Scientists Use Chili Peppers to End Pain

Researchers from the Massachusetts General Hospital and Harvard Medical School have successfully created a way of blocking pain-sensing neurons in the hopes of making trips to your surgeons or dentist less traumatic in the near future. The scientists tested their findings on rats and found a way to block the neurons that detect pain without interfering with other neurons. This procedure could do away with paralyzing or numbing sensation associated with other anesthetic.

The scientists injected the rats near their sciatic nerves causing the rats to lose the ability to feel pain in their paws but the subjects continued to move normally and reach to touch. The scientists used QX-314, an inactive derivative of the local anesthetic lidocaine, and capsaicin and which is also the active ingredient in hot peppers. The combination of QX-314 and capsaicin were able to target the neurons that send pain signals to the brain.

Professor Bruce Bean of Harvard Medical School explained that they introduced the chemicals only to a select population of neurons responsible for feeling pain so it didn't affect the other neurons that control movement or non-painful sensations, eliminating any numbness or paralyzing sensations.

Surgical pain management was only able to undergo minimal change since the demonstration of ether general anesthesia in 1846. Anesthetics work by interfering with the all nerves and not just those responsible for feeling pain which could lead to temporary paralysis or loss of consciousness. The researchers hope that their approach to pain management will eliminate these side effects.

Pain sensing neurons usually contain TRPV1. TRPV1 forms a large channel inside the neurons where molecules can pass through but this channel is usually blocked by a "gate". The "gate" can be opened when the cells are exposed to heat or in the researchers' method, capsaicin, the chili pepper ingredient. When these pain-sensing neurons are exposed to capsaicin, the channels are open but neurons which do not contain TRPV1 are not affected. The QX-314, which is usually an inactive ingredient in lidocaine, then penetrates the cell membranes to block the excitability of the cell. QX-314 usually doesn't penetrate cell membranes but since the channels of the pain-sensing neurons have been opened, QX-314 can then shut down the pain sensing neurons. QX-314 will remain outside other neurons that do not contain the TRPV1 channels.

Before the researchers' solutions can be used on humans, they must first figure out how to open the TRPV1 channels without producing a burning pain before QX-314 enters and blocks the neurons and must find a way to prolong the effects of their drug. The researchers are confident that they can overcome these hurdles.

Professor Clifford Woolf of Massachusetts General Hospital said that with their method, possibilities are endless and since itch-sensitive neurons falls into the same group as pain sensing neurons, their method may be even used to treat itch.

SOURCE:

Harvard Medical School