Compounds That Block Certain Nerve Cell Receptors May Help Relieve Fibromyalgia Pain, Mouse Study Suggests

Compounds That Block Certain Nerve Cell Receptors May Help Relieve Fibromyalgia Pain, Mouse Study Suggests
Scientists have uncovered a molecular pathway that may explain why people with fibromyalgia get no pain relief from opioids such as morphine. Their findings suggest this is caused by the activation of nerve cell receptors called NR2A-NMDA, and that opioids that are able to counteract this effect, such as methadone, may be promising therapeutic candidates for alleviating pain in those with fibromyalgia. Results were reported in the study “NR2A-NMDA receptor blockade reverses the lack of morphine analgesia without affecting chronic pain status in fibromyalgia-like mouse model,” which was published in the Journal of Pharmacology and Experimental Therapeutics. Opioids, chemical compounds that include pain relievers, analgesics, and illegal drugs, have limited effectiveness to alleviate neuropathic pain — a type of pain caused by damage or disease that affects the nervous system. One classical example is the poor effectiveness of morphine — a potent opioid used for medical purposes — at alleviating chronic pain in people with fibromyalgia. However, why morphine and other opioids fail to alleviate pain among those with fibromyalgia is still not fully understood by scientists. To pinpoint the molecular mechanisms underlying opioid inactivity in fibromyalgia, particularly morphine, researchers in Japan created a mouse model of fibromyalgia-like pain, in which the disease was induced by exposing animals to intermittent cold stress (ICS). In these animals, chronic pain is generalized, affects mainly females, and is not reversed by treatment with morphine, mirroring the condition in humans. Using this model, the researchers first investigated the relationship between chronic pain and morphine inactivity in the brain, and then focused on exploring the
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