dejerine
10-13-2005, 07:32 AM
Tony Yaksh, who is about as solid as one can get in pain research is reporting that Phospholipase A2 is giving potent antihyperalgesic effects.
Another group has found that metabotrophic glutamate receptor 5 antagonists are giving some results.
There are new substances not yet tested safe in man, which do the same thing as the cell toxin which kills cells expressing Substance P. These substances avoid the risk of transfecting man with a virus/ligand/saporin. It is even possible to achieve the same result by blocking neurokinin 1 with ondansetron, which leads to Substance P inactivation, which inactivates the acetylcholine receptors. Reuptake inhibitiors have been big sellers but not so much help for pain, so ondansetron is probably not going to be an answer.
These new avenues are encouraging, especially the one by Tony Yaksh. Although nearly all the literature for the last few years link inflammation and pain, the stuff of late is seeing a divergence, with inflammatory cytokines such as the interleukins and prostaglandins merely making the receptors more sensitive to whatever is causing pain, not causing the pain itself. We may be getting away from anti-inflammatories and their claims for pain relief and onto specifics, such as phospholipase A2, although PL2 ought to link to inflammation as well.
The work on alpha conotoxin vc1.1, which works via the acetylcholine receptors is looking very good also. We owe the latest effort here to the Australians who are no slouches when it comes to pain research and they have LOTS of cone shells to test on.
Maybe the most important will be inhibitors of the new type 3 Calcium channel that Scott Pruett posted on here. I have been trying to get more information on that but I guess the folks back at the Univ. of Virginia are not going to say more at this time.
Some scientists are also reporting that Interleukin 10 is blocking the inflammatory effects of the other interleukins. This stuff ought to be at least as good as what we have now, hopefully better, although this is still in the inflammatory area. Remember though that Central Pain patients have increased interleukins in their thalamus.
We are getting some help from heart attack studies. In heart failure, exercise causes an exaggerated rise in blood pressure, mediated in part by the TRPV1 channel. Development of meds to help save lives and avoid the blood pressure rise may STOP OUR PAIN. Work on a cancer drug, anandamide, has shown that it weakly binds to the TRPV1 channel, but with addition of cytokines may actually bind powerfully. HOPE SPRINGS ETERNAL, and we are getting some help from people who study the TPRV1 channel for reasons other than pain and it just so happens that, UNLIKE PAIN, there is tons of money to study heart attacks and cancer.
It is a fact that a useable effective pain medicine is going to make someone very very rich. This makes it hard to know just how good the various items really are. They give just enough to draw the grant money but not enough for anyone else to muscle in.
Another group has found that metabotrophic glutamate receptor 5 antagonists are giving some results.
There are new substances not yet tested safe in man, which do the same thing as the cell toxin which kills cells expressing Substance P. These substances avoid the risk of transfecting man with a virus/ligand/saporin. It is even possible to achieve the same result by blocking neurokinin 1 with ondansetron, which leads to Substance P inactivation, which inactivates the acetylcholine receptors. Reuptake inhibitiors have been big sellers but not so much help for pain, so ondansetron is probably not going to be an answer.
These new avenues are encouraging, especially the one by Tony Yaksh. Although nearly all the literature for the last few years link inflammation and pain, the stuff of late is seeing a divergence, with inflammatory cytokines such as the interleukins and prostaglandins merely making the receptors more sensitive to whatever is causing pain, not causing the pain itself. We may be getting away from anti-inflammatories and their claims for pain relief and onto specifics, such as phospholipase A2, although PL2 ought to link to inflammation as well.
The work on alpha conotoxin vc1.1, which works via the acetylcholine receptors is looking very good also. We owe the latest effort here to the Australians who are no slouches when it comes to pain research and they have LOTS of cone shells to test on.
Maybe the most important will be inhibitors of the new type 3 Calcium channel that Scott Pruett posted on here. I have been trying to get more information on that but I guess the folks back at the Univ. of Virginia are not going to say more at this time.
Some scientists are also reporting that Interleukin 10 is blocking the inflammatory effects of the other interleukins. This stuff ought to be at least as good as what we have now, hopefully better, although this is still in the inflammatory area. Remember though that Central Pain patients have increased interleukins in their thalamus.
We are getting some help from heart attack studies. In heart failure, exercise causes an exaggerated rise in blood pressure, mediated in part by the TRPV1 channel. Development of meds to help save lives and avoid the blood pressure rise may STOP OUR PAIN. Work on a cancer drug, anandamide, has shown that it weakly binds to the TRPV1 channel, but with addition of cytokines may actually bind powerfully. HOPE SPRINGS ETERNAL, and we are getting some help from people who study the TPRV1 channel for reasons other than pain and it just so happens that, UNLIKE PAIN, there is tons of money to study heart attacks and cancer.
It is a fact that a useable effective pain medicine is going to make someone very very rich. This makes it hard to know just how good the various items really are. They give just enough to draw the grant money but not enough for anyone else to muscle in.