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New Direction for Painkiller Research: Target Opioid Receptors Outside of the Brain to Reduce Side Effects- Pain News

By Staff There may be a new direction in the development of opioid medication after researchers discover a different target for opioid receptors in the brain.  Most opioid pain medications target what is called the mu opioid receptor in the brain, which result in side effects and the potential for abuse.  Researchers found that targeting…

New Direction for Painkiller Research: Target Opioid Receptors Outside of the Brain to Reduce Side Effects- Pain News

By Staff

There may be a new direction in the development of opioid medication after researchers discover a different target for opioid receptors in the brain.  Most opioid pain medications target what is called the mu opioid receptor in the brain, which result in side effects and the potential for abuse.  Researchers found that targeting delta opioid receptors on sensory neurons in peripheral tissues can avoid the side effects and abuse potential with current opioid pain medications.

“People living with chronic pain have few innovative analgesic options available to them outside of systemic opioids,” says senior study author Nathaniel Jeske of the University of Texas Health Science Center at San Antonio. “Being able to increase the responsiveness of peripheral opioid receptor systems could lead to a reduction in systemic opioid administration, thereby reducing the incidence of side effects.”

The study in rats, which was published August 25 in Cell Reports, set out to address the problem of mu opioid receptors by targeting delta opioid receptors in the peripheral nervous system rather than the brain and spinal cord, which could produce fewer side effects in animals.

Jeske and lead author Allison Doyle Brackley, also of the University of Texas Health Science Center at San Antonio found that a protein called GRK2 binds to and prevents delta opioid receptors on rat sensory neurons from responding normally to opioids.  When these peripheral neurons were exposed to a natural inflammatory molecule called bradykinin, GRK2 moved away from the delta opioid receptors, setting off a biochemical reaction that restored the functioning of these receptors.

So, the rats with the reduced GRK2 levels regained their sensitivity to the pain-relieving effects of the drug that activates the delta opioid receptors – and did so without the need for an inflammatory trigger.

“By shedding light on how inflammation activates delta opioid receptors, this research could potentially lead to the development of safer, more effective opioids for the treatment of pain,” Jeske said.

The researchers’ next steps are to attempt to replicate the findings in rats, using human tissue.

Source Nationalpainreport.com

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