TOXINS AND Na+ channels

Question

Some animals produce toxins that work by interfering with nerve conduction in the same way that local anesthetics do. For example, some organs of the pufferfish produce an extremely potent toxin, tetrodotoxin that binds to voltage-gated Na+ channels. What effect does this toxin have on the function of neurons?

a) Neurons would depolarize more rapidly.

b) The axon would be unable to generate action potentials.

c) the absolute refractory period would be shorter than normal.

d) None, because the ligand-gated sodium channels would still function.

Answer 1

B. is the answer

Na gated channels are primarily to depolarise and hence kick start an action potential, the the case of toxins this neuron depolarisation is blocked

Answer 2

There are a few distinct phases to neuron firing. First, enough neurotransmitters must be released from the axon terminal of the presynaptic neuron in order to bind to receptors on the postsynaptic dendrite and generate an action potential. That is, at the "end" of the first neuron, it pumps out chemicals. They float around in the space between it and the second neuron. There are receptors on the second neuron which the chemical can fit into, and when it does that, it causes a small change in the electrical charge of the second neuron (resting membrane potential). When enough neurotransmitters can snuggle up into those receptors, it causes the neuron to "fire", or depolarize.

There is usually much more sodium on the outside of a neuron than the inside; this maintains the electrical and chemical gradients. When the gates open, because of the differences in charge and concentration of ions, sodium will rush from the ooey gooey outside of the neuron, through the channels, and into the second neuron. This sends impulses along, causes further firing, and tra la la. Then potassium channels open up as well; there is much more potassium inside the neuron than outside, so it will go from high to low concentration - from inside the neuron to outside.

Sodium and potassium are both charged ions, 1+. So when a neuron depolarizes and sodium comes in the charge gets much higher, very quickly. (This process is nonreversible - once you pop the fun don't stop! Or, rather, once the threshold for an action potential is reached, the cell WILL depolarize, all the way. No halfsies or turny backsies.) When the potassium channels open up and potassium exits, the charge drops down, getting lower very quickly. It actually tends to get a little bit lower than the cell "likes" to be at - this is the refractory period.

The refractory period has two parts. First, the absolute - this means that no matter what, nothing absolutely nothing will make the cell depolarize again... It's not ready. Things are all in the weird wrong places and it needs to get back to normal. In the relative refractory period, the charge is still lower than normal so it is harder to make the cell depolarize... But it can be done, if there's a whoooooole bunch neurotransmitters binding to receptors on sodium channels. Eventually the cell gets things sorted out, and it is once again at it's resting membrane potential - the charge that exists when it is at homeostasis.

That's the main process. Anyways. Suppose.you get pufferfish goo all up in ya and it binds to the voltage gated sodium channels - essentially, blocking them. That means sodium can't pass through. Sure, you might get little bumps of positive from other stuff binding to various sites on the dendrite, but nowhere near enough the level to required to get to the threshold necessary, the charge at which an action potential is generated.

So. It doesn't matter how much neurotransmitter is released, how much binds to receptors. They're blocked. The neuron can't get sodium in. So the charge never gets higher real fast real big, no action potential can be created, there is no electrical impulse that travels down the neuron to the next.... Essentially, the neurons stop firing. No electric conduction, no messages sent, uh oh brain broken, you dead.

So...

a) Neurons would depolarize more rapidly.

No. They would not depolarize ever.

b) The axon would be unable to generate action potentials.

True!

c) the absolute refractory period would be shorter than normal.

No. Funnily, you kinda can look at this a couple ways. Either you never have an absolute refractory period, since you never had an action potential and repolarized a little too much, or you could consider this like a "forever" absolute refractory period. Because, this cell is absolutely not going to fire. No sodium movement, no firing, period. I don't honestly know if the definition of absolute refractory period necessitates that the cell firing is part of it, or not. But regardless, it will not be shorter. It will either be nonexistent, or longer as in forever and ever. So this answer doesn't fit.

d) None, because the ligand-gated sodium channels would still function.

Do neurons have ligand gated sodium channels? Meh. Probably. Is that how they work in order to conduct nervous impulses? No. It is changes in the electrical gradient that are involved in this process. So even if some sodium can get through these possible ligand channels, it will never result in an action potential, which again is a rapid depol/repol change in charge that goes down the neuron, causing the next to fire via the process we have described. We need a massive, fast change in voltage - that won't happen from every once in a while someone bumping a ligand channel and a few sodiums sneak in. We need a choreographed, same time, lots and lots of sodiums to get in all at once. That only happens if they are electrically stimulated to do so.

Therefore.... Let's call the answer 'B' - no more action potentials.