Biochemist Glenn King spends his days getting up close and personal with the creatures that make us shudder: spiders, centipedes and scorpions. He’s collecting their often-deadly venoms to find the perfect painkiller.
King, a researcher at the University of Queensland in Australia, studies the neurotoxins that allow these creatures to paralyze and kill their prey. The toxins shut down a channel on the membranes of different types of neurons. In humans, the same mechanism that spells doom for prey could be modified to stop pain signals in their tracks. As King explains it, this channel is the first step in the process of amplifying pain signals up the spinal cord to the brain. If researchers can use venoms to develop a drug that blocks this channel, we could provide relief for chronic pain sufferers and possibly shake our dependence on opioid-based painkillers, such as oxycodone or hydrocodone.
Derived from the opium poppy, opioids alleviate pain by binding to opioid receptors in the brain. They’ve been around for thousands of years in one form or another, both as recreational drugs and as painkillers, like morphine or codeine. Along with pain relief, opioids offer euphoria, but they also pose a risk of addiction and drug tolerance.
“It’s not simply that they’re really addictive, which makes putting someone with chronic pain on an opioid a bad idea. It’s also a bad idea because when you take an opioid on a regular basis, they can become ineffective,” says Andrew Kolodny, director of Physicians for Responsible Opioid Prescribing, a national advocacy group.
Since the resurgence of opioid-based medications to treat pain in the 1990s, the drugs have become the primary source of fatal overdoses in the United States. Seventy-one percent of the 22,767 deaths related to pharmaceutical overdose in 2013 involved prescription opioid pain relievers, according to the Centers for Disease Control and Prevention.
Animal toxins can alleviate chronic pain without inducing tolerance or addiction because they target parts of the nervous system outside the brain. It seems counterintuitive that something meant to kill or paralyze could ultimately save lives, but by studying different toxins produced by animals, scientists are gaining greater insight into how pain works in the first place. In fact, one of the first clues to understanding how pain signals make it to the brain came from an unusual source: snails. But we’re getting ahead of ourselves. First, let’s look at just how we feel pain.
A pain signal is just your body’s way of alerting you to damage in your cells. Cells respond to a threat by leaking a small sodium-ion charge through a pore in the cell membrane called voltage-gated sodium channel 1.7, or Nav 1.7. In effect, this sodium channel amplifies the pain signal so it can be “heard” by the brain, says King.
Researchers confirmed the effects of this channel a decade ago when a doctor from the United Kingdom visited Pakistan. The doctor heard about a street show where a young man could stab himself in the arm without pain, getting patched up later in a hospital. Intrigued, the doctor, a geneticist named Geoffrey Woods, eventually discovered two families who carried a genetic mutation that blocked the functioning of sodium channel 1.7. He found a mutation that kept people pain-free.