Where does the electricity come from?

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Electricity in nerves originates from the movement of ions, primarily sodium (Na+) and potassium (K+), which create an electrochemical gradient across cell membranes. When a nerve is stimulated, ion channels open, allowing these ions to flow in and out, leading to an action potential characterized by depolarization and repolarization phases. Paralytic venoms, such as those from spiders, can disrupt this process by either blocking or excessively activating ion channels, affecting muscle contractions. The discussion also touches on the Hodgkin-Huxley model, which describes the action potential mechanism but faces scrutiny regarding its assumptions and accuracy. Overall, understanding these electrical signals is crucial for grasping neurophysiology and the effects of various toxins.
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I was wondering if someone could tell me where the electricity used for the nerves come from? and could someone with a good knowledge of the matter please explain how it works to me? :)
 
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A nerve 'signal' is called an action potential. You can read the basics about them here: http://bcs.whfreeman.com/thelifewire/content/chp44/4402002.html
 
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At a glance, wikipedia seems to do a decent job: http://en.wikipedia.org/wiki/Action_potentials

A quick summary assuming I remember it correctly: the charges (from ions, Na and K I think) inside and outside of cells are different, setting up an electric gradient. When the cell is signaled to fire, it opens the ion channels and the charged particles rush in/out to eliminate the gradient, which causes some electrical thing to happen (sorry, I know the biological more than the electric part). But yeah, there are more details in the wiki article if you want them.
 
Many paralytic venoms used by spiders and other creatures affect the opening and closing of those channels. A paralytic will work either by causing the channels to open wide, causing the signals to continue non-stop, or slam shut, so no signals are sent and the muscles don't contract at all. A relaxing paralytic is not useful to a hunting, arboreal spider, since it will likely result in their prey falling out of the tree, making it hard for the spider to find and eat it. However, a convulsive paralytic will cause the prey to continue to grip, making it less likely to fall out of the tree. It does this by inducing the neurons to fire continuously. The black widow venom (latrotoxin) is an example of this, and is characterized by severe muscle cramps throughout the body, and particularly in the abdomen.
 
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RogueSpidor said:
Many paralytic venoms used by spiders and other creatures affect the opening and closing of those channels. A paralytic will work either by causing the channels to open wide, causing the signals to continue non-stop, or slam shut, so no signals are sent and the muscles don't contract at all. A relaxing paralytic is not useful to a hunting, arboreal spider, since it will likely result in their prey falling out of the tree, making it hard for the spider to find and eat it. However, a convulsive paralytic will cause the prey to continue to grip, making it less likely to fall out of the tree. It does this by inducing the neurons to fire continuously. The black widow venom (latrotoxin) is an example of this, and is characterized by severe muscle cramps throughout the body, and particularly in the abdomen.

An interesting example... The drug class you are referring to are 'neuromuscular channel blockers' and are used mainly in operations to induce muscle relaxation...

You are correct that you can induce paralysis by two different mechanisms...

For example, can induce paralysis by blocking nicotinic acetylcholine receptors (e.g. tubocurarine)... This causes sodium ion channels to remain close, neurones cannot fire and you get the 'paralytic' effect you discribe...

You can also do the opposite when induce paralysis by excessive activation of nicotinic acetylcholine receptors (e.g. suxamethonium)... Initially this would cause convulsions (due to excessive activation of neurones)... Later this would cause paralysis since excessive activation of the receptors cause them to become desensitised to the neurotransmitter...

This is only one example of a mechanism... For example, the 'latrotoxin' the black widow spider uses does not activate nAChRs like suxamethonium... It works by dramatically increasing the release of neurotransmitters, which excessively activate nAChRs...
 
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Molok said:
I was wondering if someone could tell me where the electricity used for the nerves come from? and could someone with a good knowledge of the matter please explain how it works to me? :)

Resting potential is negative mainly due to high K+ concentrations within the cell compared to outside...


And the two main stages of action potential are...

1) Na+ enters (depolarisation)
2) K+ leaves (repolarisation)
 
 
The central concept is that of an "electrochemical gradient". We have the usual notion that diffusive substances with high concentration in one area and low concentration elsewhere tend to equalize concentration across areas, over time. We also have the notion that voltage differences provide a driving force, pushing charged molecules toward high (opposite) charges.

We can combine these two notions and obtain equilibrium concentrations for ions on either side of a membrane. Normally active pumps maintain these concentrations away from their equilibrium values, however when an action potential (large depolarization) occurs, the ions are allowed to flow across the membrane and upset this equilibrium away from the norms of physiology. This perturbation away from equilibrium is the basis for all signals in neurophysiology
 
This works only if you consider that gradients remain constant. But it is impossible (at molecular level).
 
  • #10
somasimple said:
This works only if you consider that gradients remain constant. But it is impossible (at molecular level).

I'm not sure what you mean by this? The electrochemical gradients don't remain constant. This is actually what makes an action potential possible.

At resting potential, the concentration gradients are maintained by active transport.
 
  • #11
If we consider the process at a macroscopic scale, the concentrations remains constant.
But if we accept a facilitated diffusion, we admit that diffusion is driven by Coulomb forces that work only near the membrane (<50 nm).
http://www.somasimple.com/forums/showpost.php?p=38312&postcount=22
http://www.somasimple.com/forums/showpost.php?p=38545&postcount=24

The simple conclusion is that ions close to the membrane may be involved but the others can't. tHis little and simplified movie shows the rising phase of an AP. The process stops naturally because there is no more "fuel" (ions). (The movie doesn't show the water molecules involved in the ion channel)
http://www.somasimple.com/flash_anims/ICrise.swf

Of course, it implies that conductances are constant. Thus, a complete refinement of the HH model is necessary. But, but... This new model fits the facts and respects Physics.
It explains, also, refractory periods and solves the propagation, spatial and temporal summation, in an elegant manner.
 
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  • #12
At resting potential, the concentration gradients are maintained by active transport.
In the same way, this process is largely reduced and non constant. The active transport is then activated when necessary. The mystery of the "lost" energy consumption is solved.
 
  • #13
Soma Simple, if you'll fully explain what you think is wrong with the Hodgkin-Huxley model then I can show you what your mistake is. The fact is that the Hodgkin-Huxley model has stood for over 50 years with relatively few modifications and almost no radical challenges*. The theory is <at very least> quantitatively accurate in predicting neural responses.

It is almost certain that the model's mathematical formalism neglects a lot of facts about neurons which affect their responses (perhaps you have noticed some of these). However, this is taken to mean that the relative contribution of these things to overall neural behavior is small, since the overall behavior is predicted quite well within the Hodgkin-Huxley framework already.

*Recently, there has been a limited challenge to the Hodgkin-Huxley assumption that the openings of sodium channels are independent events. The alternative model is conceptually almost identical to Hodgkin-Huxley with the small modification of cooperative sodium channel openings.
 
  • #14
Soma Simple, if you'll fully explain what you think is wrong with the Hodgkin-Huxley model then I can show you what your mistake is.

here =>
http://www.somasimple.com/forums/showpost.php?p=39321&postcount=66

Please, explain how it is possible, in an equipotential wire, to have opposite currents ?
And how it is possible that a resistance is able to create energy?


BTW, I'll like to refute my assumptions about Coulomb forces interactions. Is my movie wrong? (there is a computed concentration percentage at the top right!)
 
  • #15
somasimple said:
here =>
http://www.somasimple.com/forums/showpost.php?p=39321&postcount=66

Please, explain how it is possible, in an equipotential wire, to have opposite currents ?
And how it is possible that a resistance is able to create energy?

What are you talking about? No one is claiming "equipotential wires have opposite currents" or that "resistances create energy" I'm not even sure what you mean by these.

As for the drawing on the linked website... It is also unclear what this is supposed to mean, none of those graphs are labeled. You merely circle random sections of them with no explanation of your objection.

You need to clearly explain your problem with the model, as it is, what you are saying is pretty incoherent.
 
  • #16
Cincinnatus,

I took the HH model as described by the eminent professor F Bezanilla (on his site).
I put the link of his page and the drawing comes from there.
http://www.somasimple.com/forums/showpost.php?p=39321&postcount=66

Cincinnatus said:
What are you talking about? No one is claiming "equipotential wires have opposite currents" or that "resistances create energy" I'm not even sure what you mean by these.

I'm the one that claims it!

Professor Bezanilla draws the current circulations with green arrows and I rounded with red circles the errors in the model.

You may contest it but propagation with such current circulations is made impossible because these situations may never happen.
 
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  • #17
Perhaps you missed the original link
here it is:
http://nerve.bsd.uchicago.edu/med98d.htm#Propagation

And I may add the complete description of mistakes I found:

Image C : Opposite current circulation in an equipotential wire (2 times).
Image D : Opposite current circulation in an equipotential wire and Resistance has an impossible current circulation too since it generates a current.
 
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  • #18
I see the pictures in your links and I see that you have circled various parts of them. This doesn't tell me why you think the Hodgkin-Huxley theory implies these "mistakes".

The particular explanation of the theory on the page you linked to is (IMO) not very good. There are much better explanations in textbooks by:

-Kandel et. al.
-Squire et. al.
-Dayan and Abbott

If you pick up any of these books and read their description of the model it will probably make much more sense to you than the explanation on that website.
 
  • #19
That is not a reply!
Just give your comments.
 
  • #20
You assert that there are errors in the places you circled. You never explain what these errors are. There is no comment I can make about that unless you explain what you are talking about.

I won't reply to this thread again unless you do so.
 
  • #24
Albert Einstein said:
The important thing is not to stop questioning. Curiosity has its own reason for existing. One cannot help but be in awe when he contemplates the mysteries of eternity, of life, of the marvelous structure of reality. It is enough if one tries merely to comprehend a little of this mystery every day. Never lose a holy curiosity.
Is there a biologist in the forum?
 

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