenance of pain. Since chronic pain conditions influence numerous neurochemical processes, it is helpful to have discovered a multifunctional protein that can be used specifically to disrupt the maintenance of pain, the researchers report.

Success in experiments with mice

RGS4 plays an important role in maintaining pain, regardless of whether the cause of the pain is a nerve injury or inflammation. Using genetic mouse models, the team demonstrated that preventing RGS4 activity relieves chronic pain in male and female mice. In particular, the research group used genetically modified mice to understand the role of RGS4 in the induction, intensity, and maintenance of chronic pain symptoms.

What did the inactivation of RGS4 do?

The researchers found that while genetic inactivation of RGS4 has no effect on acute pain or induction of chronic pain, it does promote the recovery of sensory hypersensitivity symptoms in preclinical models of peripheral nerve injury, chemotherapy-related neuropathy, and peripheral inflammation. Mice without RGS4 developed all of the expected symptoms of nerve injury, but recovered within three weeks. The prevention of RGS4 actions was also associated with an increase in motivation-related behavior.

More research is needed

The expression of RGS4 was also reduced in the ventral-posterior lateral nucleus of the thalamus, a pain processing center that receives impulses from the spinal cord and transmits this information to several cortical areas. Ultimately, the inhibition of RGS4 actions in the brain region reduced pain sensitivity. The laboratory is further investigating the effects of RGS4 in the spinal cord and mood-regulating areas of the brain to better understand the mechanism by which this protein affects sensory and affective pain symptoms. The therapeutic potential of RGS4 inhibitors is also being investigated. (as)

Author and source information

This text corresponds to the specifications of the medical literature, medical guidelines and current studies and has been checked by medical doctors.


  • Kleopatra Avrampou, Kerri D. Pryce, Aarthi Ramakrishnan, Farhana Sakloth, Sevasti Gaspari e. al .: RGS4 maintains chronic pain symptoms in rodent models, in Journal of Neuroscience (query: 13.10.2019), Journal of Neuroscience

Video: The Science of Pain Management (November 2021).