Describe How Synaptic Signals Become Action Potentials in a Neuron.

So…I meant to post yesterday and failed spectacularly. However, I did spend my day helping with filming and editing, so that’s a plus. Anyway, onto the post.

A psychology post today for you. With pictures and a video (neither by me, I hasten to add)! This is hopefully helping me revise.

First of all: the anatomy:


In the brain, electrically excitable neurons – the core components of the nervous system, and thus what keeps humans reacting appropriately to their environment – transmit and receive chemical and electrical signals via their dendrites and axons. (For action potential, we are only interested in the movement of electrical signals between neurons.)

These neurons have a plasma membrane: an “impermeable double-layered structure for regulating the movement of substances” – ie. a phospholipid bilayer (etymology: phospho = from phosphorus, a nitrogenic element found in all organic cells; lipid = fat/grease; bi = two). The two layers are sandwiched: hydrophobic ‘non-polar’ layer surrounded by two hydrophilic ‘polar’ layers.


A phospholipid bilayer? Understandably, the cell wall needs to allow only some substances to diffuse through. Here, those are oxygen, carbon dioxide and glucose. Action potentials rely on the idea of concentration gradient to enable the polarisation of the cell – not only that, but also a voltage gradient of free cations and anions, where the ions move their electrostatic gradients.

Inside the neuron potassium and sodium cations are balanced by various anions, which are too big to diffuse or be pumped through the membrane channels; outside the neuron, the charge is much more positive.

Let’s talk about the myelin sheaf. It’s made of fatty oligodendrocyte cells and allows the speeding up of impulses to about 430 km/h! However, because of the dense quality of the myelin sheaf, action potential and diffusion do not actually occur there. For instance, Diffusion MRI scans can identify the anisotropy (preferred direction) of fluid-flow in the brain because fluid cannot travel along the myelin. This means that myelin is the perfect layer of protection around cell soma and axons. However, it is not immune to everything. In Multiple Sclerosis, the myelin sheaf is attacked and damaged, leaving the cell membrane with hard scar tissue (hence the name). Action potential is not as effective, as the axons can no longer conduct signals as effectively, leading to the symptoms of MS, such as problems with mobility and vision.

SQUIDDid you know? The giant axons of the squid helped scientists discover the axons in our brains.

The question – in short. Ideally, a proper essay would incorporate some of the above, but I wanted to split it up for you.

An action potential is a short-lasting event of the distribution of ions into electrical potential. It is a moving exchange of ions across a neuron’s axons. In the brain, this is where a stimulus leads to information conveyed by electrical signals.

When a neuron is activated by an electrical signal received through the neuron’s dendrites as part of a neural network, it rapidly depolarises the cell walls of the neuron’s axons, causing sodium from the cell exterior to diffuse into the cell’s hydrophobic interior. Ungated potassium channels in the axon wall allow potassium cations to move freely, whilst ignoring the sodium ions; gated sodium channels respond to chemical neurotransmitters and ignore potassium ions. Potassium and sodium pumps actively pump potassium in and sodium out of the cell constantly.

This means that the axon is able to regulate its voltage. With a resting potential of about -70 millivolts inside the neuron, equilibrium is a natural aim of the cells; the difference in voltage charge creates electrical potential energy.

If changes in the soma and dendrites of a neuron reach the axon (ie. the signal from a stimulus or another neuron), sodium gates respond and more sodium enters. When the voltage gradient of the axon interior is over the threshold of about -50mV, potassium ions leave the cell to aim for equilibrium between the voltages again. This, however, leaves the voltage of the axon the reverse of its original: negative exterior and positive interior.

This is depolarisation, and tends to lead to Excitatory Postsynaptic Potential (EPSP) and the continuation of an action potential from the axon terminal to other neuron dendrites. Hyperpolarisation (threshold -80mV) occurs when there is an efflux of potassium ions, leading to Inhibitory Postsynaptic Potential (IPSP) and a lowered chance of action potential occurring. Repolarisation occurs at the finish of action potential, where the cell interior returns to its previous state, potassium ions moving out, followed by sodium ions. Repolarisation threshold is about 30 mV.

The polarisation of one axon node can produce a voltage-gated depolarisation of the next node, called Saltatory Conduction. If action potential occurs across one or two nodes, its propagation along the neuron axon creates a nerve impulse to the next synapse (the gap over which electrical potential crosses) and neuron.

Now the video, which probably explains it better than me:

Go forth and transmit!

shiny brain


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