DREAM is also a handy
acronym for the mouthful
downstream regulatory element antagonistic modulator. This is a
regulatory protein which attaches to a specific
DNA site to prevent the expression of another protein which manufactures
dynorphin. Dynorphin, in turn, is an
endorphin (an
indigenous opioid) which is normally produced in response to
pain or
stress. In other words, the presence of DREAM means less
dynorphin is manufactured, which leads to pain being perceived as more painful.
The role of DREAM was discovered by engineering a mouse that had its DREAM gene knocked out. Researchers were expecting the missing gene to cause heart problems and poor memory, but the tested mice showed neither of these problems. Instead, the mice had a dramatically (50 percent) lowered pain threshold and were otherwise completely normal. Notably, the mice didn't become addicted to their excess dynorphin -- they showed no reaction to opioid site blockers that completely stop its action.
DREAM and dynorphin work in the spinal cord to control pain messages, and are thus ubiquitous across all vectors of pain reception. This means that inhibition of DREAM would be able to lessen all forms of pain: acute, inflammatory, and neuropathic. Possible aid to neuropathic pain is the most exciting among these, as it is usually a cause of chronic pain that can last years. Common pain killers (Aspirin, COX-2 Inhibitors) only help inflammatory pain, and opioid pain killers (morphine, hydrocodone) are so effective that they tend to become addictive. A pain medicine that targeted DREAM would suffer from neither of these problems, and might be considered a "holy grail" of current pain research.