IB Biology · Theme C · C2.2

Neural signalling

From a single sodium ion crossing a membrane to billions of neurons firing together, this lesson traces how the nervous system generates, propagates, and passes on an electrical signal — and where synapses turn that signal chemical again.

Guiding questions

How are electrical signals generated and moved within neurons?

How can neurons interact with other cells?

Part one

Neuron structure and the resting potential

C2.2.1 – C2.2.2

C2.2.1

One cell body, many fibres

A neuron is a specialized cell of the nervous system whose cytoplasm and nucleus form a cell body, with elongated nerve fibres of varying length projecting outward to conduct electrical impulses.

A single long fibre called the axon carries impulses away from the cell body, often over a considerable distance to a target cell.
Multiple shorter fibres called dendrites project from the cell body and typically receive incoming signals from other neurons.
Both the axon and dendrites conduct electrical impulses — it is their number and length that distinguishes one from the other, not signalling direction alone.

Why it mattersThe data booklet shows a simple neuron without labels — be ready to label it: dendrites, cell body, nucleus, axon, myelin sheath, nodes of Ranvier and axon terminals.

A myelinated neuron like the simple neuron in the data booklet, labelled: dendrites, cell body, nucleus, axon, myelin sheath, Schwann cell nucleus, node of Ranvier and axon terminals, with an arrow showing the direction of the nerve impulse

3D render of the sodium-potassium pump in a neuron membrane: using ATP, it pumps three sodium ions out and two potassium ions in, so sodium is concentrated outside and potassium inside

C2.2.2

Charging the membrane at rest

The resting potential is the voltage difference across a neuron's plasma membrane when it is not conducting an impulse, generated and maintained by ATP-driven pumping of sodium and potassium ions in opposite directions.

The sodium-potassium pump uses energy from ATP to actively transport sodium ions out of the neuron and potassium ions into the neuron, against their concentration gradients.
Each cycle moves three Na⁺ out but only two K⁺ in, and K⁺ also leaks back out through K⁺ channels, so more positive charge ends up outside than inside — the membrane is polarized.
The resulting membrane potential is negative, roughly −70 mV, with the inside of a resting neuron negative relative to the outside.

Why it mattersThis pumping never stops, even at rest — a neuron continuously spends ATP just to maintain the gradients that make it ready to fire an impulse at any moment.

Part two

Action potentials and impulse speed

C2.2.3 – C2.2.4

C2.2.3

An impulse is an electrical event

A nerve impulse, or action potential, is a rapid, temporary reversal of the membrane potential that is generated and then propagated along a nerve fibre — it is electrical because it involves movement of positively charged ions.

An action potential only fires once a stimulus depolarizes the membrane to a threshold potential; weaker, sub-threshold stimuli produce no action potential at all.
Once threshold is reached, the action potential fires as an all-or-nothing event — every action potential in a given neuron reaches the same peak size, regardless of the stimulus.
An oscilloscope trace of a stimulated axon can record this rapid rise and fall in membrane potential over time.

Why it mattersAll-or-nothing firing means stimulus strength can't be coded in one action potential's size — it must be coded some other way, covered later in this lesson.

A voltage against time graph of a single action potential showing resting potential, threshold, rapid depolarization to a positive peak, and repolarization back down, labeled resting potential, threshold and peak

Simplified 3D render comparing a squid giant axon, with a large diameter that conducts at about 25 metres per second, with a small non-myelinated fibre that conducts at about 1 metre per second

C2.2.4

Bigger axons carry impulses faster

Conduction velocity, the speed at which an impulse travels along a fibre, varies considerably between neurons and depends strongly on axon diameter.

The squid giant axon, with an unusually large diameter, conducts impulses at about 25 m s⁻¹ — far faster than the small, non-myelinated nerve fibres of many other invertebrates (often about 1 m s⁻¹).
A wider axon offers less internal resistance to the local current that drives propagation, so an impulse spreads along it more quickly even without any insulation.
Myelination is a separate factor: large myelinated vertebrate fibres reach about 100 m s⁻¹ while staying narrow (covered later in this lesson).

Why it mattersThe squid giant axon is a classic experimental model precisely because its large size makes it physically easy to record from directly.

C2.2.4

Reading the strength of a relationship

Conduction velocity is negatively correlated with animal body size but positively correlated with axon diameter — a required application-of-skills point for interpreting data like this.

A negative correlation means one variable decreases as the other increases; a positive correlation means both variables increase together — correlation coefficients quantify the strength of each relationship.
The coefficient of determination, R², expresses the proportion of variation in conduction velocity that is explained by variation in the independent variable.
Correlation alone does not establish that one variable directly causes changes in the other, only that a statistical relationship exists in the data.

Why it mattersExpect a calculation or interpretation question that hands you a correlation coefficient or R² value directly and asks what it means about the strength of a stated relationship.

Two scatter graphs: conduction speed rises with axon diameter in non-myelinated axons (r = 0.96, R² = 0.92), and falls with animal body mass on a log scale in illustrative data (r = −0.96, R² = 0.92)

Part three

Synapses and neurotransmission

C2.2.5 – C2.2.7

A chemical synapse showing a presynaptic terminal, a narrow synaptic cleft, and a postsynaptic membrane, with a single arrow pointing from the presynaptic terminal across the cleft to the postsynaptic membrane, labeled presynaptic neuron, synaptic cleft and postsynaptic membrane

C2.2.5

A junction with only one way through

A synapse is a junction between two neurons, or between a neuron and an effector cell, across which a signal passes — this course limits synapses to chemical synapses only.

At a typical chemical synapse, the presynaptic cell releases a chemical signal that the postsynaptic cell detects, so information can only flow in one direction, presynaptic to postsynaptic.
Synapses aren't limited to connections between two neurons — the neuromuscular junction, between a motor neuron and a muscle fibre, is also a synapse under this definition.
Electrical synapses exist in some organisms but are excluded from this course; every synapse discussed here is a chemical one.

Why it mattersUnidirectional signalling at synapses is what gives a neural circuit its fixed direction of information flow, from receptor cells through to an effector.

C2.2.6

Calcium turns an impulse chemical

Release of neurotransmitter from the presynaptic membrane is triggered by depolarization of that membrane, which causes uptake of calcium ions that act as an internal signalling chemical inside the neuron.

When an action potential arrives at the presynaptic terminal, the resulting depolarization opens channels that let calcium ions enter the presynaptic cell from outside.
This calcium influx signals synaptic vesicles, each loaded with neurotransmitter, to fuse with the presynaptic membrane and release their contents into the synaptic cleft.
Without calcium entry, depolarization of the presynaptic membrane alone is not sufficient to trigger neurotransmitter release.

Why it mattersCalcium acting as an internal signal, rather than the neurotransmitter itself, is the crucial link that converts an electrical impulse into a chemical one at every synapse.

A presynaptic terminal showing a calcium ion channel with calcium ions entering the cell through it, and a synaptic vesicle fusing with the presynaptic membrane to release neurotransmitter molecules into the synaptic cleft, labeled calcium ion channel, Ca2+ entering, synaptic vesicle and neurotransmitter released

A three-step flowchart showing a neurotransmitter diffusing across the synaptic cleft, then binding a transmembrane receptor on the postsynaptic membrane, then positive ions entering through an opened channel, connected by two single-arrowhead arrows, labeled neurotransmitter diffuses, binds receptor and positive ions enter

C2.2.7

One neurotransmitter, many synapses

An excitatory postsynaptic potential (EPSP) is generated when neurotransmitter diffuses across the synaptic cleft and binds transmembrane receptors on the postsynaptic membrane, opening ion channels and depolarizing that membrane toward threshold.

Acetylcholine is the syllabus example of a neurotransmitter that generates an EPSP, and it's found in many types of synapse, including the neuromuscular junction.
Binding of acetylcholine to its transmembrane receptor lets positively charged ions cross the postsynaptic membrane, moving its potential closer to the threshold needed for an action potential.
An EPSP is a graded change in potential, not an all-or-nothing event — only the resulting action potential, if threshold is reached, is all-or-nothing.

Why it mattersThe receptor sits on the postsynaptic side, not the presynaptic side — a common point of confusion worth fixing early.

C2.2.5–7

One synapse, seven steps

A signal crosses a chemical synapse one way, from the presynaptic cell to the postsynaptic cell, in seven steps.

Steps 1–2: an action potential depolarizes the presynaptic membrane; calcium channels open and Ca²⁺ enters.
Step 3: vesicles fuse with the membrane and release neurotransmitter into the cleft.
Steps 4–5: it diffuses across the cleft and binds receptors, opening ion channels.
Step 6: positive ions enter, producing an excitatory postsynaptic potential (EPSP).
Step 7: an enzyme breaks it down and/or the presynaptic neuron takes it back up, so the response stops.

Why it mattersOnly the presynaptic side releases neurotransmitter and only the postsynaptic side has receptors, so the signal passes one way.

A labelled diagram of one chemical synapse in seven numbered steps. A presynaptic terminal sits above a wide synaptic cleft, with the postsynaptic cell below. 1: an action potential arrives at the presynaptic terminal. 2: calcium channels in the presynaptic membrane open and Ca2+ flows in. 3: vesicles of neurotransmitter, one fusing with the presynaptic membrane, release neurotransmitter. 4: the neurotransmitter diffuses across the synaptic cleft. 5: it binds transmembrane receptors in the postsynaptic membrane and ion channels open. 6: positive ions enter, giving an EPSP that depolarizes the postsynaptic membrane. 7: the neurotransmitter is removed, either broken down by an enzyme in the cleft or taken back up into the presynaptic terminal by a reuptake transporter, so the response stops. Notes say acetylcholine is an example neurotransmitter and that the signal passes one way only. A panel on the right explains each step.

Quick check

A stimulus depolarizes a neuron's membrane, but not enough to reach the threshold potential. What happens?

No action potential is generated — the stimulus produces only a small, local change in potential

A smaller-than-normal action potential fires

The neuron fires an action potential at half its normal speed

The resting potential becomes permanently positive

Correct answer: no action potential at all. Action potentials are all-or-nothing — threshold must be reached for voltage-gated sodium channels to open and trigger the full event. A sub-threshold stimulus produces only a local, non-propagated change in membrane potential, never a smaller impulse.

Part four

The action potential mechanism · HL

C2.2.8 – C2.2.11

C2.2.8 · HL

Two channels, opposite directions

Depolarization and repolarization during an action potential are produced by voltage-gated sodium and potassium channels opening in sequence, once the membrane reaches its threshold potential.

When the membrane depolarizes to threshold, voltage-gated sodium channels open, and sodium ions rush into the neuron down their electrochemical gradient, driving the rapid depolarization phase.
At the peak of the action potential, voltage-gated sodium channels inactivate while voltage-gated potassium channels open, so potassium ions flow out of the neuron, repolarizing the membrane toward resting potential.
Reaching the threshold potential in the first place is essential — below it, voltage-gated sodium channels simply do not open.

Why it mattersThe sodium-potassium pump plays no direct role in this rapid cycle — its slower job is restoring the ion gradients afterwards, not causing the voltage change itself.

3D renders of voltage-gated channels: during depolarization a sodium channel opens and sodium ions diffuse into the neuron; during repolarization a potassium channel opens and potassium ions diffuse out

C2.2.8, C2.2.10 · HL

One action potential, tied to its channels

An action potential is a rapid rise and fall in membrane potential, produced by voltage-gated sodium and potassium channels opening in sequence in the axon membrane.

Rising phase: at threshold (−55 mV) voltage-gated Na⁺ channels open and Na⁺ diffuses in down its gradient, depolarizing the membrane to about +40 mV.
Falling phase: Na⁺ channels inactivate and voltage-gated K⁺ channels open, so K⁺ diffuses out, repolarizing the membrane.
K⁺ channels close slowly, giving a brief undershoot below −70 mV before the resting potential returns.

Why it mattersEach part of an oscilloscope trace matches one channel state, which is how you interpret it.

An annotated graph of one action potential, membrane potential in millivolts against time in milliseconds, tied to a channel-state strip underneath. The curve starts flat at the resting potential of about minus 70 millivolts (phase 1, Na+ and K+ channels closed), rises through the threshold of minus 55 millivolts as voltage-gated Na+ channels open and Na+ enters (phase 2, depolarization) to a peak of about plus 40 millivolts, then falls as the Na+ channels inactivate and voltage-gated K+ channels open and K+ leaves (phase 3, repolarization), dips below minus 70 millivolts in a hyperpolarized undershoot while K+ channels are still open (phase 4), and returns to the resting potential when the K+ channels close (phase 5). Two rows show the Na+ channels (closed, open, inactivated and closed, closed) and the K+ channels (closed, open, closed) lined up with the phases. A panel on the right explains each phase.

A length of unmyelinated axon showing one depolarized region and an adjacent resting region, with short arrows showing sodium ions diffusing from the depolarized region toward the resting region both inside and outside the axon, plus one larger arrow showing the single direction of impulse propagation along the axon, labeled depolarized region, resting region and direction of impulse propagation

C2.2.9 · HL

How an impulse travels without moving

An action potential is propagated along a nerve fibre because local currents — diffusion of sodium ions inside and outside the axon — bring the adjacent membrane to threshold.

Sodium ions that entered during depolarization diffuse locally to the neighbouring, still-resting region of membrane, both inside and just outside the axon.
This local ion movement raises the neighbouring membrane's potential to threshold, opening voltage-gated sodium channels there and regenerating a full action potential at that new position.
Because the region just behind the impulse is briefly refractory and unable to fire again, this regeneration moves in one direction only, away from where it began.

Why it mattersThe action potential is not a signal passively flowing down a wire — it is actively regenerated, in full, at every point along an unmyelinated fibre.

C2.2.10 · HL

Watching a membrane's voltage change

An oscilloscope displays membrane potential against time, letting both the resting potential and the depolarization and repolarization phases of an action potential be identified and interpreted directly from the trace.

The flat, unchanging portion of a trace before a stimulus arrives corresponds to the resting potential; a sharp upward deflection marks the start of depolarization.
The number of impulses recorded within a known time window can be measured and converted to a frequency, in hertz, using impulses divided by time in seconds.
Comparing the shape, size and timing of traces from different neurons or conditions links a trace back to real, specific cellular events.

Why it mattersReading an oscilloscope trace is an application-of-skills task in its own right — expect to identify a labelled feature or calculate a frequency from a given trace.

Oscilloscope trace of membrane potential against time over 50 ms showing five identical action potentials, each peaking at about +40 mV, giving 100 impulses per second

A myelinated axon with several nodes of Ranvier as gaps in the myelin sheath, with arrows showing the action potential jumping from one node directly to the next in a single direction along the axon, labeled myelin sheath, node of Ranvier and direction of impulse

C2.2.11 · HL

Jumping from node to node

Saltatory conduction is the faster form of impulse propagation in myelinated fibres, where ion pumps and channels are clustered at gaps in the myelin sheath called nodes of Ranvier.

The myelin sheath insulates long stretches of the axon between nodes, so the membrane beneath it cannot generate an action potential directly.
Because ion channels are concentrated at the nodes of Ranvier, the action potential is only regenerated at these points, and appears to jump from node to node along the fibre.
Since far fewer points need active regeneration compared with a continuously conducting unmyelinated fibre, saltatory conduction achieves substantially faster impulses for a similar axon diameter.

Why it mattersMyelin itself does not conduct the signal — it's a passive insulator that forces conduction to become node-to-node instead of continuous.

Part five

Synaptic transmission in depth · HL

C2.2.12 – C2.2.14

C2.2.12 · HL

Blocking the receiving end

Neonicotinoid pesticides are the syllabus example of an exogenous chemical that blocks synaptic transmission by acting on the postsynaptic membrane, rather than the presynaptic terminal.

Neonicotinoids bind to acetylcholine receptors on the postsynaptic membrane, and acetylcholinesterase cannot break them down, so the receptors stay occupied.
Acetylcholine can then no longer pass signals across, so this binding blocks the insect's usual synaptic transmission at cholinergic synapses, ultimately causing paralysis and death.
This receptor-blocking mechanism is distinct from an enzyme-blocking mechanism — neonicotinoids do not act on any enzyme that breaks down neurotransmitter.

Why it mattersNeonicotinoids are widely used agricultural insecticides, which has made their effect on non-target pollinating insects a genuine environmental concern.

3D render of a neonicotinoid molecule bound in the acetylcholine binding site of a receptor in the postsynaptic membrane; the channel stays blocked and no signal passes

3D render of a synapse: vesicles of dopamine in the presynaptic terminal, a reuptake transporter blocked by cocaine, dopamine building up in the synaptic cleft, and the postsynaptic membrane with its receptors

C2.2.12 · HL

Blocking the sending end

Cocaine is the syllabus example of a drug that affects synaptic transmission by blocking reuptake of neurotransmitter at the presynaptic terminal, rather than acting at the postsynaptic receptor.

Normally, a transporter protein in the presynaptic membrane removes neurotransmitter such as dopamine from the synaptic cleft after it has acted, ending the signal and recycling the neurotransmitter.
Cocaine blocks this reuptake transporter, so neurotransmitter stays in the synaptic cleft for longer, prolonging its stimulatory effect on the postsynaptic membrane.
Because neonicotinoids and cocaine act at opposite sides of the synapse and by different mechanisms, they should never be treated as interchangeable examples.

Why it mattersCocaine's prolonged dopamine signalling in reward pathways of the brain is central to why the drug is so strongly associated with addiction.

C2.2.13 · HL

Pushing a membrane further from firing

An inhibitory postsynaptic potential (IPSP) is generated when an inhibitory neurotransmitter binds its receptor and causes the postsynaptic membrane to become hyperpolarized — more negative than its resting potential.

Hyperpolarization moves the membrane potential further from the threshold needed to trigger an action potential, making the postsynaptic neuron less likely to fire.
An IPSP is a real, measurable change in potential, not simply the absence of excitatory input — it actively works against any EPSPs arriving at the same time.
Inhibitory and excitatory neurotransmitters can act at entirely different synapses onto the very same postsynaptic neuron, giving it competing inputs to reconcile.

Why it mattersMixing up EPSP and IPSP — depolarizing toward threshold versus hyperpolarizing away from it — is one of the most common exam errors on this topic.

3D render of an inhibitory neurotransmitter bound to its receptor in the postsynaptic membrane, opening a channel through which ions flow so the inside becomes more negative; beside it, a graph of an IPSP dipping below the resting potential, away from threshold

3D render of two presynaptic neurons forming two synapses on the dendrite and cell body of one postsynaptic neuron; beside it, a graph showing that each EPSP alone stays below threshold but the two together sum to reach it

C2.2.14 · HL

Adding up different inputs

Spatial summation is the addition of postsynaptic potentials arriving at the same moment from different synapses on a postsynaptic neuron.

Two or more presynaptic neurons can each contribute an EPSP arriving at essentially the same instant, from different points on the postsynaptic neuron's surface.
Each individual EPSP may be too small to reach threshold alone, but their combined, summed effect at that instant can trigger an action potential.
The name reflects where the inputs come from — different locations — rather than when they arrive, which is what temporal summation is about instead.

Why it mattersA single synapse rarely decides whether a neuron fires — spatial summation lets it integrate simultaneous input from many sources at once.

C2.2.14 · HL

Adding up the same input, over time

Temporal summation is the addition of postsynaptic potentials generated in quick succession by a single presynaptic neuron at one synapse.

If one presynaptic neuron fires repeatedly fast enough, each new EPSP arrives before the last one has fully decayed, so their effects build on top of each other.
This build-up can push the membrane potential up to threshold even though no single impulse from that synapse would have been enough alone.
The same location is involved each time — only the timing of repeated inputs changes, which is what distinguishes it from spatial summation.

Why it mattersTemporal summation means firing rate, not just whether a synapse fires at all, carries real information the postsynaptic neuron can use.

Graph of temporal summation: three impulses from one presynaptic neuron produce EPSPs that add together, step by step, until threshold is reached and an action potential fires

Quick check · HL

A postsynaptic neuron receives an EPSP that would reach threshold on its own. At the same moment, it also receives an IPSP from a different presynaptic neuron. What is the most likely outcome?

The neuron may not fire, because the IPSP's hyperpolarization can counteract the EPSP's depolarization when the two are summed

The neuron always fires, because at least one EPSP reached threshold

The IPSP is ignored entirely, since EPSPs always take priority

The neuron fires twice, once for each signal

Correct answer: summation can prevent firing. Postsynaptic potentials are graded and summate — a simultaneous IPSP hyperpolarizes the membrane, counteracting the EPSP's depolarization. Whether the neuron fires depends on the combined, summed potential at the axon hillock reaching threshold, not on any single input in isolation.

Part six

Pain and consciousness · HL

C2.2.15 – C2.2.16

C2.2.15 · HL

Free endings that sense danger

Free nerve endings in the skin detect pain-associated stimuli such as high temperature, acid, or capsaicin, using channels for positively charged ions that open in response.

When a stimulus such as high temperature or acid is detected, channels for positively charged ions open in the free nerve ending, allowing these ions to enter.
Entry of positive ions brings the local membrane to threshold, generating nerve impulses that pass through the sensory neuron toward the brain.
Capsaicin, the compound behind the heat of chilli peppers, opens these same channels directly, which is why it produces a genuine sensation of heat and pain without real tissue-damaging temperature.

Why it mattersPain itself is perceived in the brain, not at the skin — the free nerve ending only detects the stimulus and generates the impulse that eventually reaches it.

3D cutaway render of skin: high temperature at the surface stimulates free nerve endings in the epidermis, opening channels for positive ions; impulses travel along the sensory neuron through the dermis to the CNS

An abstract, warmly lit network of many interconnected glowing neurons forming a brain-like web, with no text or labels, suggesting a single emergent property arising from countless individual connections

C2.2.16 · HL

A property of the whole network

Consciousness is described in this course as an emergent property — one that arises from the interaction of many individual neurons in the brain, and that no single neuron possesses on its own.

A single neuron studied in isolation shows no sign of consciousness — the property only appears at the level of a large, interconnected network.
This is one example of a wider theme in biology: emergent properties are features of a whole system that cannot be predicted from studying its parts separately.
Billions of neurons, each following the same resting-potential, action-potential and synaptic rules covered in this lesson, together give rise to this one emergent property.

Why it mattersThis idea ties the lesson together — every mechanism here, from a single ion pump to a single synapse, scales up into something new once enough of them interact.

Key vocabulary

Worth being able to define in a single sentence each

Resting potential

The voltage difference across a neuron's membrane at rest, generated by active pumping of Na⁺ and K⁺ in opposite directions.

Action potential

An all-or-nothing electrical impulse triggered once a stimulus depolarizes the membrane to threshold.

Synapse

A chemical junction between two neurons, or between a neuron and an effector cell, across which a signal passes in one direction.

Threshold potential

The minimum depolarization needed to trigger an action potential.

EPSP

Excitatory postsynaptic potential: a depolarizing, graded shift in postsynaptic membrane potential toward threshold.

Saltatory conductionHL

The "jumping" of an action potential from node to node in a myelinated fibre, achieving faster impulses.

Refractory periodHL

The brief period after an action potential during which a neuron cannot (absolute) or is less able (relative) to fire again.

IPSPHL

Inhibitory postsynaptic potential: a hyperpolarizing, graded shift in postsynaptic membrane potential away from threshold.

SummationHL

Combining multiple EPSPs and IPSPs at a postsynaptic neuron into one all-or-nothing firing decision.

Where this shows up again

B2.1

The sodium-potassium pump (B2.1) maintains the Na⁺ and K⁺ gradients essential for action potentials. State how many Na⁺ and K⁺ ions the pump moves for each ATP used, and explain why this helps make the inside of the neuron negative.

B1.2

The structure of proteins (B1.2) determines the specificity of neurotransmitter receptors. Explain how the tertiary structure of a ligand-gated ion channel enables it to open only in response to a specific neurotransmitter.

B3.3

At the neuromuscular junction (B3.3), acetylcholine triggers muscle contraction. Compare the postsynaptic response at the NMJ with that at a neuron-neuron synapse in the central nervous system.

C2.1

Many psychoactive drugs affect synaptic transmission. Using cocaine (dopamine reuptake inhibitor) as an example, explain how altering synaptic transmission can lead to addiction.

C2.2 Neural signalling — one-page recap

Screenshot this slide to revise from

Neuron structure & resting potential

Neuron: cell body (cytoplasm + nucleus) with one long axon and multiple shorter dendrites, all conducting impulses.
Resting potential (~−70 mV, inside negative): maintained by ATP-driven pumping of Na⁺ out and K⁺ in, in opposite directions.

Action potentials & impulse speed

Action potential: all-or-nothing electrical event, triggered only once threshold is reached; read on oscilloscope traces.
Conduction velocity is negatively correlated with body size, positively correlated with axon diameter (R² quantifies each relationship's strength).

Synapses & neurotransmission

Synapse: junction (neuron–neuron or neuron–effector) where a signal passes one direction only; depolarization → Ca²⁺ entry → neurotransmitter release.
EPSP: neurotransmitter (e.g. acetylcholine) diffuses across the cleft, binds a receptor, depolarizes the postsynaptic membrane toward threshold.

HL · The action potential mechanism

Depolarization = Na⁺ influx via voltage-gated Na⁺ channels; repolarization = K⁺ efflux via voltage-gated K⁺ channels.
Local currents regenerate the impulse point-by-point (unmyelinated); saltatory conduction jumps node-to-node at nodes of Ranvier (myelinated) for speed.

HL · Synaptic transmission in depth

Neonicotinoids block the postsynaptic acetylcholine receptor; cocaine blocks presynaptic reuptake of neurotransmitter (e.g. dopamine) — different sides, different mechanisms.
IPSP hyperpolarizes the postsynaptic membrane; summation (spatial + temporal) combines many EPSPs/IPSPs into one all-or-nothing firing decision.

HL · Pain & consciousness

Free nerve endings open positive-ion channels in response to heat, acid or capsaicin, sending impulses to the brain, where pain is perceived.
Consciousness is an emergent property arising from the interaction of billions of individual neurons, not a property any single neuron has alone.

Next step

Now test yourself on C2.2

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Every thought, one ion at a time

From a single sodium ion crossing a membrane to billions of neurons interacting to produce consciousness itself, this lesson traces the nervous system's electrical and chemical signalling from the smallest scale to the largest.

C2.2 Neural signalling · BioCentral IB