Nerves, aka the not-so-good wires

Author’s note:

So, just before we explore the workings of message transfer in the human body, I would like to clarify the origins of this blog post. On Saturday 5th November 2016, Cambridge University held a Medicine Taster Day at the Lady Mitchell Hall. This consisted of sample lectures and a run through of the teaching system, among other tips for entry. One of the lectures was titled something along the lines of “How do nerves work?”. As fabulous and interesting as the other lectures were, this one really gave me the most “food for thought”, as they say, and it is on the notes that I made during the lecture that is blog post is based.

Thus, I implore you to understand that writing notes on a topic which a lecturer is comfortably pacing through and later trying to make out the beginning and end of your scrawls is no easy feat (as I’m sure we’ll all find out about in a few years’ time and become masters of note taking). I admit that I wanted to write this solely on my notes to a) review the lecture and b) to see if I understood anything that was being said.

But before any of you future Biology stars start panic (or panic further as may be the case), I did ask for my Biology teacher to look over this post. The message is this: this is a very simplified version of what is happening in real life, especially in the case of amplification. We shall, of course, come to study the topic of nerves in more detail and finesse further in the A Level course.

Oh, and another thing. If any of you dear readers come to learn that any of the figures are incorrect, I sincerely apologise and please do not hesitate to let me know. In the meantime, feel free to blame my poor eyesight (I did find out a while later that my right eye has deteriorated 🙂 ) or my incomprehensible handwriting for any mistakes made.


Nerves work in a similar fashion to wires, but when you look at their basic structure, to be honest, they’re a bit of a disappointment to the wire family.

So, if nerves are the “ok” version of copper wires, how do we manage to stay alive?

Firstly, we’ll look at how nerves work, then the problems they encounter and finally how they try to overcome the issues of transferring current.

Trying hard to be a wire

When a pain fibre is stimulated, pain channels are opened and sodium ions (which have a positive charge) enter at one end of the nerve while the rest remains negatively charged. The next stages are similar to those of a battery, as, the differently charged ions create a current which spreads positive charge through the nerve and this results in the potential of activating something else, such as a synapse.

In comparison to a copper wire in which the speed of this is 28,000,000 m/s, the nerve’s speed is between 0.6 to 100 m/s. However, although this is significantly lower, this is not a limiting factor in the body’s reactions, as the message still travels in milliseconds.

The difficulties begin

As usual, there are problems with all wires, however this is particularly true of nerves, and the problem nerves face is that current leaks out.


Fig 1. Diagram showing longitudinal and membrane resistance in a nerve.

In the diagram above (Fig 1.), RL (red line) is the longitudinal resistance and it is a measure of the resistance the current encounters as it travels along the nerve. The lower this resistance, the easier it is for the current to travel.

Rm (blue line) is the membrane resistance and this is a measure of the resistance given to the current by the cell membrane. The higher this resistance, the less current will escape.

How far can a nerve conduct?

Voltage decreases exponentially, meaning it leaks less.

The distance at which the voltage has decreased by half is called lambda (λ), and it is a ratio of the two resistances aforementioned. In effect, it is a ratio of how much voltage continues travelling along the nerve to how much has leaked out.


This means that high membrane resistance and low longitudinal resistance results in a good signal.

We must also remember that resistance is calculated by:

R = p x l/A


  • R is resistance
  • p is resistivity
  • l is length
  • A is cross-sectional area


Nerves are very narrow as they normally have a diameter between 0.2 to 2.0 micrometres, meaning that RL is large.

The cell membranes are also very thin, typically between 7.0 to 9.0 nanometres, so Rm is small. This is due to the fact that the membrane is made of two molecules – specifically two phospholipids, as cell membranes are bilayers.

In addition, the axon, which is mainly cytoplasm, has a resistivity of 50 To put this into perspective, copper wires have a resistivity of 1.7×108 The poor axon resistivity is because, since nerves are part of the body, they have to be able to change shape, which is the advantage of a conducting liquid.

As a result, a 1 metre long, 1 micrometre diameter nerve has the same resistance as a 22-gauge copper wire, which in other words is a 0.65 nanometre diameter piece of copper stretching to Saturn and back. Five times.

A much-needed rescue

To put it nicely, nerves are probably not the material you would be reaching for if you wanted to transfer some current. As a result of their physical properties of being narrow, thin-walled and not very conductive, their resistance is high, and even non-physics students know that this is not ideal for conducting electricity.

After reading all of this, I’m sure your question is: how are we still alive? This was my question too.

Thankfully, nerves have some tricks up their sleeves, something similar to pulling a rabbit out of a hat.


One of these features is myelination of the nerve fibre. The myelin sheath increases the membrane resistance and it means that the signal can travel 3 millimetres more. However taking into consideration that the length of a nerve fibre running from your foot to the central nervous system can be around 1 metre, in the grand scheme of things, 3 millimetres are not that helpful, although certainly much appreciated.


The real show stopper trick and literal life saver is the nerve’s power of amplification. This process keeps allowing ions to enter the nerve cell by sodium gated voltage channels in order to sustain the voltage. This makes the signal bigger, as when the channel opens, more positive sodium ions enter and this increases the concentration gradient, as there is more positive charge. Furthermore, the channel is also charged, meaning it moves if voltage changes. This means the channel itself detects a change in the voltage and is able to react to make it greater. Figure 2 demonstrates this process.


Fig 2. Graph showing the effect of amplification [1].

Problems persist

Because the amplification process requires sodium channels, and channels are required to stimulate pain, the myelin sheath cannot be too thick, as otherwise the sodium channels could not be present, meaning the effect of myelination is not at its highest potential, as it needs to compromise with the other processes.

Moreover, the transmission takes time because the passive movement of the signal (i.e. when the signal is not aided by amplification) is still faster than the active movement (the points where amplification takes place) since the amplification process, as we now know, involves sodium channels opening, moving and opening again, which overall is time consuming. 

In addition, there is also the factor of positive feedback. The main idea is that it is triggered by something that it causes and so it is an all or nothing response. What this means is that as one sodium channel opens, then more will open. If the stimulus is not powerful enough, then nothing happens, so the stimulus must be greater than the threshold.


Overall, the structure of the nerve results in it being a poor conductor, however it is because of features such as myelination and amplification that we are still here today, reading this biology blog post.


As I have mentioned before: this post has been written from my notes which I took during the lecture: “How do nerves work?” as part of the Medicine Taster Day at Cambridge University. The information is from the lecturer given on the day: 5Th November 2016.



With thanks to:

·Cambridge University for organising the taster day and to the lecturer for providing the fascinating information.

·Miss Lasouska who kindly read this post.


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