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tarantula venom could be a step towards non-addictive painkillers
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many common painkillers, including opiates, work by blocking some of the ion channels that lead to the nerve cells. getty
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a tarantula with an incredibly painful bite could help us understand more about chronic pain — and may even help scientists develop non-addictive painkillers.
australian researchers began looking into the king baboon spider, a tarantula native to kenya and tanzania. the king baboon is a burrowing spider, which, unfortunately for those of us who fear them, burrows underground. (an even scarier detail: they often burrow with their fangs.)
they also have a ferocious and extremely painful bite. and while it isn’t fatal in humans, getting bitten by a king baboon results in days of excruciating pain, along with swelling and muscle spasms.
it’s the specific way the tarantula’s venom takes hold in the body that’s being studied.
“there are many components in spider — and other animals’ — venoms able to cause pain,” the study’s co-authors rocio k. finol-urdaneta, david j. adams, and paul f. alewood
told inverse. “yet the particular ‘cocktail’ delivered by each spider will determine the mechanisms through which pain is elicited.”
in breaking down the elements of the king baboon’s venom, researchers found that it contained a peptide called pm1a, which manages our body’s responses in a collection of cell bodies called the dorsal root ganglion. essentially, this one peptide is largely responsible for the extreme and continuous pain caused by the spider bite.
the researchers found that mice who were given synthetic pm1a had “hyperexcitability” — meaning the pain neurons were firing in a rapid, intense way — through three channels of their nerve cells: sodium, potassium and calcium. that hyperexcitability is similar in the nerves of people with specific kinds of chronic pain, a finding that has important implications for people studying chronic pain.
“drugs that could reduce excitability in pain neurons through the simultaneous modulation of several molecular players may provide more effective, alternative treatments for pain,” the researchers wrote in the study.
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why some painkillers are addictive and some aren’t
many common painkillers, including opiates, work by blocking some of the ion channels that lead to the nerve cells,
vox explains. the neurons remain “unexcited,” dulling the pain. but one of the major reasons so many painkillers are addictive is because our neurons get desensitized to them, and need higher doses to perform the same action.
in the same way that pm1a causes intense pain, other peptides can prevent it. pm1a is a “promiscuous” peptide because it impacts so many different channels leading to different neurons. promiscuous peptides are less likely to lead to the desensitization of an individual neuron — meaning doctors wouldn’t have to keep increase dosing for them to work.
“the benefit of using spider-derived venom peptides are that these peptides do not cause dose dependence and addiction,”
christina schroeder, a researcher who
studies venom-inspired painkillers,explained
to vox. (schroeder was not part of the study.) significantly, those peptides don’t rely on the same receptors that oxycodone and morphine do.
painkillers have typically been designed to focus in on just a few ion channels. but trying to target a broader swath of the parts of our brain and nervous system that feel pain could be safer and more effective, schroder said: “this study highlights that we should probably reexamine the way we approach the development of novel pain therapeutics.”
opioids like oxycontin, fentanyl, and vicodin, are just some of the powerful drugs often prescribed to treat the pain that follows surgery. even a few weeks of use can trigger dependence, according to dr. karsten kueppenbender, an addiction psychiatrist at harvard-affiliated mclean hospital.
“any patient who is treated with opioids for 30 days or longer will develop opioid tolerance,”
kueppenbender said. “this causes them to suffer withdrawal symptoms if the medication is stopped abruptly. users may also begin to want more of these drugs to achieve the same effect. it can happen to anybody.”
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maija kappler is a reporter and editor at healthing. you can reach her at mkappler@postmedia.com
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