Neuroscience: Neurons, Action Potentials & Synapses
CollegeA thought, a reflex, a memory — all of it ultimately reduces to charged ions crossing membranes at precise moments. This chapter opens the electrical and chemical machinery behind the nervous system introduced in Chapter 15.
The resting membrane potential
A resting neuron holds its inside at about −70 mV relative to the outside. This resting potential is maintained by the Na⁺/K⁺ ATPase, which pumps 3 Na⁺ out and 2 K⁺ in per ATP (building concentration gradients: Na⁺ high outside, K⁺ high inside), combined with the membrane being more permeable to K⁺ than Na⁺ at rest via leak channels, so K⁺ diffuses out along its gradient until an electrical force pulls it back in balance — settling near the K⁺ equilibrium potential.
The action potential
If a stimulus depolarises the membrane past a threshold (~−55 mV), voltage-gated Na⁺ channels snap open, Na⁺ rushes in, and the membrane rapidly depolarises, briefly overshooting to about +30 mV. Na⁺ channels then inactivate and voltage-gated K⁺ channels open, K⁺ flows out, and the membrane repolarises, typically overshooting slightly into a brief hyperpolarisation before the resting potential is restored. During the absolute refractory period, Na⁺ channels are inactivated and a new action potential cannot fire no matter how strong the stimulus; during the following relative refractory period, only an unusually strong stimulus can trigger one. This is an all-or-none event: below threshold, nothing happens; above threshold, a full-sized action potential fires regardless of how far past threshold the stimulus was. In myelinated axons, the action potential appears to leap between the gaps in the insulation (nodes of Ranvier) — saltatory conduction — which is far faster than continuous conduction along an unmyelinated axon.
Synaptic transmission
When an action potential reaches the axon terminal, voltage-gated Ca²⁺ channels open; the resulting Ca²⁺ influx triggers synaptic vesicles to fuse with the membrane (via SNARE proteins) and release neurotransmitter into the synaptic cleft. The neurotransmitter binds receptors on the postsynaptic cell: ionotropic receptors are ligand-gated ion channels that act within milliseconds (e.g. Na⁺ influx gives an excitatory postsynaptic potential, EPSP; Cl⁻ influx gives an inhibitory postsynaptic potential, IPSP); metabotropic receptors act more slowly via G-proteins and second messengers. Many small EPSPs and IPSPs are combined at the axon hillock through summation (spatial — from many synapses at once; temporal — from rapid repeated firing at one synapse); only if the combined effect crosses threshold does the postsynaptic neuron fire its own action potential.
A digital spike built from analogue votes
The nervous system elegantly combines two different kinds of signal. Synaptic potentials (EPSPs and IPSPs) are graded — analogue, variable in size, and they add together like votes being tallied at the axon hillock. But once that tally crosses threshold, the neuron responds with an action potential that is digital — always the same size, an all-or-none spike, regardless of how far above threshold the trigger was. This division of labour is efficient: graded potentials allow fine, flexible integration of many simultaneous inputs (some excitatory, some inhibitory, some strong, some weak), while the all-or-none spike allows a signal to travel long distances down an axon without losing strength or information, since it is regenerated at full size at every point along the way rather than fading like a graded signal would.
Because the patch of membrane just behind an advancing action potential is briefly refractory (its Na⁺ channels are inactivated), the spike cannot re-trigger backward into territory it just came from — it is physically forced to propagate in one direction only, from soma to axon terminal. Without refractoriness, signals could reflect back and forth chaotically.
Worked example: conduction velocity in a myelinated axon
A myelinated axon has nodes of Ranvier spaced 1.5 mm apart. The action potential "jumps" from one node to the next, and each jump takes about 15 microseconds (µs).
- Convert units. 1.5 mm = 0.0015 m; 15 µs = 0.000015 s.
- Apply the formula. velocity = distance ÷ time.
- Compute. 0.0015 m ÷ 0.000015 s = 100 m/s.
- Compare. This is roughly 10–100 times faster than conduction along a comparable unmyelinated axon (~0.5–2 m/s), which must regenerate the action potential continuously along every patch of membrane rather than jumping between sparse nodes.
- Connect to disease. This calculation shows why demyelinating diseases like multiple sclerosis are so disruptive: stripping the myelin removes the "jumps," forcing slower, continuous conduction (or blocking it entirely if the axon can no longer maintain the current between distant nodes).
Test yourself
Q1 Explain why the refractory period ensures an action potential travels in only one direction along an axon.
Immediately after an action potential passes a point on the membrane, the voltage-gated Na⁺ channels there enter an inactivated state and cannot reopen until the membrane repolarises and recovers — the absolute refractory period. Since the region just behind the advancing spike is refractory, the depolarisation cannot re-trigger a new action potential there; it can only propagate forward, into fresh membrane whose Na⁺ channels have not yet been used. This one-way constraint is what forces signal propagation to be unidirectional, from the point of initiation toward the axon terminal.
Q2 Multiple sclerosis destroys myelin. Explain the physiological consequence for action potential conduction.
Myelin normally allows saltatory conduction, in which the action potential effectively jumps between the exposed nodes of Ranvier, since the insulated internodal membrane doesn't need to regenerate it. When myelin is destroyed, the axon must instead regenerate the action potential continuously along its full length (if it can still conduct at all), which is far slower and requires the current to spread passively over a longer stretch of now-uninsulated membrane, often failing entirely if the distance between remaining functional patches becomes too great for the current to bridge — producing the conduction slowing and blockade responsible for MS symptoms.
Q3 A postsynaptic neuron receives one EPSP of +5 mV and, almost simultaneously, one IPSP of −3 mV at a nearby synapse. Explain what happens and name the process.
This is spatial summation: the postsynaptic membrane potential changes contributed by both synapses are added algebraically at the axon hillock, giving a net change of +5 + (−3) = +2 mV. Whether this actually triggers an action potential depends on whether the combined change is enough to bring the membrane past threshold; a single +2 mV shift is generally far too small on its own, illustrating why a neuron typically needs many simultaneous excitatory inputs, only partly offset by inhibitory ones, to fire.
Q4 Why does the amplitude of an action potential not vary with the strength of the triggering stimulus, and how does the nervous system then encode stimulus intensity?
The action potential is all-or-none: once threshold is crossed, the same fixed sequence of voltage-gated Na⁺ and K⁺ channel opening and closing occurs regardless of how far past threshold the trigger was, producing a spike of constant amplitude every time. Stimulus intensity is instead encoded by frequency coding — a stronger stimulus causes the neuron to fire a higher rate of action potentials per second (and can recruit more neurons), rather than producing a bigger individual spike.
Q5 SSRIs (selective serotonin reuptake inhibitors) are used to treat depression. Explain their mechanism at the synaptic level.
After serotonin is released into the synaptic cleft and binds postsynaptic receptors, it is normally cleared from the cleft largely by reuptake — transporter proteins on the presynaptic neuron pump serotonin back inside for reuse, ending the signal. An SSRI blocks these reuptake transporters, so serotonin lingers longer in the synaptic cleft and can continue stimulating postsynaptic receptors for an extended time, effectively increasing serotonergic signalling — the basis for their use in modulating mood-related neural circuits.
How the ideas connect
Every key idea in this chapter, branching from the core concept — use it to see the whole picture at a glance.
The process, step by step
Worked problems, step by step
Follow each solution line by line, then try to reproduce it on paper before moving on.
Example 1An impulse travels 1.2 m along an axon in 0.01 s. Find the conduction velocity.
- Velocity = distance / time
- 1.2 / 0.01 = 120
Example 2Why does a stronger stimulus not make a bigger action potential?
- Action potentials are all-or-nothing above threshold
- Stronger stimuli raise the frequency of spikes, not their size
Now you try
Work each one out first, then tap to reveal the worked answer.