Researchers Find An Off Switch For Pain

Researchers Find An Off Switch For Pain
(Image source)
In research published in the medical journal Brain, researchers have discovered a way to block a pain pathway in animal models of chronic neuropathic pain including pain caused by chemotherapeutic agents and bone cancer pain suggesting a promising new approach to pain relief. The research demonstrates that turning on a receptor in the brain and spinal cord counteracts chronic nerve pain in male and female rodents.
 
Activating the A3 receptor - either by its native chemical stimulator, the small molecule adenosine, or by powerful synthetic small molecule drugs invented at the NIH - prevents or reverses pain that develops slowly from nerve damage without causing analgesic tolerance or intrinsic reward (unlike opioids).

Pain is an enormous problem. As an unmet medical need, pain causes suffering and comes with a multi-billion dollar societal cost. Current treatments are problematic because they cause intolerable side effects, diminish quality of life and do not sufficiently quell pain. The most successful pharmacological approaches for the treatment of chronic pain rely on certain "pathways": circuits involving opioid, adrenergic, and calcium channels.
 
For the past decade, scientists have tried to take advantage of these known pathways - the series of interactions between molecular-level components that lead to pain. While adenosine had shown potential for pain-killing in humans, researchers had not yet successfully leveraged this particular pain pathway because the targeted receptors engaged many side effects.

In new research, researchers have demonstrated that activation of the A3 adenosine receptor subtype is key in mediating the pain relieving effects of adenosine. Researchers are excited to note that A3AR agonists are already in advanced clinical trials as anti-inflammatory and anticancer agents and show good safety profiles.