23 February 2011

Spikes without sodium

ResearchBlogging.orgNeuroscience is concerned with human, mammals, and vertebrates, in that order. The one example of an invertebrate that appears in many narratives for students learning the field is the squid giant axon, which was used to work out the mechanism underlying action potentials.

From the squid axon, we learned that the action potential, in a nutshell, was:

Sodium in, potassium out.

The electrical signal of a neuron was made possible because charged atoms passed into and out of the cell through channels. These channels opened due to the internal electrical state of the neuron, specifically the voltage. In most species, anything that blocks these voltage-gated sodium channels is nasty stuff indeed. Tetrodotoxin is just one of these toxins, and can be found in many animals, but is most famous as pufferfish poison.

“Sodium in, potassium out” was so common and widespread that you could be forgiven that every animal on Earth does things this way. You’d still be wrong, mind you... but forgiven.

Because one of the most studied organisms on the planet can’t get sodium into its neurons.

Caenorhabditis elegans is a little worm that has two big advantages as model nervous system. It was the first animal in which the connections between every neuron in the body was worked out; it was one of the first organisms to have its genome sequenced.

And when the genome was sequenced, people noticed that there were no genes for voltage gated sodium channels.

Gao and Zhen have a new paper that shows how these worms are managing to run their nervous system without voltage-gated sodium channels. They were focusing on the muscles, which also work with sodium in many critters.

They did several experiments, and the bottom line to them all is that in this worm, it’s calcium in, potassium out. The experiment that’s easiest to explain is that when the calcium concentration surrounding the cell was messed up (no calcium), the spikes were messed up (they stopped).

There are several reasons that this is not a huge surprise. Calcium spikes have been found in other animals. And when channels open, calcium tends to do the same thing, electrically speaking, as sodium: it makes the inside of the neuron more positive. In fact, if anything, it’s a surprise that more cells don’t make calcium spikes, because every calcium ion packs twice the electrical “punch” of a sodium atom.

Alas, examples like this rarely seem to get into neuroscience textbooks.

There’s another piece of this paper that is a nice demonstration of the diversity of nervous systems, but I’ll save that for another post.


Gao S, Zhen M. 2011. Action potentials drive body wall muscle contractions in Caenorhabditis elegans. Proceedings of the National Academy of Sciences 108(6), 2557-2562. DOI: 10.1073/pnas.1012346108

Photo by derPlau on Flickr; used under a Creative Commons license.


Björn Brembs said...

Yet another great post!

Neuromancy said...

Wow, I had just assumed that when even stuff like paramecium use Na+/K+ chemistry was fairly standard across all organisms.

How would a change from Na+ to Ca2+ affect the physiology of the cell? You say Ca2+ "packs twice the electrical punch", but how many Navs do you get on a standard neuron? I always just assumed it was more than just a few, so I wouldn't see the entry of a Ca2+ molecule rather than Na+ would cause a much bigger change in the membrane potential.

Is there anything else Na+ related that might be affected? Would an equivalent to Na+/K+ATPase work very differently?

Neuromancy said...

Wait, aren't vertebrate muscle contractions driven by calcium influx? Is the finding that the motor neurons (and other neurons) in C. elegans use Ca2+ as well? Obviously I defer to the authors' experience.

Neuromancy said...

No, ignore that comment... I double checked and it was Ca2+ influx that triggered vesicle release.

It's too early in the morning!