Action potentials and synapses
- Neurons communicate with each other via electrical events called ‘action potentials’ and chemical neurotransmitters.
- At the junction between two neurons (synapse), an action potential causes neuron A to release a chemical neurotransmitter.
- The neurotransmitter can either help (excite) or hinder (inhibit) neuron B from firing its own action potential.
- In an intact brain, the balance of hundreds of excitatory and inhibitory inputs to a neuron determines whether an action potential will result.
Neurons are essentially electrical devices. There are many channels sitting in the cell membrane (the boundary between a cell’s inside and outside) that allow positive or negative ions to flow into and the cell.
Normally, the inside of the cell is more negative than the outside; neuroscientists say that the inside is around -70 mV with respect to the outside, or that the cell’s resting membrane potential is -70 mV.
This membrane potential isn’t static. It’s constantly going up and down, depending mostly on the inputs coming from the axons of other neurons. Some inputs make the neuron’s membrane potential become more positive (or less negative, e.g. from -70 mV to -65 mV), and others do the opposite.
These are respectively termed excitatory and inhibitory inputs, as they promote or inhibit the generation of action potentials (the reason some inputs are excitatory and others inhibitory is that different types of neuron release different neurotransmitters; the neurotransmitter used by a neuron determines its effect).
Action potentials are the fundamental units of communication between neurons and occur when the sum total of all of the excitatory and inhibitory inputs makes the neuron’s membrane potential reach around -50 mV (see diagram), a value called the action potential threshold.
Neuroscientists often refer to action potentials as ‘spikes’, or say a neuron has ‘fired a spike’ or ‘spiked’. The term is a reference to the shape of an action potential as recorded using sensitive electrical equipment.
A neuron spikes when a combination of all the excitation and inhibition it receives makes it reach threshold. On the right is an example from an actual neuron in the mouse's cortex. (Image: Alan Woodruff / QBI)
Synapses: how neurons communicate with each other
Neurons talk to each other across synapses. When an action potential reaches the presynaptic terminal, it causes neurotransmitter to be released from the neuron into the synaptic cleft, a 20–40nm gap between the presynaptic axon terminal and the postsynaptic dendrite (often a spine).
After travelling across the synaptic cleft, the transmitter will attach to neurotransmitter receptors on the postsynaptic side, and depending on the neurotransmitter released (which is dependent on the type of neuron releasing it), particular positive (e.g. Na+, K+, Ca+) or negative ions (e.g. Cl-) will travel through channels that span the membrane.
Synapses can be thought of as converting an electrical signal (the action potential) into a chemical signal in the form of neurotransmitter release, and then, upon binding of the transmitter to the postsynaptic receptor, switching the signal back again into an electrical form, as charged ions flow into or the postsynaptic neuron.
An action potential, or spike, causes neurotransmitters to be released across the synaptic cleft, causing an electrical signal in the postsynaptic neuron. (Image: By Thomas Splettstoesser / CC BY-SA 4.0)
Concepts and definitions
Axon – The long, thin structure in which action potentials are generated; the transmitting part of the neuron. After initiation, action potentials travel down axons to cause release of neurotransmitter.
Dendrite – The receiving part of the neuron. Dendrites receive synaptic inputs from axons, with the sum total of dendritic inputs determining whether the neuron will fire an action potential.
Spine – The small protrusions found on dendrites that are, for many synapses, the postsynaptic contact site.
Membrane potential – The electrical potential across the neuron's cell membrane, which arises due to different distributions of positively and negatively charged ions within and outside of the cell. The value inside of the cell is always stated relative to the outside: -70 mV means the inside is 70 mV more negative than the outside (which is given a value of 0 mV).
Action potential – Brief (~1 ms) electrical event typically generated in the axon that signals the neuron as 'active'. An action potential travels the length of the axon and causes release of neurotransmitter into the synapse. The action potential and consequent transmitter release allow the neuron to communicate with other neurons.
Neurotransmitter – A chemical released from a neuron following an action potential. The neurotransmitter travels across the synapse to excite or inhibit the target neuron. Different types of neurons use different neurotransmitters and therefore have different effects on their targets.
Synapse – The junction between the axon of one neuron and the dendrite of another, through which the two neurons communicate.
QBI Laboratories working on neurons and neuronal communication: Professor Stephen Williams, Professor Pankaj Sah
QBI Laboratories working on synapses: Dr Victor Anggono, Professor Joseph Lynch, Professor Frederic Meunier
How do neurons work?
Neurons conduct electrical impulses by using the Action Potential. This phenomenon is generated through the flow of positively charged ions across the neuronal membrane. I'll explain…….
Neurons, all cells, maintain different concentrations of certain ions (charged atoms) across their cell membranes.
Imagine the case of a boat with a small leak below the water line. In order to keep the boat afloat, the small amount of water entering through the leak has to be pumped out, which maintains a lower water level relative to the open sea. Neurons do the same thing, but they pump out positively charged sodium ions.
In addition, they pump in positively charged potassium ions (potash to the gardeners out there!!) Thus there is a high concentration of sodium ions present outside the neuron, and a high concentration of potassium ions inside.
The neuronal membrane also contains specialised proteins called channels, which form pores in the membrane that are selectively permeable to particular ions. Thus sodium channels allow sodium ions through the membrane while potassium channels allow potassium ions through.
OK, so far so good. Now, under resting conditions, the potassium channel is more permeable to potassium ions than the sodium channel is to sodium ions. So there is a slow outward leak of potassium ions that is larger than the inward leak of sodium ions.
This means that the membrane has a charge on the inside face that is negative relative to the outside, as more positively charged ions flow the neuron than flow in.
This difference in the concentrations of ions on either side of the membrane gives rise to the membrane potential and the membrane is said to be polarised.
Let's go back to the boat. Now, in the boat, there is a pressure for water to enter and if a big hole is punched in the side, the rate at which water flows into the boat in massively increased. Similarly, there is a pressure for the sodium ions to enter the neuron, but they are prevented from doing so by the membrane and the pumping mechanisms that remove any ions that manage to get in. However, if the sodium channels are opened, positively charged sodium ions flood into the neuron, and making the inside of the cell momentarily positively charged — the cell is said to be depolarized. This has the effect of opening the potassium channels, allowing potassium ions to leave the cell. Thus, there is first an influx of sodium ions (leading to massive depolarization) followed by a rapid efflux of potassium ions from the neuron (leading to repolarisation). Excess ions are subsequently pumped in/ the neuron.
This transient switch in membrane potential is the action potential. The cycle of depolarization and repolarization is extremely rapid, taking only about 2 milliseconds (0.002 seconds) and thus allows neurons to fire action potentials in rapid bursts, a common feature in neuronal communication.
How does the action potential propagate along the axon?
The sodium channels in the neuronal membrane are opened in response to a small depolarization of the membrane potential. So when an action potential depolarizes the membrane, the leading edge activates other adjacent sodium channels.
This leads to another spike of depolarization the leading edge of which activates more adjacent sodium channels … etc. Thus a wave of depolarization spreads from the point of initiation.
If this were all there was to it, then the action potential would propagate in all directions along an axon. But action potentials move in one direction.
This is achieved because the sodium channels have a refractory period following activation, during which they cannot open again. This ensures that the action potential is propagated in a specific direction along the axon.
The speed of propagation is related to the size of the axon
The speed of action potential propagation is usually directly related to the size of the axon. Big axons result in fast transmission rates. For example, the squid has an axon nearly 1 mm in diameter that initiates a rapid escape reflex. Increasing the size of the axon retains more of the sodium ions that form the internal depolarisation wave inside the axon.
However, if we had to have axons the size of the squid giant axon in our brains, doorways would have to be substantially widened to accommodate our heads!!! We could only have a few muscles located at any great distance from our brains — so we'd all be extremely short with very large heads….not really feasible, is it? The answer is to insulate the axonal membrane to prevent the dissipation of the internal depolarisation in small axons — myelin.
So what does Myelin do?
Myelin is the fatty membranes of cells called Oligodendroglia (in the CNS) and Schwann Cells (in the PNS) that wraps around the axon and acts as an insulator, preventing the dissipation of the depolarisation wave.
The sodium and potassium ion channels, pumps and all the other paraphernalia associated with action potential propagation are concentrated at sites between blocks of myelin called the Nodes of Ranvier.
This myelin sheath allows the action potential to jump from one node to another, greatly increasing the rate of transmission.
Without the myelin sheath, we cannot function.
This is demonstrated by the devastating effects of Multiple Sclerosis, a demyelinating disease that affects bundles of axons in the brain, spinal cord and optic nerve, leading to lack of co-ordination and muscle control as well as difficulties with speech and vision. For further information on this disease, visit the MS Society's web site.