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Myelin Sheath


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The myelin sheath of neurons in the CNS is formed by cells called oligodendrocytes, but in the PNS it is formed by Shwann cells. Both of these cells act as electrical insulators surrounding the axon. They work by laying down layer upon layer of their own plasma membrane in a tight spiral fashion, this myelination decreases the ability of the neuronal membrain to retain electric charge and therefore the depolarization spreads faster and farther.

 

I hope this helps, personally I think the nodes of Ranvier stuff is more fascinating :)

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  • 1 month later...

hey you seem to know your stuff, instead of making a new topic i was wondering if i could ask my question here..

 

Do you think you could possibly explain, in simple terms (if you can) the nerve impulse transmission process to me? My text book explains it in such a way that it seems very confusing to me :mad:

 

that help would really be appreciated, thanks!

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Can anyone tell me the composition of the Schwann Cells that makes them unique the way they are?

As for the composition, the plasma membrane is just the usual phospholipid bilayer (mainly fat), and many layers of this makes a very good electrical insulator.

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hey you seem to know your stuff' date=' instead of making a new topic i was wondering if i could ask my question here..

 

Do you think you could possibly explain, in simple terms (if you can) the nerve impulse transmission process to me? My text book explains it in such a way that it seems very confusing to me :mad:

 

that help would really be appreciated, thanks![/quote']

Ok. (deep breath) There are three forces at work whilst a neuron is at rest. There is an electrical potantial, there is a concentration gradient and there is a sodium/potassium pump.

 

The electrical potential is due to the high concentration of large, negatively charged proteins (albumin) inside the cell, so the inside of the cell (at rest) has a negative charge of -70mv compared to the outside. This is called the resting potential.

 

The concentration gradient is to do with the concentrations of sodium and potassium ions (both positively charged ions); there are many fewer sodium ions inside the resting cell than outside, and many more potassium ions inside than outside.

 

The sodium potassium pump is an active transport mechanism that pums sodium out and potassium in. This helps to maintain the concentration gradient.

 

When the cell is stimulated, sodium channels in the membrane open, and sodium rushes in down its concentration gradient, and towards the more negative inside of the cell (remember, these ions are +ve). The resting potential begins to change. Once it has gone from -70mv to the threshold level of around -15mv, the local change in charge causes local voltage gated sodium channels to open and sodium ions flood in. The potential changes from around -15mv, to around +40mv. This is known as an action potential (AP) and is a very local event.

 

However, action potentials propogate. This local change in membrane potential creates a local current which triggers voltage gated sodium channels further down the axon. These open, sodium rushes in and so the AP travels down the axon.

 

In myelinated cells, the local current cannot open channels in the myelinated sections, but it is strong enough to 'leap' to the next node (the non-myelinated sections between the schwann cells are called the Nodes of Ranvier), and cause voltage gated sodium channels concentrated at these nodes to open. This mechanism of the current 'leaping' from node to node is called Saltatory conduction (from the Latin; Saltare: To Leap), and is a much faster method of propogation than happens in non-myelinated axons (e.g. C fibres).

 

This leaping propogation of the AP travels down to the axon terminal, where the current causes calcium channels to open, allowing calcium ions to enter the presynaptic membrane. This calcium causes vesicles filled with neurotransmitter substance to move to the presynaptic membrane, where they burst, like bubbles coming to the surface of water (a process known as exocytosis), releasing the neurotransmitter into the synaptic cleft.

 

The transmitter molecules diffuse across the cleft and bind with ligand gated channels (i.e. channels that require a substance to open them like a key in a lock, as voltage gated channels). When the transmitter binds to these ligand gated channels, they open and sodium rushes in and the whole process starts again in the next neuron.

 

I hope that's simple enough?

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Thank you so much, Glider. Thais is very helpfull and i can understand the process now a great deal better now. However, some of the information you gave is beyond what is expected of me at the moment (highschool bio), a more indepth explanation makes the process easier to understand than a greatly simplified one which leaves out some critical aspects of it.

 

thanks.

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Reading that it seems like the process would take a long time, and then far longer to set it back up to happen again. I know it happens many times a second, but it's kinda shocking hearing it like that when I'm not used to it;)

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I know what you mean. A lot happens in a very short space of time. Once an AP has passed, the membrane hyperpolarises and the sodium channels become 'locked', (known as the refractory period), which prevents tetany. But even this lasts only around 2 milliseconds.

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