how does the paralytic neurotoxin of Pyemotes tritici work?

[kimagurealex]

Describe the biological acitivty of the toxin please, I look all over the internet including the NCBI sites but I couldn't find a paper that describe the mechanism.

 

[Looney]

That's one of the reasons why i dropped biology... it freaking makes me stutters.

 

[Jfur]

good luck

 

[kimagurealex]

Did I mention I 've looked all over the internet? but thanks for the input, Jfur, I've been to that website and it didn't help, no mechanism was described, such as action potential blocked, or stuffs like that...you know what I mean?

 

[Jfur]

maybe contact the guy in Texas -- he may respond?

 

[exp]

Obtain copies of the research papers cited on the web-page Jfur provided. The Tomalski ones should have what you are looking for.

 

[kimagurealex]

I've read the abstract of every single one of his papers I could found on Entrez, but I don't have access to those paper in whole. I 've found something that kinda imply the toxin affect the voltage gate Calcium channel, is there any physiologist here that can explain what could be going on? I am under time constraint here, so can't really go and start flipping pages now. Thanks in advance.

 

[Looney]

I've read the abstract of every single one of his papers I could found on Entrez, but I don't have access to those paper in whole. I 've found something that kinda imply the toxin affect the voltage gate Calcium channel, is there any physiologist here that can explain what could be going on? I am under time constraint here, so can't really go and start flipping pages now. Thanks in advance.


I can't wait until the day they decide to make the entire articles in digital form rather than just the abstracts. I've run into the same problem as you, i'll find something on medline or psychinfo from my home, but then need to take a 45 min drive back to the library to look up the journals.

 

[kimagurealex]

not likely in the near future, copyright and intelletual properties issues.....

 

[Looney]

Well, you can already photocopy it at will... i assume as long as it's properly credited it would be ok. Magazine articles etc are being hosted online, i can't see why these articles can't... especially since they're not exactly profitable to begin with.

 

[BD2003]

Geez, now I know what my mom feels like when I tell her:

"I think I found the problem...the PCI IDE Controller had an IRQ conflict with the onboard SCSI. Damn ACPI."

or

"No mom, its not the amount of megahertz you have, its a combination of FSB Speed, DDR Memory, and FPU performance that matters. Hardware texture and lighting is nice, and some fillrate here or there wouldnt hurt."

 

[exp]

<< I've found something that kinda imply the toxin affect the voltage gate Calcium channel, is there any physiologist here that can explain what could be going on? >>



Well, I will give it a shot but it would help if you knew what types of neurons the toxin acted on. Assuming the toxin in question is acting on motor neurons at the neuromuscular junctions there are two sets of Ca2+ voltage-gated channels there that could be affected. The first set is in the plasma membrane of the neuron axon and is opened in response to an action potential. Ca2+ influx then triggers the release of the neurotransmitter acetylcholine. Acetylcholine is released into the synapse between the neuron and the muscle cell and triggers the opening of Na+ channels in the plasma membrane of the muscle cell. Depolarization of the membrane by influx of Na+ causes the second set of Ca2+ channels to open and release stored Ca2+ from the sarcoplasmic reticulum.

Unfortunately we don't know how this particular toxin affects the Ca2+ channels--it could activate them or inhibit them--although we could figure that out if we knew what kind of paralysis it inflicted. I have heard of Ca2+ channel blockers before so this may be one of them. If it is a blocker then it would likely induce catatonic paralysis by either 1) preventing action potentials from reaching the muscles (if it acts on the first set of Ca2+ channels), or 2) preventing muscle contraction by inhibiting Ca2+ release from the second set of channels.

I am no physiologist, though, so you should probably get some other opinions. Does this sound right to everyone?

Anyway, definitely hit the library and get those papers if at all possible.

 

[exp]

One more thing...the title of one of those Tomalski papers suggests that p. tritici TxP-1 toxin is at least partly homologous with Tox21A. If that is true then maybe there is more data available on that one than on TxP-1. You might try looking for information on Tox21A or other homologous proteins, since they would presumably have the same, or similar, mechanism of action as TxP-1.

 

[kimagurealex]

Thank you so much exp. I guess the logical question that follows would be, does insects have the same motorneruon model as mammalian cells? I know the model you provided is valid with mammalian cells, but I am not sure about invertebrate. Thanks once again.

 

[MajesticMoose]

/me smiles and nods

m00se

 

[exp]

<< I guess the logical question that follows would be, does insects have the same motorneruon model as mammalian cells? >>



Good question...you are quite right, that was the model for human cells I gave. However, I do know that much of our knowledge about vertebrate nervous system function has come from studying insects (good ol' Drosophila). Like humans, insects do have K+, Na+, and Ca2+ channels that are responsible for propagating action potentials. Also, acetylcholine is a ubiquitious neurotransmitter and can be found in both vertebrates and invertebrates.

Beyond that, I don't know. The actual arrangement and even role of Ca2+ channels could very well be different for insects. It might be difficult to find information on something so specific as insect ion channels but you could always try a web search and see what pops up.