Any biology wizzes out there?

[Mo0o]

I need help on this group presentation we need to do

Our task is to design a droup that counters Tetrodotoxin poisoning. The only problem is theres no current antidote. What im thinking is apply Batrachotoxin since it opens the permeability of the sodium gates which antagonizes TTX which closes the sodium gates down. And if theres any BTX sideeffects apparently theres a drug called DigiBind that fights it. This is all speculation of course because im not sure if BTX can reopn the sodium gates after TTX has firmly bound itself into the sodium gates

Yes this is a blatant cry for help in a hw assignment. But I have done research and im just asking for input.

 

[Wallydraigle]

Here.



But seriously, you design an antidote for tetrodotoxin and turn it in, your professor publishes it and obtains the patent, ten years down the road the FDA approves it and tetrodotoxin becomes the anesthetic of the twenty first century. Your professor rakes in teh billions, and you're left at Burger Shak asking greasy people if they want fries with that. Run. Run far away.

 

[DrNoobie]

Mmmm...pufferfish. I believe that researchers were looking into 4-aminopyridine as a possible antidote. It's a K-channel blocker, and was successful in the treatment of lab animals. I don't know where that went, however. You might consider something along those lines. Instead of trying to prevent something from happening, treat the damage that was done. I don't know, I'm just a premed student throwing out ideas.

 

[Mo0o]

I read about that as well, but how does K channel blocker treat the damage. I was under the impression the K channel needs to be open during repolarization.

 

[DrNoobie]

Originally posted by: Mo0o
I read about that as well, but how does K channel blocker treat the damage. I was under the impression the K channel needs to be open during repolarization.

It's not the blockage of the K-channel that treats the damage, 4-aminopyridine heals damaged nerve endings, though I forget exactly how.

 

[Mo0o]

But the problem still remains of TTX staying bound to the Na channels

 

[tweakmm]

::woooooooosh::

Do you know what that was the sound of? That was the sound of this thread going waaay over my head.

 

[Mo0o]

Originally posted by: lirion
Here.



But seriously, you design an antidote for tetrodotoxin and turn it in, your professor publishes it and obtains the patent, ten years down the road the FDA approves it and tetrodotoxin becomes the anesthetic of the twenty first century. Your professor rakes in teh billions, and you're left at Burger Shak asking greasy people if they want fries with that. Run. Run far away.

yeah i also noticed a little fishiness with this assignment. although i gues they figured college freshman aren't gonna find a cure where realy scientists and docs have failed

 

[DrNoobie]

Originally posted by: Mo0o
But the problem still remains of TTX staying bound to the Na channels

TTX poisoning naturally gets better after a 24-48 hour time period (depending on the amount ingested), the problem is most people who become poisoned die within 6 hours. 4-aminopyridine reverses the effects of TTX, restores normal breathing patterns and heart rate patterns, and keeps the patient long enough for the body to naturally heal.

 

[Mo0o]

bleh i feel so stupid, i still dont get it. withint those 24-48 hours, when the TTX is still affecting the sodium channels, how does 4-aminopyridine help? from what i read, and your explanation it only affects potassium channels.

edit: i think my biggest question is how does altering k channels affect the na channels? i thought k channels only come into play during repolarization after an action potential. if sodium channels are blocked then there would'nt even be depolarization.

 

[Mo0o]

omg i think i get it. is it because since 4aminopyridine blocks k channels, it prolongs any depolarization bursts done by none affect sodium channels. ?