Transmission of Neural Impulses: From Resting Potential to Synapse
Resting membrane potential, the action potential, impulse propagation, and synaptic transmission — explained for the MCAT.
Neurons communicate by generating electrical signals and converting them into chemical messages. This page follows that process in order: the resting state a neuron starts from, how the axon hillock decides whether to fire, the phases of the action potential itself, how that signal propagates down the axon, and finally what happens at the synapse.
Key Takeaways
The resting membrane potential (~−70 mV) results from potassium leaking out (making the inside more negative), sodium leaking in (making the inside less negative), and the Na⁺/K⁺ ATPase (3 Na⁺ out, 2 K⁺ in) restoring both gradients.
The axon hillock integrates excitatory (depolarizing) and inhibitory (hyperpolarizing) inputs; reaching threshold (−55 to −40 mV) triggers an all-or-nothing action potential, aided by temporal and spatial summation.
The action potential proceeds through depolarization (Na⁺ influx, peak ~+30 mV), repolarization (K⁺ efflux), hyperpolarization, and recovery via the Na⁺/K⁺ ATPase.
Absolute and relative refractory periods prevent immediate re-firing and enforce one-directional signal propagation.
Myelination enables saltatory conduction between nodes of Ranvier, and larger axon diameter reduces resistance — both increase conduction speed; stronger stimuli increase firing frequency, not signal size.
At the synapse, calcium influx triggers neurotransmitter release, which is cleared from the cleft by enzymatic breakdown, reuptake, or diffusion.
The Resting Membrane Potential
The resting membrane potential is the voltage difference across a neuron's membrane when the cell isn't actively signaling. In most neurons, this value is about −70 mV — the negative sign means the inside of the neuron is more negatively charged than the outside.
This voltage difference comes from the movement of ions — mainly potassium (K⁺) and sodium (Na⁺) — across the membrane, driven by concentration gradients and controlled by dedicated channels and transporters.
Potassium and Sodium Leak Channels
Potassium is concentrated inside the cell, so it naturally moves out through always-open potassium leak channels. As positively charged K⁺ leaves, it takes positive charge with it, making the inside more negative. Potassium's effect alone would pull the membrane potential down to about −90 mV, its equilibrium potential.
Sodium is concentrated outside the cell, so it drifts in through sodium leak channels. This inward flow of positive charge makes the inside slightly less negative, partially counteracting potassium's effect. Sodium's effect alone would push the membrane potential up to about +60 mV, its equilibrium potential.
Because potassium leak channels vastly outnumber sodium leak channels, the resting potential ends up much closer to potassium's equilibrium potential (−90 mV) than sodium's (+60 mV) — landing at the observed −70 mV.
The Na⁺/K⁺ ATPase
Since leak channels constantly let ions drift down their gradients, something has to move them back against those gradients to keep the resting potential stable. That job belongs to the sodium-potassium ATPase (Na⁺/K⁺ pump), which uses ATP to actively transport ions against their concentration gradients. Each cycle, it pumps 3 sodium ions out of the cell and 2 potassium ions in, maintaining the ion distribution the neuron needs to keep firing properly.
How each ion shapes the resting potential:
Potassium exits via leak channels — makes the inside more negative.
Sodium enters via leak channels — makes the inside more positive.
The Na⁺/K⁺ pump restores both gradients, maintaining the overall −70 mV resting potential.
This resting state matters because it sets the baseline the neuron works from — without this voltage difference, the neuron couldn't respond to stimuli or fire a signal.
The Axon Hillock and Signal Integration
The axon hillock — the region where the soma transitions into the axon — serves as the integration center for all incoming signals. By the time signals from the dendrites reach the axon hillock, the neuron has to decide: is the combined input strong enough to trigger an action potential?
Depolarization vs. Hyperpolarization
Not all incoming signals are equal:
Excitatory signals make the neuron more likely to fire. They cause depolarization — the membrane potential becomes less negative, moving closer to zero (the inside becomes more positive).
Inhibitory signals do the opposite. They cause hyperpolarization — the membrane potential becomes even more negative, pushing the neuron further from threshold and making it less likely to fire.
The axon hillock sums all incoming excitatory and inhibitory input. If the net result brings the membrane potential to threshold — typically between −55 and −40 mV — the neuron fires an action potential. If it doesn't reach threshold, no action potential occurs. Like the action potential itself, this is an all-or-nothing response.
Temporal and Spatial Summation
A single input often isn't strong enough on its own to reach threshold, so neurons rely on summation to combine multiple signals:
Temporal summation: multiple signals arrive from the same neuron in rapid succession, close enough in time to add together.
Spatial summation: signals arrive simultaneously from multiple different neurons at different points on the dendritic tree, combining their effects.
Only when the total combined input — from either or both types of summation — reaches threshold does the axon hillock trigger an action potential.
The Action Potential
Once the axon hillock reaches threshold, it triggers an action potential: a rapid, stereotyped electrical signal that unfolds in a predictable sequence of phases.
The action potential, step by step:
Rest: the neuron sits at its resting potential (~−70 mV); voltage-gated channels are closed.
Threshold reached: a stimulus brings the membrane to about −55 mV, opening voltage-gated sodium channels.
Depolarization: Na⁺ floods into the cell down both its concentration and electrical gradients, sharply raising the membrane potential to roughly +30 mV.
Repolarization: sodium channels inactivate and close; voltage-gated potassium channels open, letting K⁺ flow out and driving the potential back down.
Hyperpolarization: potassium efflux overshoots, briefly making the inside more negative than the resting potential.
Recovery: the Na⁺/K⁺ ATPase restores the resting ion gradients (3 Na⁺ out, 2 K⁺ in), returning the membrane to its baseline −70 mV.
Refractory Periods
The hyperpolarization phase sets up two refractory periods that control the timing of subsequent action potentials:
Absolute refractory period: no action potential can occur, no matter how strong the stimulus, because sodium channels are inactivated and need time to reset.
Relative refractory period: an action potential can occur, but it requires a stronger-than-normal stimulus, since the cell is still hyperpolarized and farther from threshold.
These refractory periods temporarily reduce the neuron's excitability, ensuring signals travel in one direction without immediately re-triggering.
Impulse Propagation Down the Axon
Once generated — usually at the axon hillock — the action potential must travel down the axon to the axon terminal. This process, called impulse propagation, is a self-perpetuating wave of depolarization: each segment's depolarization triggers the next segment to reach threshold and fire in turn, moving the signal step by step down the axon.
The signal only travels in one direction, toward the axon terminal, because the segment that just fired is in its refractory period and can't fire again immediately — preventing the signal from moving backward.
Myelination, Saltatory Conduction, and Axon Diameter
In unmyelinated axons, the action potential propagates continuously, with each segment depolarizing and repolarizing in turn — a relatively slow process.
In myelinated axons, conduction is much faster thanks to saltatory conduction. The myelin sheath insulates most of the axon, leaving small exposed regions — the nodes of Ranvier — packed with voltage-gated ion channels. The action potential effectively jumps from node to node, dramatically increasing conduction speed.
Axon diameter also affects speed: larger axons conduct impulses faster because they offer less internal resistance to ion flow.
Stimulus Strength and Firing Frequency
A stronger stimulus does not produce a bigger action potential — action potentials are always the same magnitude once triggered. Instead, a stronger stimulus increases the frequency of action potentials fired over a given period. Stronger input means faster firing, not a larger signal.
Synaptic Transmission
When the action potential reaches the end of the axon, it arrives at the presynaptic terminal (axon terminal), where the electrical signal must convert into a chemical message to reach the next cell.
Neurotransmitter Release
The synaptic cleft is the tiny gap separating the presynaptic neuron from the postsynaptic neuron — neurons never physically touch, so the signal must cross this gap chemically.
At the presynaptic terminal, vesicles filled with neurotransmitters wait near the membrane. When the action potential arrives, it opens voltage-gated calcium channels, letting Ca²⁺ enter the terminal. This calcium influx causes the vesicles to fuse with the membrane and release neurotransmitters into the synaptic cleft. The neurotransmitters diffuse across the cleft and bind receptors on the postsynaptic cell — either ion channels or G-protein coupled receptors — which, depending on the receptor type, either excite or inhibit the next neuron.
Clearing the Synapse
To reset the system and stop the signal, neurotransmitters must be cleared from the synaptic cleft; otherwise they would keep stimulating the postsynaptic cell indefinitely. There are three main clearance mechanisms:
Mechanism | How It Works |
|---|---|
Enzymatic breakdown | Enzymes in the cleft chemically degrade the neurotransmitter into inactive components (e.g., acetylcholine is broken down this way). |
Reuptake | Transporters carry the neurotransmitter back into the presynaptic neuron, where it can be reused or broken down internally. |
Diffusion | The neurotransmitter simply drifts away from the cleft over time — slower, but still contributes to clearance. |
Together, these mechanisms keep synaptic signaling brief, specific, and controlled.
Common MCAT Mistakes
Thinking a stronger stimulus produces a bigger action potential. Action potentials are all-or-nothing and always reach the same peak (~+30 mV) once triggered; a stronger stimulus increases firing frequency, not amplitude.
Mixing up which ion drives which phase. Depolarization is driven by Na⁺ influx through voltage-gated sodium channels; repolarization is driven by K⁺ efflux through voltage-gated potassium channels — reversing these flips the whole mechanism.
Confusing the absolute and relative refractory periods. During the absolute refractory period, no stimulus (however strong) can trigger another action potential because sodium channels are inactivated; during the relative refractory period, a stronger-than-normal stimulus can still fire one.
Assuming resting potential comes only from ion channels. Leak channels set up the passive gradient, but the Na⁺/K⁺ ATPase is what actively restores those gradients (3 Na⁺ out, 2 K⁺ in) — without it, repeated firing would collapse the ion distributions.
MCAT-Style Concept Check
Question: A researcher records from a neuron and observes that, immediately after an action potential fires, no stimulus — regardless of strength — can trigger a second action potential for a brief period. Shortly after, a second action potential can be triggered, but only with a stronger-than-normal stimulus. What ionic event underlies the first (absolute) phase, and why does the second (relative) phase require extra stimulus strength?
A) The first phase is caused by open potassium leak channels; the second requires extra strength because sodium leak channels are closed.
B) The first phase is caused by inactivated voltage-gated sodium channels, which cannot reopen regardless of stimulus; the second requires extra strength because the membrane is still hyperpolarized, farther from threshold.
C) The first phase is caused by the Na⁺/K⁺ ATPase pausing; the second requires extra strength because potassium leak channels are closed.
D) The first phase is caused by depolarization overshoot; the second requires extra strength because voltage-gated calcium channels are inactivated.
Answer: B
Explanation: During the absolute refractory period, voltage-gated sodium channels are inactivated and cannot reopen no matter how strong the stimulus, making a second action potential impossible. During the subsequent relative refractory period, sodium channels have reset, but the membrane is still hyperpolarized from the potassium efflux that closed out the first action potential — so it sits farther from threshold, meaning only a stronger-than-normal stimulus can bring it back to threshold and fire again. The other options misattribute the mechanism to potassium leak channels, the Na⁺/K⁺ ATPase, or calcium channels, none of which are responsible for the refractory periods.
FAQ
What causes the resting membrane potential?
The resting membrane potential (~−70 mV) results from potassium leaking out through leak channels (making the inside more negative), sodium leaking in through leak channels (making the inside less negative), and the Na⁺/K⁺ ATPase actively restoring both gradients by pumping 3 Na⁺ out and 2 K⁺ in each cycle.
What triggers an action potential?
An action potential fires when the axon hillock's integrated input — combined through temporal and/or spatial summation of excitatory and inhibitory signals — brings the membrane potential to threshold (about −55 to −40 mV), opening voltage-gated sodium channels in an all-or-nothing response.
Why does myelination speed up impulse conduction?
Myelin insulates most of the axon, leaving only the nodes of Ranvier exposed. Instead of regenerating the signal continuously along the membrane, the action potential jumps from node to node — saltatory conduction — which is much faster than the continuous propagation seen in unmyelinated axons.
What happens at the synapse when an action potential arrives?
The action potential opens voltage-gated calcium channels at the presynaptic terminal, and the resulting Ca²⁺ influx causes neurotransmitter-filled vesicles to fuse with the membrane and release their contents into the synaptic cleft, where the neurotransmitters bind receptors on the postsynaptic cell.
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