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PKG in the On Position Results in Chronic Pain

Richard Ambron from Columbia University in New York City has discovered that chronic pain occurs as a result of hyper-excitable neurons.

Richard Ambron from Columbia University in New York City has discovered that chronic pain occurs as a result of hyper-excitable neurons.

He and his colleagues were studying chronic pain at the molecular and cellular level. Normally at the molecular level a pain stimulus occurs and the neurons becomes excited and begin to send signals to the brain and the individual sense pain but when the stimulus is removed the nerves become dormant and there is no sense of pain. In case of patients suffering from chronic pain the nerves remain the hyper- excitable stage and remains so even if there is a very mild stimulus.

This is because of the enzyme called protein kinase G or PKG. if it is in the on position then the nerves keep sending signals long after the injury that originally caused the pain has healed. Hence drugs should be developed to target this enzyme and shut down the enzyme. It is a new approach to pain relief for the millions suffering from chronic pain. Statistics show that about 48 million Americans suffer from long-lasting pain. Current pain drugs have side effects such as drowsiness and sometimes do not work with certain individuals. The study is done in mice and will be published in the journal Neuroscience.


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