New Research has uncovered a target for chronic Pain Medication

Pain medications
New drug target may change chronic pain medication, that may lead to better medicine for those suffering from pain within the future.
Chronic pain is “the commonest reason for long disability,” according to the National Institutes of Health (NIH).

In fact, a recent analysis from the NIH estimates that quite twenty five million individuals within the u. s. (or over 11 p.c of the country’s adult population) suffer chronic pain. this implies that they have experienced pain on a daily basis for the past three months.

While in some cases chronic pain could have been initially triggered by an incident like an injury or an infection, most of the time, the reason for chronic pain is unknown.

Because its causes remain mostly unknown, chronic pain cannot nevertheless be cured. However, medicine typically help, and researchers are hard at work trying to come up with more effective treatments.

Now, a new study – published in the journal PLOS Biology – has identified a potential novel therapeutic target for chronic pain, which could help researchers to develop an alternative medication to treat pain in the near future.

The team was led by Dr. Matthew Dalva, of the Department of Neuroscience at Thomas Jefferson University in Philadelphia, PA. He and his team have investigated a process called phosphorylation and its impact on how chronic pain occurs and what sensations it triggers.

Phosphorylation is a term that describes a common biological process whereby a protein changes in response to external stimuli.

Identifying a new pain receptor
Previous research has identified a pain receptor called N-methyl-D-aspartate (NMDA) and the fact that it plays a key role in pathologic pain.

However, this receptor is also important in memory and learning, so drugs that would target this receptor would also affect these functions.

But in the new study, Dr. Dalva and colleagues identified a second receptor that also plays a crucial role in pain. In their study, the scientists examined neurons in particular.

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Specifically, by conducting a series of laboratory tests in cell cultures and in vivo, the team were ready to see that, in response to injury-induced pain, the protein ephrin B modifies outside of the brain cell. This phosphorylation outside of the cell permits the ephrin B receptor to connect to the NMDA receptor, moving it into the synapses.

This method alters the function of the NMDA receptor, that results in higher sensitivity to pain.

As the authors make a case for, pathologic pain differs from pain caused by an injury or inflammation because it’s a results of cellular disfunction.

Because pain happens at the cellular level, it doesn’t depart even after the initial cause has gone – as is that the case with chronic pain or the common migraine.

For a cell to perform properly, proteins should be within the right location. however what the new study shows is that in the case of chronic pain, the questionable method of phosphorylation “moves” the proteins far from the nerve cell, therefore triggering cell disfunction and pathologic pain.

Importantly, employing a mouse model, the scientists were additionally able to take a look at some chemicals that managed to block the unwanted synergy between the ephrin B receptor and also the NMDA receptor.

Interrupting this communication between the 2 receptors stopped the pain. And conversely, bringing the two receptors along led to an excessive sensitivity to pain.

The senior author of the study comments on the importance of the findings, saying, “Because the protein modification that initiates nerve sensitivity to pain occurs outside of the cell, it offers us a better target for drug development. this can be a promising advance within the field of pain management.”

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