"Off Switch" for pain relief?

     On Wednesday, November 26, 2014 scientific efforts led by Salvemini at Saint Louis University Medical Center believe that the finding of blocking a pain pathway in animal models will lead to a "promising" new approach to pain relief.  The findings have produced the results that blocking a pain pathway in animal models of chronic neuropathic pain including pain caused by chemotherapeutic agents and bone cancer pain suggesting a promising new approach to pain relief.  Ultimately, it was demonstrated that turning on a receptor in the brain and spinal cord counteracts chronic nerve pain in male and female rodents.  The activation of the A3 receptor by either the natural chemical stimulator, adenosine, or a powerful synthetic drug invented by the NIH, prevents or reverses pain that slowly develops from nerve damage. 

     These findings are significant because pain is a significant issue that many individuals suffer from on a daily basis.  Additionally, some treatments result in intolerable side effects and do not prevent the pain.  The pathways that are typically targeted are circuits involving opioid, adrenergic, and calcium channels where scientists take advantage of the molecular-level component interactions.  

     Moreover, Salvemini and colleagues demonstrated that the activation of A3 adenosine is key in mediating the pain relieving effects of adenosine.  Salvemini states that, "It has long been appreciated that harnessing the potent pain-killing effects of adenosine could provide a breakthrough step towards an effective treatment for chronic pain."  Researchers are excited to note that A3AR agonist are already in advanced clinical trials as an anti-inflammatory and anticancer agents which also display good safety profiles.

     I found this article to be quite interesting and intriguing to read about.  Pain is a persistent annoyance that many individuals go through on a daily-basis, myself included and these findings can be a step in the right direction to helping out so many individuals live a healthy and active life. 

Main article: http://www.sciencedaily.com/releases/2014/11/141126132639.htm

The Case of the Girl Who Couldn’t Feel Pain

        A recent article unveils that reduced pain perception might actually be the result of a single gene mutation. Typically, such drastic medical complications are the result of the interactions and mutations of multiple genes. In this new study, an anonymous woman, “Index Subject 1,” was studied by an entire team of scientists because of her unusual condition: she has the inability to feel pain. Her condition is a dangerous one; she has suffered severe injuries, all of which healed slowly because she was unable to detect that she was hurt. 
Researchers targeted the woman’s mutation not only by studying the genomes of both of the woman’s parents, but also by comparing her family’s genes to several human databases. These databases include the genes of 1,092 people from 14 different populations. In each case, the researchers located a single gene mutation that was displayed in Index Subject 1, but not in a
ny other genome that they studied; the gene called SCN11A was affected by the mutation and caused the woman to not feel pain. The SCN11A gene produces a protein that controls the amount of sodium that passes through cells in the human body; nerves utilize many of these sodium channels in order to indicate to the rest of the body a message of pain. In the case of Index Subject 1, the mutation specifically affected a sodium channel that is abundant in nociceptors, the particular nerves that sense pain. 
After researchers identified that Index Subject 1 has a mutation affecting the SCN11A gene, they then studied the genetic composition of 58 other individuals who had reduced pain perception. Another individual, a man they named Index Subject 2, was identified as having the same mutation as Index Subject 1. Researchers went even further to test whether the mutation affecting the SCN11A gene really did cause a dramatic reduction in pain perception. Scientists found that of the 101 lab mice that were given the SCN11A mutation, 11 gave themselves self-inflicted wounds. Mutated mice were able to withstand high temperatures, and they did not protect a swollen paw as a normal mouse would. 
       I chose to post this article not only because it reports a super-rare genetic mutation, but also because it suggests a medical revolution. The studied mutation could be used as a model for pharmaceutical companies to create future painkillers. The impact that this genetic mutation could have on the medical and pharmaceutical communities will come at a relief for individuals who suffer from chronic pain. I believe that this study will have a significant impact on the way that individuals are treated for their pain. Rather than taking multiple pain medications to treat pain, it is possible to create one medication that affects the SCN11A gene, thus diminishing the individual’s pain. 

Reduce pain through meditation!
http://www.youtube.com/watch?v=tnABHy6tjL8

Centipede Toxin Kills Pain

Chinese red-headed centipede

    In a test done by Glenn King of the University of Queensland in St. Lucia, Australia,  purified a molecule of 46 amino acids from the toxin, or venom of the Chinese red-headed centipede.  When it was tested in rat neurons by IV, the peptide inhibited pain-associated sodium ion channel and had little effect on related channels.
    Researchers then compared the molecule injected into mice that were exposed to noxious chemicals or heat and saw that the higher the does the less they felt pain and showed no obvious side effects.  The researchers came to the conclusion that this molecule and maybe others from centipede toxins could provide powerful pain treatments for chronic pain. However it only mentioned the studying being done with Chinese red-headed centipedes, so it leaves me to wonder how other centipede venom would act.  I thought this was a very interesting article, like I stated above though, I wonder if other centipede venom reacts the same way or if different centipede venom can help with things other than pain.

http://doi.org/n35
http://ezproxy.stockton.edu:2048/login?url=http://search.proquest.com.ezproxy.stockton.edu:2048/docview/17584456?accountid=29054

Boost potency of natural pain relief chemicals

This article discusses a way of enhancing the effects anandamine, a natural chemical in the body that provides pain relief.  Researchers have discovered a protein, named FLAT, in brain cells that transports anandamine to sites within the cell that break it down and that by blocking this protein the potency of anandamine increases.  Anandamine has been shown to play key roles in regulating food consumption, antianxiety, and antidepressant.  Experiments were conducted to better understand how the protein FLAT binds to anandamine and takes it to sites within the cell to be broken down.  The researchers speculate that inhibiting FLAT could be useful in controlling certain forms of pain and reducing addiction to pain medications.  Blocking FLA activity enhances several effects of anandamine without producing the “high” seen in marijuana.  They found that compounds that boost the natural abilities of anandamine could be used to create medications that don’t produce addiction, sedation, or other common side effects.  The researchers hope that by using the analgesic properties of marijuana new safe drugs can be created by amplifying the actions of natural marijuana like chemicals.