Anatomy and Physiology 2e · The Nervous System and Nervous Tissue

Communication Between Neurons

7 min read
Synaptic cleft dimensions and timing are commonly taught reference concepts — verify against current texts.
Want it in plain words first? Jump to Eli explains — the same idea, no jargon.
On this page 9 sections
  1. In 30 seconds
  2. Why this matters
  3. The college version
  4. Eli explains
  5. Worked example
  6. Key takeaway
  7. Check yourself
  8. Study tools
  9. Sources & references

In 30 seconds

An action potential is a neuron's private electrical message, but neurons do not touch — they are separated by a tiny gap called the . Communication Between Neurons is the study of how a signal crosses that gap and influences the next cell. The junction where this happens is the , and the process is synaptic transmission.

Two broad types of synapses exist. Electrical synapses connect cells directly through gap junctions, letting ions flow from one cell to the next almost instantly — useful where synchronized, rapid firing matters, such as in some smooth and cardiac muscle. Chemical synapses are far more common in the nervous system. An arriving action potential triggers the release of chemical messengers called neurotransmitters, which diffuse across the cleft and bind receptors on the postsynaptic cell, changing its membrane potential. The effect depends on which receptor is engaged: the postsynaptic cell may be nudged toward firing (excitatory) or away from it (inhibitory), and the final decision is made by summing all the inputs it receives at once.

Why this matters

The synapse is where the nervous system makes its decisions — and where most psychoactive and neurological drugs act. Antidepressants, anesthetics, and many pain medications work by altering release, , or receptor binding, so understanding transmission is essential for anyone entering nursing, medicine, or pharmacology. Synaptic dysfunction is also central to disorders from depression and anxiety to Parkinson disease and myasthenia gravis (impaired signaling at the neuromuscular junction). On exams, synaptic transmission is a perennial favorite: expect EPSPs versus IPSPs, , and the sequence of events from action potential to neurotransmitter release.

The college version

Core Concepts

Anatomy of a chemical synapse

  • Presynaptic terminal — the axon's swollen end, holding synaptic vesicles packed with neurotransmitter.
  • Synaptic cleft — the narrow fluid-filled gap (commonly taught as ~20–40 nanometers) across which the signal travels.
  • Postsynaptic membrane — the receiving cell's membrane, studded with receptors.

The postsynaptic "cell" may be a neuron, a muscle fiber (neuromuscular junction), or a gland cell.

The steps of chemical transmission

  1. An action potential arrives and depolarizes the presynaptic terminal.
  2. Depolarization opens voltage-gated Ca²⁺ channels.
  3. Calcium enters, triggering vesicles to fuse with the membrane (), releasing neurotransmitter into the cleft.
  4. Neurotransmitter diffuses across and binds postsynaptic receptors.
  5. Binding opens or closes ion channels, changing the postsynaptic membrane potential.
  6. The signal is terminated: neurotransmitter is removed so the effect does not last forever.

The whole sequence takes well under a millisecond — fast enough for reflexes that must happen in a blink.

Receptors: the message decoders

The same neurotransmitter can produce different effects depending on the receptor:

  • Ionotropic receptors are themselves ion channels (ligand-gated). Binding opens the channel directly — immediate, brief effects.
  • Metabotropic receptors are not channels; binding triggers intracellular signaling cascades (often via G proteins) that indirectly alter channels or gene expression — slower but longer-lasting and amplifiable.

This is why one molecule can do many jobs: the nervous system reuses messengers with different receptors in different circuits.

EPSPs, IPSPs, and summation

Binding produces small, local voltage changes called postsynaptic potentials:

  • An (excitatory postsynaptic potential) depolarizes the membrane toward threshold — firing becomes more likely.
  • An (inhibitory postsynaptic potential) hyperpolarizes (or stabilizes) the membrane away from threshold — firing becomes less likely.

One EPSP is far too small to trigger an action potential alone, so neurons integrate inputs:

  • Temporal summation: one presynaptic neuron fires rapidly, and successive EPSPs add before the first decays.
  • Spatial summation: several presynaptic neurons fire together, and their EPSPs/IPSPs add across the membrane.

If the summed potential reaches threshold at the axon hillock (the trigger zone), an action potential fires. The neuron is a tiny voting machine: excitatory inputs vote "fire," inhibitory inputs vote "don't," and the tally at the trigger zone decides.

Clearing the signal

  • Reuptake: transporters pump neurotransmitter back into the presynaptic terminal for recycling.
  • Enzymatic degradation: enzymes in the cleft break the neurotransmitter into inactive pieces.
  • Diffusion: neurotransmitter drifts away.

Drugs that block reuptake (many antidepressants) or block degradation (some treatments for myasthenia gravis) work by prolonging neurotransmitter action.

Common Confusions

Do Not ConfuseWithDifference
SynapseSynaptic cleftThe synapse is the whole junction; the cleft is just the gap
EPSPAction potentialAn EPSP is small, graded, local, decaying; an action potential is large, all-or-none, propagating — EPSPs may trigger one, they are not one
NeurotransmitterHormoneNeurotransmitters act locally across a cleft in milliseconds; hormones travel in blood, acting broadly over seconds to hours
Temporal summationSpatial summationTemporal = same input, repeated over time; spatial = many inputs, simultaneous across the membrane
"Excitatory neurotransmitter""Always excites"The effect depends on the receptor, not the molecule
ReuptakeDegradationReuptake = transporter pumps it back; degradation = enzymes destroy it in the cleft
Eli, the EliExplains learning guide

Eli explains

The same idea, in plain words

Explain it like I’m 10

Neurons are like kids playing "telephone," but they can't whisper directly — there's a gap between them. So the first kid writes the message on a paper ball and throws it across. The second kid reads it and decides what to do: get excited and pass it along, or stay quiet. Lots of notes can arrive at once, and the kid only shouts onward if enough notes pile up (or one really fast stream). After reading, the notes go in the recycle bin so the message doesn't echo forever.

Worked example

Consider the knee-jerk (patellar) reflex:

  1. A tap stretches the muscle, exciting a sensory neuron.
  2. Its action potentials reach the spinal cord and release an excitatory neurotransmitter (acetylcholine is the classic example) onto a motor neuron.
  3. The motor neuron receives an EPSP; if the summed EPSPs reach threshold, it fires and the quadriceps contracts — the kick.
  4. Simultaneously, the sensory neuron excites an inhibitory interneuron, which releases an inhibitory neurotransmitter onto the opposing (hamstring) motor neuron. That neuron receives an IPSP and stays quiet, so the hamstring relaxes rather than fighting the quadriceps.

The circuit shows every key idea: Ca²⁺-triggered release, EPSPs and IPSPs, summation at the trigger zone, and receptor-dependent effects — and why inhibition matters: coordinated movement requires some muscles to be told "don't fire."

Key takeaways

  • Order of events: action potential → Ca²⁺ entry → vesicle exocytosis → neurotransmitter release → receptor binding → postsynaptic potential → termination.
  • Calcium is the trigger for release — no Ca²⁺ entry, no release.
  • EPSP depolarizes toward threshold; IPSP moves away. Both are graded, local, and rapidly decaying.
  • Temporal summation = one input, rapid repeats; spatial summation = many inputs, simultaneous. The axon hillock decides.
  • Ionotropic receptors = fast, direct; metabotropic receptors = slower, longer-lasting, cascades.
  • Signal termination is essential; drugs exploit reuptake and degradation to change synaptic strength.
  • The receptor, not the neurotransmitter, determines excitation vs. inhibition.

Check yourself

5 review questions from the chapter. Try each one, then open the answer.

  1. List, in order, the steps of chemical synaptic transmission.

    Show answer

    Action potential arrives → Ca²⁺ channels open → Ca²⁺ triggers exocytosis → neurotransmitter diffuses across the cleft → binds receptors, changing membrane potential → signal terminated by reuptake, degradation, or diffusion.

  2. What ion must enter the presynaptic terminal for neurotransmitter release?

    Show answer

    Calcium (Ca²⁺); its entry is the trigger for vesicle fusion and release.

  3. A neuron receives five simultaneous EPSPs from five different presynaptic neurons. What kind of summation is this?

    Show answer

    Spatial summation — multiple inputs arriving simultaneously from different neurons.

  4. A drug prevents the enzyme that breaks down acetylcholine in the cleft. What happens to the postsynaptic effect?

    Show answer

    The acetylcholine stays in the cleft longer, so the postsynaptic effect is prolonged and strengthened (the logic behind certain myasthenia gravis treatments).

  5. Why can the same neurotransmitter excite one synapse and inhibit another?

    Show answer

    Because the effect is determined by the receptor and the ion channels it controls, not by the molecule: a receptor that opens Na⁺ channels is excitatory; one that opens Cl⁻ or K⁺ channels is inhibitory.

Keep learning

Ready to build on this? Continue to the next lesson.

Study tools & related lessonsKey vocabulary · Related

Key vocabulary

Synapse
The functional junction between neurons
Synaptic cleft
The narrow gap between presynaptic and postsynaptic membranes
Neurotransmitter
A chemical messenger released by a neuron
Synaptic vesicle
A sac that stores and releases neurotransmitter
Exocytosis
Vesicle fusion releasing contents outside the cell
Ionotropic receptor
A receptor that is itself an ion channel
Metabotropic receptor
A receptor that triggers intracellular signaling cascades
EPSP
Excitatory postsynaptic potential — a depolarizing nudge
IPSP
Inhibitory postsynaptic potential — a hyperpolarizing nudge
Summation
Adding postsynaptic potentials in time or space
Reuptake
Pumping neurotransmitter back into the terminal

Sources & references

  1. openstax.org — Anatomy And Physiology 2e

This lesson was adapted from the open educational references above; their licenses and attributions are preserved. See Copyright & Licensing.

Educational content only. It is not medical, legal or professional advice. Found an error? Tell us.