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Wangers
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#1
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k, can someone clear this up please:

non myelinated conduction - slow because impule is dissipated, without reaching target effectors? (thats what ive always thought)

but the markschemes and stupid notes teacher gave us say - that it is slower then saltatory conduction because saltatory conduction only needs depolarisation at the nodes of Ranvier.

This to me sounds ******ed - Surely immpulses have to travel down the length of the nerve cell axon, irrespective of wether it is insulated ot not. And since the nodes do not amplify the amplulse, how does this work??

:Confused: any help appreciated.

Thanks people
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Ancient Beast
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Myelinated is faster because action potentials can only be initiated at the nodes (contain Na channels). Therefore the impulses jump from node to node, thus conductions are quicker.
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miki_da_magpie
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Hm, not sure if this'll help you but I'll try. Non-myelinated conduction is slow because the impulse dissipitates, this is correct. It's shown in people who have multiple sclerosis. The glial cells (schwann cells and oligodendrocytes) insulate the axon so that little current leaks out of it. The nodes of ranvier are where the Na ions are concentrated, but its not insulated. Since the insulated bits keep so much electrical current in, the AP moves quickly from node to node. Thus the nodes dont DO anything, but the glial cells allow the axon to be as efficient as possible. (Jumping from node to node is Saltatory conduction).
If the axons are not insulated then more electrical current is wasted in dealing with the in and outs of Na and K ions, thus the AP will lose its strength.
Thus, saltatory conduction is much quicker and efficient that non-myolated conduction.
Hope that helps, and you might want to double check with something, im no expert.
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Wangers
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So the myelination allows impulses to travel between nodes with greater speed, while still retaining their *strength*.

Presumably in the non myelinated (or where the sheath has been destroyed) the "whole impulse" travels slower because each individual impulse takes longer to reach the next conduction point, ot dosnt reach it at all?

Do the Nodes act as normal na/k+ depolarisation sites then? ie the usual chain of events, with a threshold potential etc etc....

Do the strength of the impulses from the node depend on the grand resultant potential, ie are they conditionable, or just constant?

Thank you
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miki_da_magpie
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The myelination is only a "wrap" of sheats around the axon, whereas at the nodes, there is no "wrap" just the axon, so essentially the myelination only insulates the axon so that less of the potential is lost. The AP depolarises each Node, which elevates the voltage of the next Node, which causes it to depolarise. So the AP is not a fluid motion, but more like hops from one node to the next. This means they travel faster than normal (I dont know why, hopping seems to be faster than moving along the axon normally). So when the nodes are destroyed the AP is slower... but still works. In MS, the nodes keep being replaced by new ones, which causes scar tissue to build up and eventually stop the axon from firing. This is also handy to keep in mind: "Apart from increasing the speed of the nerve impulse, the myelin sheath helps in reducing energy expenditure as the area of depolarization and hence the amount of sodium/potassium ions that need to be pumped to bring the concentration back to normal, is decreased." - wikipedia (very handy)
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Revenged
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(Original post by miki_da_magpie)
In MS, the nodes keep being replaced by new ones, which causes scar tissue to build up and eventually stop the axon from firing.
Multiple sclerosis is an autoimmune disorder that causes demyelination and neuronal death...

It is the myelin sheath that is replaced - not the nodes...

It is not true to say that when an myelinated neurone demylinates it still functions but slower than normal... This isn't the case, the neurone simply dies without a sufficient myelin sheath...

and it is the death of neurones in certain part of the brain and/or optic nerve that causes multiple sclerosis...
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Revenged
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(Original post by Wangers)
Do the strength of the impulses from the node depend on the grand resultant potential, ie are they conditionable, or just constant?
Action potentials are "all or nothing"...

An increased stimulus will have an increased frequency of action potentials and would generate action potentials in more neurones...
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miki_da_magpie
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(Original post by Revenged)
It is the myelin sheath that is replaced - not the nodes...
Sorry, i meant the myelin sheath

(Original post by Revenged)
It is not true to say that when an myelinated neurone demylinates it still functions but slower than normal... This isn't the case, the neurone simply dies without a sufficient myelin sheath...
Myelin sheaths are replaced are they not? Just because one section of the axon is demylinated doesnt mean the whole neurone dies, does it? As I said, I'm no expert... I thought that the sheaths were replaced by new sheaths (less efficient), therefore neurone function is limited but not completely stopped until MS is advanced...

(Original post by Revenged)
and it is the death of neurones in certain part of the brain and/or optic nerve that causes multiple sclerosis...
Yes, MS was used as an example for what happens when there are no myelin sheaths...
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Revenged
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(Original post by miki_da_magpie)
Myelin sheaths are replaced are they not? Just because one section of the axon is demylinated doesnt mean the who neurone to die does it? As I said, I'm no expert... I thought that the sheaths were replaced, therefore neurone function is limited but not completely stopped until MS is advanced...
Yes, myelin sheath is being replaced... there is a remitting period where there is death of myelin sheath but it is being replaced and so there are no symptoms... but this doesn't last forever and the replaced myelin isn't like the original and eventually you get total demyelination, which causes death of neurones...

Myelinated neurones cannot function when they are completely demyelinated, which is what the problem is in multiple sclerosis... neurones simply die and with cell death you get symptoms of multiple sclerosis... Unlike peripheral nerves when central nerves are damaged, this damage is permanent and they cannot be repaired... In fact, the body stops such replication by astrocytes forming scars at the end of neurones...

Well, that's what i think happens...

Typically with someone with MS, they will be young... have had a previous symptom of upper motoneurone damage a few years before... and then will present with some damage to vision and/or various uppermotor disorders (sign of central nerve system damage) a few years later... IgG antibodies in the cerebrospinal fluid and white patches on a MRI scan are signs...
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Wangers
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why would the body want to form the scar tissue? Surely the intuitive thing to do is to continue repair efforts?
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miki_da_magpie
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(Original post by Wangers)
why would the body want to form the scar tissue? Surely the intuitive thing to do is to continue repair efforts?
I dont think its a case of "wanting" to form scar tissue. Just like scin scars I guess the body wants to make sure everything is covered so it over does the repair... I ahve no clue if im on the right path, it just makes sense. Like if you get a wound on your arm and you get a scar... its just extra skin and tissue to make sure the wound is completely closed up... :confused:
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(Original post by Wangers)
why would the body want to form the scar tissue? Surely the intuitive thing to do is to continue repair efforts?
Yes but some things in the body are so complex that they are beyond repairing... The central nervous system is so complex that if the body did even try to repair itself it would probably make things a hell of a lot worse... So it has developed ways to prevent the regrowth of central nerones...

but the paradox is that the liver can basically completely regrow even if you took about three quarters of it... and it can function with only about twenty five percent... well, it's something like that... i have just made up those figures... i don't really why the liver can regrow and other organs such as the brain cannot...
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miki_da_magpie
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(Original post by Revenged)
but the paradox is that the liver can basically completely regrow even if you took about three quarters of it... and it can function with only about twenty five percent... well, it's something like that... i have just made up those figures... i don't really why the liver can regrow and other organs such as the brain cannot...
Is it because NS cells cannot undergo mitosis? Neurone's are born and last a lifetime rite? And all other cells undergo mitosis throughout one's life. I read somewhere that liver cells complete development in about a year. So if part of your liver is surgically removed, it'll grow back over time. Is it because liver tissue is non-specific? But then why can't the pancreas grow itself back, too small? The liver really is quite extraordinary...
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Revenged
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(Original post by miki_da_magpie)
Is it because NS cells cannot undergo mitosis? Neurone's are born and last a lifetime rite? And all other cells undergo mitosis throughout one's life. I read somewhere that liver cells complete development in about a year. So if part of your liver is surgically removed, it'll grow back over time. Is it because liver tissue is non-specific? But then why can't the pancreas grow itself back, too small? The liver really is quite extraordinary...
I don't really know the answer... but peripheral nerve cells can regenerate and i doubtful they do so due to mitosis... some peripheral nerve cells are about a metre long... maybe wrong though...

what you do at uni btw?
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miki_da_magpie
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Biomedical sciences Just finished first semester and we did quite a bit on excitatory cells. What bout you, why do you know so much :P?
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Wangers
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maybe because the liver plays a more vital homeostatic function - ie advantagous to the holistic survival of the body? whereas concievably you could get away with MS damage on a nerve?

and when you say regenerate - do you mean crawling fibres?? I cant remember if thats what they're called - the ones that bridge the gaps and stuff.
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miki_da_magpie
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[QUOTE=Wangers]maybe because the liver plays a more vital homeostatic function - ie advantagous to the holistic survival of the body?QUOTE]

True it does play a vital part in homeostatic function, but then so do kidney's (osmoregulation etc) and erm the longs as well... and the heart, cant forget the heart... but why can none of those cells "regrow" whereas the liver cells can?
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(Original post by miki_da_magpie)
Biomedical sciences Just finished first semester and we did quite a bit on excitatory cells. What bout you, why do you know so much :P?
2nd year medic... and i don't know that much mate... but i like what i do and you find that you pick a lot up when you enjoy what you are doing...
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miki_da_magpie
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I wish I was doing med, I aplied and divvn get in, instead of a gap year I chose to do biomed, I hope it gets a little more humane...less sciency you know, im more of a people person but the study is giving me good background i figure. I have a mate who is doing med and he's loving it, hard work but loving it. Hopefully I will still want to do medicine after I get my bachelors
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Revenged
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(Original post by Wangers)
maybe because the liver plays a more vital homeostatic function - ie advantagous to the holistic survival of the body? whereas concievably you could get away with MS damage on a nerve?

and when you say regenerate - do you mean crawling fibres?? I cant remember if thats what they're called - the ones that bridge the gaps and stuff.
With MS parts of the brain die... and you lose nervous function... your brain cannot really compensate...

and if part of the liver degenates then you have no problems...

i don't know what you mean by crawling fibres?... the only thing i can think about is climbing fibres but this is to do with the central nervous system, which doesn't regenerate...

and i don't really know how peripheral nerves regenerate...
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