There may be a treatment for those suffering from chronic pain, thanks to research from a new animal study.
Researchers from the New York University School of Medicine studied mice suffering from chronic pain as the result of peripheral nerve damage and a leg surgery. The researchers said that changing the way neurons operate after peripheral nerve damage, which can cause weakness, numbness and pain, could help prevent chronic pain.
“Our findings suggest that manipulating interneuron activity after peripheral nerve injury could be an important avenue for the prevention of pyramidal neuron over-excitation and the transition from acute postoperative pain to chronic centralized pain,” the researchers said.
Though the study was conducted on mice and is supported by human as well as animal studies, it would need to be repeated and verified in order for the research to move forward. When studying the mice, the researchers noticed that peripheral nerve damage blocked brain cells known as somatostatin interneurons (SOM), which help to stem pain.
Since the SOM interneurons weren’t present, the pain signals within the brain became even more active. The researchers manually activated the SOM interneurons themselves and helped to prevent chronic pain.
In order to understand the way the brain operates in the face of chronic pain, the researchers operated on the mice and precisely damaged the peripheral nerves in the left thigh. By using a two-photon calcium imaging process, the researchers were able to observe how the mice responded.
In mice with chronic pain, the neurons within the primary sensory region of the brain were hyperactive compared to the mice that had the operation. The SOM interneurons and other neurons that help to control pain signals were less active, the researchers said.
By injecting a genetically engineered virus that was able to control the SOM interneurons in mice with chronic pain, the researchers were able to stop the hyperactivity found in the brain’s sensory region. The researchers said activating the SOM interneurons effectively prevented chronic pain from ever happening.
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“Our study provides, to our knowledge, the first direct evidence that impaired SOM cell activity is involved in the development of neuropathic pain,” the researchers said.
The study, published in Nature Neuroscience, could lead to new ways to target the SOM interneurons specifically. Regardless of what the results could lead to, the study shows how chronic pain starts and where it can end.
“These findings reveal cortical circuit changes that arise during the development of neuropathic pain and identify the activation of specific cortical interneurons as therapeutic targets for chronic pain treatment,” the researchers concluded.
Tori Linville is a freelance writer and editor from Clarksville, Tennessee. When she isn’t writing or teaching, she’s faithfully watching her alma mater, the University of Alabama, dominate the football field.