This animal could kill seven people.
No wonder it looks a little smug.
That newt could well be thinking, “Sure, you might try and eat me, but when your brain stops, I’ll have the last laugh, sucker.”
And it wouldn’t be kidding.
Some rough skinned newts (Taricha granulosa) have something in common with poison dart frogs, blue-ringed octopus, and pufferfish. They all contain within them a poison called tetrodotoxin.
Tetrodotoxin is a neurotoxin that stops neurons from initiating action potentials. It’s most famous as the stuff that makes fugu, pufferfish sushi, notoriously tricky to prepare and serve, because if you do it wrong, eating it kills.
Some garter snakes (Thamnophis sirtalis), however, have evolved the ability to resist tetrodotoxin – which lets them eat newts with impunity. There’s been quite a few studies on this predator-prey arms race, and the latest, by Lee and colleagues, looks at the properties of the neuron that allow the snake to tough out tetrodotoxin.
Using molecular techniques, Lee and company expressed the voltage gated sodium channels (which are critical to starting action potentials) in frog eggs. They used three different kinds of sodium channels, each of which was based on three different snake populations: one with no resistance to the toxin, two others with different mutations that provided resistance.
“Wait! Frog? You never mentioned anything about frogs...” The frog has nothing to do with the ecology here. It’s just a convenient way to get a lot of cell membrane with the voltage gated sodium channel expressed in it.
The ion channels with the toxin resistance were different from the normal ion channels in several ways. It was harder (roughly and loosely speaking) to open toxin resistant channels then normal ones. To be more precise, they needed a larger membrane potential depolarization to reach activation threshold.
The point of a sodium channel is to let sodium pass through the membrane: the more sodium rushes into the neuron from opening the channel, the better. Here again, the normal channels let more sodium though than the toxin resistant ion channels.
Both of these results suggest that the way to make an ion channel immune to a toxin is to make it a crummy ion channel. Harder to open, and it doesn’t work as well when it does open.
This paper talks about the implications of all this in a way that is mostly geared towards ion channel aficionados. Lee and crew are interested in the molecules, not the animals. But there’s been a series of papers before this that have shown resistant garter snakes don’t fare as well as non-resistant ones in various kinds of physiological tests. This does seem to have consequences at the whole animal level.
What I love about this story is that it’s one piece in a much larger puzzle that is becoming a classic in integrative biology. People have studied this predator / prey relationship all the way from the large scale ecology down to this paper on molecules, which might be as fine an analysis as you can reasonably expect to get.
Lee C, Jones D, Ahern C, Sarhan M, Ruben P. 2010. Biophysical costs associated with tetrodotoxin resistance in the sodium channel pore of the garter snake, Thamnophis sirtalis. Journal of Comparative Physiology A. DOI: 10.1007/s00359-010-0582-9
Newt picture by randomtruth on Flickr, snake picture by squamatologist on Flickr. Both used under a Creative Commons license.