The bark scorpion (Centruroides sculpturatus) delivers one of the most painful stings of all members of the scorpion family. Humans that have been stung by the bark scorpion compare the pain to being branded like livestock. Nevertheless, the 25-gram grasshopper mouse routinely kills and eats these scorpions, even though the scorpions sting them repeatedly. Ashlee Rowe, evolutionary neurobiologist at the University of Texas, Austin, has been studying the grasshopper mouse since she was in graduate school. She has discovered why the small mouse doesn’t react to the scorpion stings.
She milked venom from nearly 500 bark scorpions and injected venom into the hind paws of laboratory mice. She observed that the lab mice furiously licked their hind paws at the point of injection for several minutes. However, when she injected venom into grasshopper mice, they licked their paws for a few seconds and then went about their business as if nothing happened. In fact, the grasshopper mice seemed to be more irritated by injections of the saline solution she used as a control.
Rowe was aware that the mice weren’t impervious to pain because they responded to other painful chemicals such as formalin, but not bark scorpion venom. Rowe and colleagues decided to find out how the venom affects the nervous system. Fortunately, pain sensation involves only a few of the chemical channels, so it was easy to home in on two of these channels which include Nav1.7 and Nav1.8, and they control the flow of sodium ions in and out of cells.
Nav1.7 initiates a pain signal and Nav1.8 transmits the pain signal to the brain. Both channels need to be activated for a pain sensation to be registered. With an in vitro application (petri dish), Rowe and colleagues observed that bark scorpion venom targets 1.7 in both lab mice and grasshopper mice. However, in grasshopper mice, 1.8 shuts down in the presence of scorpion venom.
Rowe notes, “The [pain] signal might get generated by sodium channel 1.7, but it does not get sent to the brain by 1.8.”
Glenn King, a structural biologist at the University of Queensland in Australia, who was not involved in the research, comments, “They’ve actually shown the molecular basis by which an animal has evolved [pain] resistance, and that’s very cool.” Rowe notes, pain resistance is an unusual adaptation for animals. Pain is a necessary sense that has evolved to protect an individual from harm. Rowe believes that grasshopper mice have evolved their resistance to scorpion venom because they are an important food source. The bark scorpions are abundant in the Arizona desert where grasshopper mice habitat.
Rowe noticed that the grasshopper mouse became temporarily insensitive to other pain stimuli once bark scorpion venom shut down their 1.8 channels. This suggested to Rowe that this type of phenomena could be useful for engineering a new kind of painkiller for humans.
According to Ewan Smith, a neuroscientist at the University of Cambridge in the United Kingdom, who was also not involved in the current research, “The ideal painkiller is one that you take and your pain goes away but nothing else is affected.” Nav1.7 and Nav1.8 simply trigger pain. A drug could target one or both of these channels and inhibit pain without disturbing other sensations. Additionally, there would be no side effects to contend with including addictions that often come with other painkillers.