[JustOneVoice]

Active Ingredients In Marijuana Found To Spread And Prolong Pain
ScienceDaily (Aug. 14, 2009) — Imagine that you're working on your back porch, hammering in a nail. Suddenly you slip and hit your thumb instead — hard. The pain is incredibly intense, but it only lasts a moment. After a few seconds (and a few unprintable words) you're ready to start hammering again.
How can such severe pain vanish so quickly? And why is it that other kinds of equally terrible pain refuse to go away, and instead torment their victims for years?
University of Texas Medical Branch at Galveston researchers think they've found at least part of the answer—and believe it or not, it's in a group of compounds that includes the active ingredients in marijuana, the cannabinoids. Interestingly enough, given recent interest in the medical use of marijuana for pain relief, experiments with rodents and humans described in a paper published in the current issue of Science suggest these "endocannabinoids," which are made within the human body, can actually amplify and prolong pain rather than damping it down.
"In the spinal cord there's a balance of systems that control what information, including information about pain, is transmitted to the brain," said UTMB professor Volker Neugebauer, one of the authors of the Science article, along with UTMB senior research scientist Guangchen Ji and collaborators from Switzerland, Hungary, Japan, Germany, France and Venezuela. "Excitatory systems act like a car's accelerator, and inhibitory ones act like the brakes. What we found is that in the spinal cord endocannabinoids can disable the brakes."
To get to this conclusion, the researchers began by studying what happened when they applied a biochemical mimic of an endocannabinoid to inhibitory neurons (the brakes, in Neugebauer's analogy) on slices of mouse spinal cord. Electrical signals that would ordinarily have elicited an inhibitory response were ignored. They then repeated the procedure using slices of spinal cord from mice genetically engineered to lack receptors where the endocannabinoid molecules could dock, and found that in that case, the "brakes" worked. Finally, using electron microscopy, they confirmed that the receptors were in fact on inhibitory, not excitatory neurons. Endocannabinoids docking with them would suppress the inhibitor neurons, and leave pain signals with a straight shot to the brain.
"The next step was to make the leap from spinal slices to test whether this really had anything to do with pain," Neugebauer said. Using anesthetized rats, he recorded the spinal cord electrical activity produced by an injection in the hindpaw of capsaicin– a chemical found in hot peppers that produces a level of pain he compared to a severe toothache. Although the rats were unconscious, pain impulses could be detected racing up their spinal cords. What's more, formerly benign stimuli now generated a significant pain response — a response that stopped when the rats were treated with an endocannabinoid receptor blocker.
"Why was this non-painful information now gaining access to the spinal "pain" neurons?" Neugebauer said. "The capsaicin produced an overstimulation that led to the peripheral nerves releasing endocannabinoids, which activated receptors that shut down the inhibitor neurons, leaving the gates wide open."
Finally, the researchers recruited human volunteers to determine whether a compound that blocked endocannabinoid receptors would have an effect on the increased sensitivity to pain (hyperalgesia) and tendency for normally non-painful stimuli to induce pain (allodynia) often reported in areas of the body near where acute pain had been inflicted. In this case, the researchers induced pain by passing electricity through the volunteers' left forearms, with the intensity of the current set by each volunteer to a 6 on a scale of 1 to 10. At a second session a month later, the volunteers who had received the receptor blocker showed no reduction in perceived acute pain, but had significantly less hyperalgesia and allodynia — a result that matched up well with the endocannabinoid hypothesis.
"To sum up, we've discovered a novel mechanism that can transform transient normal pain into persistent chronic pain," Neugebauer said. "Persistent pain is notoriously difficult to treat, and this study offers insight into new mechanisms and possibly a new target in the spinal cord."
It also raises questions about the efficacy of marijuana in relieving acute pain, given that endocannabinoids and the cannabinoids found in marijuana are so biochemically similar. "If you had a toothache, you probably wouldn't want to treat it with marijuana, because you could actually make it worse," Neugebauer said. "Now, for more pathological conditions like neuropathic pain, where the problem is a dysfunction within the nerves themselves and a subsequent disturbance throughout the nervous system that's not confined to the pain system, marijuana may be beneficial. There are studies that seem to show that. But our model shows cannabinoids over-activating the pain system, and it just doesn't seem like a good idea to further increase this effect."

http://www.sciencedaily.com/releases...0813170848.htm

Uhhhhh, I disagree and my study is over 30 years in the making!!!!!!!!!

[JustOneVoice]

There it was, the headline every medical marijuana patient dreads to see, “Discovery That Active Ingredients In Marijuana Spread And Prolong Pain Has Implications For Medical Use Of Drug And Concepts Of Chronic Pain.” Then as I kept reading the article it became clear where the facts were hidden- in the last paragraph.

While the study, which is so eloquently editorialized by University of Texas Medical Branch at Galveston Senior Science Writer, Jim Kelly, speaks of the research done on slices of mice spine and the “biochemical mimic of an endocannabinoid” used to perform said research, the article is void of the most important information until the final paragraph. I say it is the most important, because it completely contradicts the title of the article.

The following statement appears as the final three of four sentences in the article:

"If you had a toothache, you probably wouldn't want to treat it with marijuana, because you could actually make it worse," Neugebauer said. "Now, for more pathological conditions like neuropathic pain, where the problem is a dysfunction within the nerves themselves and a subsequent disturbance throughout the nervous system that's not confined to the pain system, marijuana may be beneficial. There are studies that seem to show that.”

I guess I am just having an issue understanding how the above quote shows any implications for “medical use…and concepts of chronic pain.” This information simply supports what any medical marijuana patient who uses cannabis to treat their chronic pain will tell you, and have been saying for years. Marijuana doesn’t kill the pain like opiates, but rather changes one’s perception of that pain. Additionally, I have yet to find anyone in any of the 13 states with medical marijuana programs who has been given a medical marijuana recommendation for acute pain, like a toothache. People who are using marijuana for chronic pain are using it in place of long-term opiate “treatment” which is known to present potential of overdose and life-destroying addiction.

No offense, but it seems like Mr. Kelly is implying more than anyone or anything related to this study. Using a substance that mimics another substance is hardly scientific evidence of anything other than a reaction to that substance that was actually used. Since marijuana was not actually used in this experiment it is not quite valid when it comes to the effects of delta-9-tetrahydrocannabinol.

http://www.examiner.com/x-17593-NORM...y-of-marijuana

[kmk420kali]

It is really very simple-- I have heard the same thing for years, and will verify it, from many years of investigation--
Cannabis will not help acute pain...(Sharp Pain)
But it will help with chronic pain (Dull Pain)
As was said above, it will not stop acute pain, but will help in the way that chronic pain is perceived--

[GREENCROSSHOLISTIC]

Or "Not percieved" !!
GCH