Biology for AP Courses · The Nervous System
How Neurons Communicate
On this page 9 sections
In 30 seconds
Neurons communicate in two stages. Within a single neuron, the message is electrical — a wave of ion movement called an action potential The all-or-none electrical spike traveling down the axon Full entry → traveling down the axon. Between neurons, the message becomes chemical — neurotransmitters released into a tiny gap, the synaptic cleft, bind receptors on the next cell. This electrical → chemical → electrical relay is the backbone of everything the nervous system does, from reflexes to memory.
Communication depends on ion gradients built by the sodium-potassium pump and ion channels. Resting potential, action potential, propagation, and synaptic transmission form the most heavily tested cluster of ideas in nervous system physiology on the AP® Biology exam.
Why this matters
This topic is where biology meets pharmacology. Local anesthetics block voltage-gated sodium channels so action potentials cannot fire; antidepressants prolong neurotransmitter A chemical released at a synapse that binds postsynaptic receptors Full entry → action at synapses. Understand the steps of signaling and you can predict what a drug acting at any single step will do. The same knowledge explains why myelination speeds conduction, why some venoms paralyze (they block receptors), and why a neuron's message strength is coded in firing rate rather than spike size.
The college version
Core Concepts
The resting membrane potential
A resting neuron is polarized: the inside is negative relative to the outside, about −70 mV (a commonly taught textbook value; it varies with cell type). Three features hold this gradient: unequal ion distribution (cytoplasm rich in K⁺ and negative proteins; extracellular fluid rich in Na⁺ and Cl⁻); the Na⁺/K⁺ pump, which uses ATP to push 3 Na⁺ out and 2 K⁺ in; and leak channels, which let K⁺ escape, carrying positive charge out. The resting potential is the neuron's charged battery.
The action potential: an all-or-none event
When a stimulus depolarizes the membrane to threshold The voltage (~−55 mV) that must be reached to fire Full entry → (about −55 mV), the neuron fires a rapid, stereotyped voltage change that either happens completely or not at all:
- Depolarization: voltage-gated Na⁺ channels open, Na⁺ rushes in, and the membrane shoots toward roughly +30 to +40 mV.
- Repolarization: Na⁺ channels inactivate, and voltage-gated K⁺ channels open; K⁺ leaves, returning the membrane negative.
- Hyperpolarization (undershoot): K⁺ channels close slowly, so the membrane briefly dips below −70 mV before returning to rest.
Because the event is all-or-none, a stronger stimulus does not produce a bigger spike — it produces a higher frequency of identical spikes. Information is coded in firing rate, not spike height.
Refractory periods: why signals go one way
During the absolute refractory period Window after a spike when firing is impossible (absolute) or harder (relative) Full entry →, Na⁺ channels are inactivated, so no stimulus can trigger another spike. During the relative refractory period, the membrane is hyperpolarized, so only a stronger-than-usual stimulus works. Refractory periods also force one-way travel: the region behind a spike cannot re-fire, so the signal cannot double back.
Propagation: continuous and saltatory conduction
In unmyelinated axons, the spike triggers the next patch of membrane in a slow continuous wave. In myelinated axons, voltage-gated channels concentrate at the nodes of Ranvier (gaps between myelin segments), and the depolarization jumps node to node — saltatory conduction — which is much faster and uses far less ATP. Large myelinated fibers approach ~100 m/s, while unmyelinated fibers manage only ~1 m/s (commonly taught order-of-magnitude references).
The synapse: chemical transmission
At the synapse The junction where a neuron signals another cell Full entry →, the presynaptic terminal sits ~20 nm from the postsynaptic cell. Transmission steps:
- The action potential arrives and opens voltage-gated Ca²⁺ channels.
- Ca²⁺ enters and triggers exocytosis of synaptic vesicles.
- Neurotransmitter diffuses across the cleft and binds receptors on the postsynaptic membrane.
- Receptor binding opens ion channels, producing a small postsynaptic potential.
- The signal ends: transmitter is reuptaken, degraded by enzymes, or diffuses away.
EPSPs, IPSPs, and summation
A single synaptic event produces only a small, graded change. Excitatory postsynaptic potentials (EPSPs) depolarize (Na⁺ or Ca²⁺ entry); inhibitory postsynaptic potentials (IPSPs) hyperpolarize (Cl⁻ entry or K⁺ efflux). Whether the postsynaptic neuron fires depends on summation Adding synaptic effects in time (temporal) or space (spatial) Full entry →: temporal (one synapse fires rapidly, adding effects in time) or spatial (many synapses fire at once, adding effects in space). If summed depolarization reaches threshold at the axon hillock, a spike fires.
Neurotransmitter families
Small-molecule transmitters include acetylcholine (neuromuscular junctions, much of the PNS), amino acids such as glutamate (main excitatory transmitter in the brain) and GABA (main inhibitory one), and biogenic amines such as dopamine, serotonin, and norepinephrine (mood, reward, arousal). Neuropeptides like endorphins modulate longer-lasting effects. A transmitter's effect depends on the receptor: acetylcholine excites skeletal muscle but slows the heart.
How It Works / Step-by-Step Process
From fingertip to muscle — one complete signaling cycle:
- A skin receptor is stimulated and depolarizes the sensory neuron's membrane.
- If threshold is reached at the axon hillock, an action potential fires.
- The spike propagates down the axon; in myelinated regions it jumps node to node.
- At the terminal, the spike opens Ca²⁺ channels; Ca²⁺ floods in.
- Vesicles fuse and release neurotransmitter into the cleft.
- Transmitter binds receptors on the next neuron, producing an EPSP.
- EPSPs sum; if threshold is reached, a new spike fires in the next cell.
- Enzymes and reuptake clear the transmitter so the synapse resets.
Common Confusions
| Do Not Confuse | With | Difference |
|---|---|---|
| Graded potential (EPSP) | Action potential | Graded = small, local, size varies; action potential = large, all-or-none, travels |
| Depolarization | Repolarization | Na⁺ in toward positive vs. K⁺ out back toward negative |
| Absolute refractory | Relative refractory | Na⁺ channels inactivated (nothing fires) vs. hyperpolarized (stronger stimuli fire) |
| Spike size | Stimulus strength | Spikes are always full-size; stronger stimuli raise firing rate |
| Reuptake | Enzymatic degradation | Transporter pulls transmitter back for reuse vs. enzymes destroy it in the cleft |
| Transmitter identity | Transmitter effect | Acetylcholine excites muscle but slows the heart — effect depends on the receptor |
| Saltatory | Continuous conduction | Node-to-node jumps in myelinated axons vs. slow wave in unmyelinated |
Eli explains
The same idea, in plain words
Explain it like I’m 10
A neuron is like a line of people passing a bucket of water, but the bucket is a spark. The spark races down the wire (that's the electrical part). At the end, the neuron can't touch the next person, so it throws tiny water balloons — the chemical message — across a gap. If enough balloons land, the next person gets splashed hard enough to start their own spark. That's how a message hops from cell to cell.
Worked example
Why a local anesthetic stops pain. A dentist applies a local anesthetic (such as lidocaine) near a nerve. The drug blocks voltage-gated Na⁺ channels from inside the membrane. Even when pain receptors in the tooth are stimulated, the sensory neuron cannot produce the Na⁺ influx needed for an action potential — the all-or-none event simply never starts. No spike means no signal reaches the CNS, so no pain is perceived. This is a perfect exam illustration: block the Na⁺ channel and you block the entire electrical message, no matter how strongly the receptor is stimulated.
Key takeaways
- Resting potential ≈ −70 mV, maintained by the Na⁺/K⁺ pump (3 Na⁺ out, 2 K⁺ in per ATP) and K⁺ leak.
- Sequence: threshold → Na⁺ in (depolarize) → Na⁺ channels inactivate → K⁺ out (repolarize) → undershoot → restore.
- All-or-none: stimulus strength is encoded in firing frequency, not spike size.
- Absolute refractory = Na⁺ channels inactivated; relative = hyperpolarized, needs stronger stimulus.
- Saltatory conduction (myelinated) is faster and cheaper than continuous.
- Synapse: Ca²⁺ in → vesicle exocytosis → transmitter diffuses → receptor binds → postsynaptic potential → reuptake/degradation.
- EPSP depolarizes, IPSP hyperpolarizes; temporal + spatial summation decide firing.
- Acetylcholine's effect depends on the receptor — excitatory at muscle, inhibitory at heart.
Check yourself
6 review questions from the chapter. Try each one, then open the answer.
What three mechanisms maintain the resting membrane potential The neuron's resting voltage (~−70 mV), inside negative Full entry →?
Show answer
Unequal ion distribution, the Na⁺/K⁺ pump (3 Na⁺ out, 2 K⁺ in per ATP), and K⁺ leak channels making the inside negative.
List the phases of an action potential in order, naming the ion movement in each.
Show answer
Depolarization (Na⁺ in), repolarization (K⁺ out), hyperpolarization/undershoot (slow K⁺ closing), then rest. Na⁺ channel inactivation separates rising and falling phases.
Why can't an action potential travel backward along an axon?
Show answer
The region behind the spike is in its absolute refractory period, so the depolarization cannot re-trigger it; the signal can only move forward into resting membrane.
What is the role of Ca²⁺ at the axon terminal?
Show answer
Ca²⁺ enters when the spike arrives and triggers vesicles to fuse and release neurotransmitter by exocytosis.
Five excitatory signals arrive at one synapse far apart in time; the neuron stays silent. Why — and what would change if they arrived together?
Show answer
Each EPSP is small and decays before the next arrives, so they never sum to threshold. Arriving together (temporal summation) or from many synapses at once (spatial summation), they could reach threshold and fire.
Why does blocking voltage-gated Na⁺ channels stop pain completely?
Show answer
The action potential is all-or-none and depends on Na⁺ influx; block the channels and no spike can form, so no signal is sent even if the receptor is strongly stimulated.
Study tools & related lessonsKey vocabulary · Related
Key vocabulary
- resting membrane potential
- The neuron's resting voltage (~−70 mV), inside negative
- depolarization / repolarization
- Membrane becomes less negative (Na⁺ in) / returns negative (K⁺ out)
- threshold
- The voltage (~−55 mV) that must be reached to fire
- action potential
- The all-or-none electrical spike traveling down the axon
- refractory period
- Window after a spike when firing is impossible (absolute) or harder (relative)
- synapse
- The junction where a neuron signals another cell
- neurotransmitter
- A chemical released at a synapse that binds postsynaptic receptors
- EPSP / IPSP
- Small depolarizing (excitatory) / hyperpolarizing (inhibitory) change
- summation
- Adding synaptic effects in time (temporal) or space (spatial)
Sources & references
This lesson was adapted from the open educational references above; their licenses and attributions are preserved. See Copyright & Licensing.
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