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Painful stimuli begins in receptors beneath the skin, in joints, and in many internal organs. Specialized nerve fibers relay these signals through the spinal column to the brain, where pain becomes conscious.

In the spinal column the messenger molecule amino butyric acid (GABA) is released to act as a kind of pain filter by activating chloride channels on neighboring cells, which then relay the pain signals to the brain.

Ulrich Zeilhofer, Professor at Institute of Pharmacology and Toxicology, University of Zürich had known that chronic inflammatory disease patients, such as rheumatoid arthritis or nerve damage patients, the GABA becomes compromised. As a result, pain signals are nearly unfiltered. Drugs known as benzodiazepines (i.e. Valium®) enhance the action of GABA when injected into the spinal canal. However, such injections are done in in very selected cases. More often benzodiazepines are administered with tablets, which means that it not only works on the spinal cord but also the brain. As a result there can be an undesired effect, like sedation, impaired memory, or addiction.  Over time their effectiveness can fade.

Benzodiazepines have at least 4 different subtypes of GABA receptors and have remained largely neglected as potential targets for pain treatment. The researchers used genetically altered mice with either a slight inflamed hind paw or an irritated sciatic nerve. Through the use of benzodiazepine injected into the spinal canal the researchers were able to identify 2 subtypes of GABA receptors which mediate spinal pain control.

Researchers feel drugs designed to target only the 2 GABA subtype receptors would be a big step forward in pain therapy. This approach would help those with chronic pain to be treated with medication that has fewer side effects.