An alternative to chronic pain treatment may be on the horizon.
According to the National Institutes of Health (NIH), chronic pain is the most common cause of long-term disability. Over 11% of the United States’ adult population live with chronic pain. This means that 25 million people across the country have experienced pain every day for the past three months.
To this day, the causes of chronic pain are largely unknown. While drugs tend to ease the experience, researchers are working diligently on more effective treatments.
Initially explored by Medical News Today, researchers have identified a new potential therapeutic target for chronic pain.
This new study, published in the journal PLOS Biology, was led by Dr. Matthew Dalva of the Department of Neuroscience at Thomas Jefferson University in Philidelphia, PA. Dalva and his team investigated a process called phosphorylation and its impact on how chronic pain occurs and the sensations it triggers.
Phosphorylation describes a common biological process in which a protein changes in response to external stimuli.
Pathologic pain differs from pain caused by an injury or inflammation because it’s a result of cellular dysfunction. Because this pain occurs at the cellular level, it doesn’t dissipate after the initial cause has ceased.
The pain receptor called N-methyl-D-aspartate (NMDA) has previously been identified as a key player in pathologic pain. However, NMDA also plays an important role in memory and learning, which means targeting this receptor can have serious side effects.
By conducting a series of laboratory tests in cell structures, the team was able to identify a second receptor they believed to also play a crucial role in pain. In response to injury-induced pain, the protein ephrin B modifies outside the brain cell. This phosphorylation allows the ephrin B receptor to attach to the NMDA receptor, moving it into the synapses and altering its function, triggering a higher sensitivity to pain.
Using a mouse subject, the scientists were able to interrupt communication between the two receptors, thus ending the pain experience. Conversely, bringing the two receptors back together led to an excessive sensitivity to pain.
Proteins must be in the right location for a cell to function properly. This new study illustrates that in the case of chronic pain, phosphorylation occurring outside the cell “moves” the proteins away from the neuron, effectively triggering cell dysfunction and pathologic pain.
“This is a promising advance in the field of pain management,” says Dalva. “Although we have yet to discover the exact mechanism that causes this modification … this finding offers both a target for developing new treatments and a strong new tool for studying synapses in general.”
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