IB Biology · Theme C Interaction and interdependence · Cells
C2.2 Neural signalling
Neurons carry electrical impulses: action potentials made by sodium and potassium ions crossing the membrane. At synapses the signal becomes chemical, as neurotransmitter diffuses across a cleft to receptors. Speed depends on axon diameter and myelin; summation of inputs decides whether a neuron fires.
Compiled from the IB Biology guide (first assessment 2025, updated May 2026 for 2028) and our question bank ·
Specialist review in progress
· How these pages are made
Assessed in Paper 1A (multiple choice), Paper 1B (data-based) and Paper 2 (short and extended response). IB Biology guide (first assessment 2025, updated May 2026 for 2028).
Learn
C2.2.1 A neuron is one cell with a body and long fibres
From 2028 this is supplied in the Biology data booklet — you need to recognise and interpret it, not reproduce it from memory.
A neuron is a nervous system cell that carries electrical impulses.
The cell body holds the nucleus and most of the cytoplasm.
One long single fibre is the axon; multiple shorter fibres are dendrites.
Impulses are conducted along these nerve fibres, which are part of the neuron itself.
Students often think nerve and neuron mean the same. In fact a neuron is one cell; a nerve is a bundle of fibres from many neurons.
Students often think a neuron has several axons. In fact it has one axon; the other fibres are dendrites.
C2.2.2 Pumping ions sets up the resting potential
The sodium–potassium pump uses ATP to move Na⁺ out and K⁺ in, against their gradients.
Three Na⁺ leave for every two K⁺ that enter.
The membrane potential is the voltage across the membrane, inside relative to outside.
A resting neuron is polarised at about −70 mV, inside negative.
The inside is negative because of the 3:2 pumping, faster K⁺ leakage out, and trapped negative proteins.
Students often think the pump is a channel that needs no ATP. In fact it is active transport, powered by ATP.
Students often think a resting neuron uses no energy. In fact the pump runs continuously to maintain the gradients.
C2.2.3 A nerve impulse is a travelling reversal of membrane potential
A nerve impulse is an action potential propagated along a fibre.
The inside briefly becomes positive (depolarisation) then returns to negative (repolarisation).
It is electrical because positively charged ions cross the membrane.
It travels without getting smaller.
Students often think the impulse is electrons flowing like a wire. In fact it is a wave of membrane change; ions cross at each point in turn.
Students often think neurotransmitter molecules travel along the axon. In fact the axon signal is electrical; chemicals are used only at synapses.
C2.2.4 Wider and myelinated fibres conduct faster
Speed is positively correlated with axon diameter.
The squid giant axon, about 1 mm wide, conducts at about 25 m s⁻¹.
Narrow non-myelinated fibres, about 1 µm wide, manage about 1 m s⁻¹.
Myelinated fibres conduct faster still, over 100 m s⁻¹ in mammals.
Across animals, conduction speed is negatively correlated with animal size. The correlation coefficient r runs from −1 to +1: sign gives direction, magnitude gives strength. R² = r² gives the fraction of variation explained.
Students often think r = 0.9 means 90% explained. In fact R² = 0.81, so 81% is explained.
Students often think a strong correlation proves cause. In fact it shows association only; cause needs an experiment or mechanism.
C2.2.5 Synapses join neurons to neurons or to effectors, one way only
A synapse is a junction between a neuron and another neuron or an effector cell.
Effectors include muscle fibres and gland cells; a neuromuscular junction is one example.
The presynaptic neuron releases neurotransmitter; the postsynaptic cell carries the receptors.
A signal crosses a typical synapse in one direction only.
Students often think impulses cross synapses in either direction. In fact they go from presynaptic to postsynaptic only.
Students often think the impulse jumps the gap as a spark. In fact it stops; a chemical crosses and starts a new potential.
Free nerve endings of sensory neurons in the skin have channels for positive ions.
High temperature, acid or capsaicin open them; ions enter; threshold is reached.
Impulses pass along the neuron to the brain, where pain is perceived.
Capsaicin opens the same channels as heat, so chilli feels hot without warmth.
Students often think pain is felt in the skin. In fact the skin detects; the brain perceives.
Students often think separate receptor cells detect pain. In fact the neuron's own free ending has the channels.
C2.2.16 Consciousness emerges from neurons interacting HL
An emergent property belongs to a whole system, not to any component.
Consciousness arises from the interaction of very many neurons.
No single neuron is conscious, even a little.
No single region or chemical produces it.
Students often think one brain region stores consciousness. In fact it emerges from interactions across the brain.
Students often think each neuron adds a bit of consciousness. In fact an emergent property is absent from every component.
Diagnostic a bearings check, not a test
10 questions, one per part of the topic where we can. Answer them, then see which statements you own and which to read.
1 Which description of the structure of a neuron is correct?
Answer and reasoning
A cell body of cytoplasm and a nucleus, with one long axon and several shorter dendrites projecting from it. — Cytoplasm and a nucleus form the cell body of a neuron, with elongated nerve fibres projecting from it: an axon is a long single fibre, and dendrites are multiple shorter fibres. Electrical impulses are conducted along these fibres.
A cell body of cytoplasm and a nucleus, with many long axons of equal length projecting from it in all directions. — A student who counts every fibre leaving the cell body as an axon picks this. In fact a neuron has a single axon; the other, shorter fibres are dendrites.
A bundle of many nerve fibres wrapped in connective tissue, with cell bodies spaced along the length of the bundle. — A student who treats 'nerve' and 'neuron' as the same thing picks this. In fact this describes a nerve; a neuron is one cell with its own cell body and fibres.
A cell body of cytoplasm and a nucleus, joined to other cell bodies by separate connecting fibres that are not part of any cell. — A student who pictures neurons as cell bodies linked by external wires picks this. In fact the fibres are projections of the neuron itself, enclosed by its plasma membrane.
2 How does the sodium–potassium pump contribute to the resting potential of a neuron?
Answer and reasoning
It uses energy from ATP to move potassium ions out of the neuron and sodium ions in across the membrane, building up concentration gradients of both ions. — A student who has the two ions the wrong way round picks this. In fact sodium ions are pumped out and potassium ions in, so the cytoplasm is high in potassium ions and low in sodium ions.
It lets sodium and potassium ions diffuse down their concentration gradients through its channel, without using any ATP at all. — A student who confuses a pump with a channel picks this. In fact the pump moves ions against their gradients, which requires energy from ATP; diffusion cannot build a gradient.
It uses energy from ATP to move sodium ions out of the neuron and potassium ions in, building up concentration gradients of both ions. — Energy from ATP drives the pumping of sodium and potassium ions in opposite directions across the membrane: sodium ions out and potassium ions in. The gradients this establishes, together with unequal leakage of the two ions, generate the negative resting potential.
It is switched off while the neuron is at rest, so that no ATP is used until an impulse arrives at the membrane of the neuron. — A student who thinks 'resting' means inactive picks this. In fact the pump works continuously at rest, and it is this pumping that maintains the resting potential.
3 In a study of axon diameter and conduction speed, the correlation coefficient was r = +0.90. Which statement about the coefficient of determination is correct?
Answer and reasoning
R² = 0.81, so about 81% of the variation in speed is explained by variation in diameter. — The coefficient of determination is the square of the correlation coefficient: 0.90² = 0.81. It evaluates the degree to which variation in the independent variable (diameter) explains the variation in the dependent variable (speed), here 81%.
R² = 0.90, so about 90% of the variation in speed is explained by the variation in diameter. — A student who uses r itself as the proportion explained picks this. In fact R² is r squared, 0.81, so 81% of the variation is explained.
R² = 0.81, so about 81% of the fibres measured conducted faster when they had a larger diameter. — A student who reads R² as a fraction of data points picks this. In fact R² describes how much of the variation in speed is accounted for by diameter, not how many fibres follow the trend.
R² = 0.81, which proves that a larger diameter is the cause of the faster conduction speed. — A student who treats a strong correlation as proof of cause picks this. In fact R² measures the strength of the statistical association; causation would need experimental evidence or a mechanism.
A signal can pass across it in either direction, depending on which of the two neurons is stimulated first. — A student who pictures the synapse as a simple gap picks this. In fact only one side releases neurotransmitter and only the other has receptors, so transmission is one-way.
It is found only where two neurons meet, so muscle fibres are stimulated directly by the nerve impulse. — A student who has only seen neuron-to-neuron synapses picks this. In fact synapses also occur between neurons and effector cells; a neuromuscular junction is a synapse.
A signal can pass across it in one direction only, from the presynaptic cell to the postsynaptic cell. — A signal can only pass in one direction across a typical synapse, because neurotransmitter is released from the presynaptic membrane and its receptors are on the postsynaptic membrane.
The action potential jumps across the gap as an electrical spark, so no chemical is needed to cross the cleft. — A student who assumes electricity bridges the cleft picks this. In fact the signal crosses the cleft as a neurotransmitter that diffuses to receptors on the postsynaptic membrane.
5 How does acetylcholine generate an excitatory postsynaptic potential?
Answer and reasoning
It diffuses across the cleft and enters the postsynaptic cell, where it depolarizes the membrane from the inside. — A student who thinks the neurotransmitter goes into the next cell picks this. In fact acetylcholine binds to receptors on the outer surface of the postsynaptic membrane and stays outside; ions entering through the opened channels cause the depolarization.
It is actively transported across the cleft by carrier proteins, which use ATP to push it into the postsynaptic cell. — A student who thinks crossing the cleft needs active transport picks this. In fact acetylcholine diffuses across the narrow cleft and binds to receptors; it is not pumped and it does not enter the cell.
It diffuses across the cleft and binds to transmembrane receptors, opening channels through which sodium ions enter the postsynaptic cell. — Acetylcholine diffuses across the synaptic cleft and binds to transmembrane receptors on the postsynaptic membrane. Binding opens channels for positively charged ions, mainly sodium ions, which enter and depolarize the membrane, producing an excitatory postsynaptic potential.
It diffuses across the cleft and binds to receptors, opening channels through which potassium ions enter the postsynaptic cell. — A student who has the ions swapped picks this. In fact the channels opened by acetylcholine at an excitatory synapse let sodium ions enter; potassium ions are more concentrated inside and would not enter.
6 How do local currents propagate an action potential along an axon? HL
Answer and reasoning
Sodium ions that entered at the start travel along the whole axon to its end, carrying the depolarization with them. — A student who thinks the same ions travel the length of the axon picks this. In fact each region admits its own sodium ions once it reaches threshold; the ions that entered move only to the neighbouring region.
Sodium ions that entered diffuse to the next region and depolarize it fully, so no voltage-gated channels are needed there. — A student who thinks the local current carries the whole depolarization picks this. In fact local currents only bring the next region to threshold; its own voltage-gated sodium channels then produce the full depolarization.
Electrons released when the sodium channels open flow along the inside of the axon, depolarizing the whole length at once. — A student who thinks the impulse is electron flow picks this. In fact local currents are movements of ions, and the action potential is regenerated region by region, not all at once.
Sodium ions that entered diffuse along the inside of the axon to the next region, bringing it to threshold so its sodium channels open. — Sodium ions entering at the depolarized region diffuse along the inside of the axon to the adjacent region, while outside the axon sodium ions diffuse towards the depolarized region. These local currents reduce the membrane potential of the adjacent region until threshold is reached and its voltage-gated sodium channels open, regenerating the action potential.
7 An oscilloscope trace of an axon shows a steady −70 mV, then a rapid rise to +30 mV at 1 ms, a fall back through −70 mV by 3 ms, a brief dip to −80 mV, and a return to −70 mV. What is happening between 1 ms and 3 ms? HL
Answer and reasoning
Repolarization: voltage-gated potassium channels are open and potassium ions are entering the axon. — A student who has the direction of potassium movement wrong picks this. In fact potassium ions leave the axon, removing positive charge and so making the inside negative again.
Repolarization: voltage-gated potassium channels are open and potassium ions are leaving the axon. — The fall from the +30 mV peak back to the resting potential is repolarization. It is caused by voltage-gated potassium channels opening after the sodium channels close, so that potassium ions diffuse out and the inside becomes negative again. The dip to −80 mV is a brief hyperpolarization: the voltage-gated potassium channels are slow to close, so potassium ions continue to leave for a moment after the resting potential is reached, and the membrane returns to −70 mV once they have closed.
Repolarization: the sodium–potassium pump is actively moving sodium ions back out of the axon. — A student who credits the pump with repolarization picks this. In fact a fall of 100 mV in 2 ms is produced by potassium ions diffusing out through voltage-gated channels; the pump restores gradients much more slowly afterwards.
Depolarization: the membrane potential is becoming more negative as the polarity is being removed from it. — A student who thinks depolarization means becoming more negative picks this. In fact depolarization is the rise to +30 mV before 1 ms; the return to negative values is repolarization.
8 How do neonicotinoid pesticides block synaptic transmission in insects? HL
Answer and reasoning
They block the reuptake of acetylcholine into the presynaptic neuron, so the insect's synapses soon run out of neurotransmitter. — A student who has merged the two examples picks this. In fact blocking reuptake is the mechanism of cocaine; neonicotinoids act at the acetylcholine receptors.
They inhibit the enzyme acetylcholinesterase in the cleft, so acetylcholine is not broken down at all after it has been released. — A student who expects a pesticide to target the enzyme picks this. In fact that is the action of other insecticides; neonicotinoids bind to the receptors, not the enzyme.
They prevent calcium ions from crossing the synaptic cleft, so the postsynaptic membrane is not depolarized at all. — A student who thinks calcium crosses the cleft picks this. In fact calcium acts inside the presynaptic neuron, and neonicotinoids act on the postsynaptic acetylcholine receptors.
They bind to acetylcholine receptors at the insect's synapses, so acetylcholine can no longer transmit signals across them. — Neonicotinoids bind to acetylcholine receptors on postsynaptic membranes in the insect's central nervous system. The receptors can then no longer respond normally to acetylcholine, so synaptic transmission is blocked and the insect is paralysed and dies.
9 What happens at the postsynaptic membrane when an inhibitory neurotransmitter binds to its receptors? HL
Answer and reasoning
Channels open that make the inside more negative than the resting potential, so the membrane is hyperpolarized and further from threshold. — Inhibitory neurotransmitters open channels that let negative ions such as chloride ions in or positive ions such as potassium ions out. The postsynaptic membrane becomes hyperpolarized, generating an inhibitory postsynaptic potential that makes an action potential less likely.
Channels open that depolarize the membrane, but by a smaller amount than an excitatory neurotransmitter would. — A student who thinks 'inhibitory' just means 'weaker' picks this. In fact inhibitory neurotransmitters move the membrane potential the opposite way, making it more negative.
Channels open that make the inside more positive than the resting potential, which is called hyperpolarization. — A student who reads 'hyper' as 'more positive' picks this. In fact hyperpolarization means more polarized: more negative inside than at rest.
Nothing happens at this membrane, because inhibitory neurotransmitters act by stopping release from the presynaptic neuron. — A student who thinks inhibition switches off the presynaptic neuron picks this. In fact the inhibitory neurotransmitter is itself released and acts on the postsynaptic membrane, hyperpolarizing it.
10 Eating chilli peppers causes a burning pain in the mouth. Which explanation is correct? HL
Answer and reasoning
Capsaicin raises the temperature of the tissue in the mouth, and this heat is what the free nerve endings then detect. — A student who takes 'hot' literally picks this. In fact the tissue does not warm; capsaicin opens the same channels that heat opens, so the brain perceives the same burning.
Capsaicin stimulates free nerve endings, which perceive the pain in the mouth and then send a report of it to the brain. — A student who locates perception at the site of the stimulus picks this. In fact the nerve endings only detect the stimulus and generate impulses; pain is perceived in the brain.
Capsaicin causes receptor cells in the mouth to release neurotransmitter onto sensory neurons, which then carry the pain. — A student who expects separate receptor cells picks this. In fact the free nerve endings are part of the sensory neurons themselves, and capsaicin acts directly on their ion channels.
Capsaicin opens channels for positive ions in free nerve endings, so threshold is reached and impulses pass to the brain, where pain is perceived. — Free nerve endings have channels for positively charged ions that open in response to high temperature, acid, or chemicals such as capsaicin. Entry of positive ions brings the membrane to threshold, and the impulses that result pass to the brain, where the pain is perceived.
Read the ones marked not yet in Learn, then Verify.
Verify confirm before you go
24 more questions. Every wrong answer here is a real misconception, and you see why it is wrong straight away.
1 A motor neuron has its cell body in the spinal cord and a single fibre about 1 m long that reaches a muscle in the foot. What is this fibre?
Answer and reasoning
One of the neuron's several axons, each of which reaches a different muscle in the leg. — A student who thinks a neuron has several axons picks this. In fact a neuron has a single axon; its branches near the end are terminals of that one axon.
An axon: a single long fibre along which impulses are conducted away from the cell body. — An axon is a long single fibre projecting from the cell body. A motor neuron's axon can extend about a metre from the spinal cord to a muscle, and impulses are conducted along it.
A nerve, because a fibre this long must be made of many neurons joined end to end. — A student who confuses a nerve with a neuron picks this. In fact one neuron's axon can be a metre long; a nerve is a bundle of many such fibres.
A connecting fibre that links the neuron to the muscle but is not part of the neuron itself. — A student who sees fibres as separate wiring picks this. In fact the fibre is part of the neuron: an extension of its cytoplasm surrounded by its own membrane.
2 Measurements on a resting neuron show that potassium ions are about 30 times more concentrated inside than outside and sodium ions about 10 times more concentrated outside than inside, yet the inside is at −70 mV relative to the outside. Which explanation of the negative resting potential is consistent with these measurements?
Answer and reasoning
All the positively charged ions are pumped out of the cytoplasm by the sodium–potassium pump, leaving only negatively charged ions inside the neuron. — A student who reads 'inside negative' as meaning no positive ions inside picks this. In fact the cytoplasm is rich in potassium ions; the negative potential comes from a small imbalance, not the absence of positive ions.
Positive ions diffuse out through the pump faster than they diffuse in, because the pump is simply a channel that favours movement outwards. — A student who thinks the pump is a channel picks this. In fact the pump uses ATP to move ions against their gradients; it is not a channel and ions do not diffuse through it.
The membrane is completely impermeable at rest, so the charge left over from the last impulse cannot leak away across it. — A student who thinks nothing happens at rest picks this. In fact ions leak across the resting membrane continuously and the pump works continuously to maintain the gradients.
The pump moves three sodium ions out for every two potassium ions in, and potassium ions leak back out faster than sodium ions leak in. — Each cycle of the pump removes more positive charge than it brings in, and the membrane is much more permeable to potassium ions than to sodium ions, so more positive charge leaks out than in. Negatively charged proteins that cannot leave the cytoplasm add to the effect, so the inside is about −70 mV relative to the outside.
3 A neuron is treated with a chemical that stops it producing ATP. Which prediction about its resting potential is correct?
Answer and reasoning
It gradually falls towards zero, because the pump stops and the ion gradients run down as ions leak across the membrane. — The resting potential depends on gradients that are maintained by pumping driven by ATP. Without ATP the pump stops, leakage of ions continues, and the gradients and the potential they generate decay gradually.
It stays the same, because a neuron at rest is inactive and does not need to use ATP for anything until an impulse arrives. — A student who thinks a resting neuron uses no energy picks this. In fact maintaining the resting potential is an active process that consumes ATP continuously.
It stays the same, because the pump moves ions passively down their gradients and does not need ATP in order to work. — A student who confuses the pump with a channel picks this. In fact the pump moves ions against their gradients and cannot work without energy from ATP.
It becomes more positive straight away, because the pump can no longer remove the positive ions that had all been kept outside. — A student who thinks the resting potential comes from all positive ions being outside picks this. In fact the cytoplasm is rich in potassium ions; the gradients run down gradually by leakage, so the potential decays slowly towards zero rather than jumping positive.
4 Why is a nerve impulse described as an electrical signal?
Answer and reasoning
It consists of electrons flowing along the inside of the fibre, in the same way as a current in a metal wire. — A student who applies the wiring analogy literally picks this. In fact no electrons flow along the axon; the charge carriers are ions crossing the membrane.
It consists of positively charged ions moving across the membrane, which changes the membrane potential. — A nerve impulse is electrical because it involves movement of positively charged ions, sodium and potassium ions, across the membrane of the nerve fibre, reversing and then restoring the membrane potential.
It consists of neurotransmitter molecules travelling along the fibre and carrying their electrical charge with them. — A student who generalizes the chemical signal at synapses to the whole neuron picks this. In fact neurotransmitters act only at synapses; along the fibre the signal is a change in membrane potential.
It consists of sodium ions flowing along the whole length of the fibre from one end of it to the other. — A student who thinks the ions themselves travel the length of the axon picks this. In fact ions cross the membrane at each point in turn; the impulse travels but the individual ions move only a short distance.
5 Electrodes inside and outside an axon show that the inside briefly becomes positive relative to the outside as an impulse passes. What causes this change?
Answer and reasoning
Potassium ions move into the axon across the membrane at that point. — A student who has the ion directions swapped picks this. In fact potassium ions move out of the axon, and they do so later, restoring the negative inside.
Electrons move out of the axon along the inner surface of its membrane. — A student who thinks of the impulse as electron flow picks this. In fact there is no flow of electrons; positive ions entering the axon make the inside positive.
Sodium ions move into the axon across the membrane at that point. — During an action potential sodium ions diffuse into the axon through the membrane, adding positive charge inside so that the membrane potential briefly reverses to positive. The impulse is electrical because of this movement of positively charged ions.
Sodium ions arriving from further back along the axon accumulate at that point. — A student who thinks ions travel along the axon picks this. In fact the sodium ions that make this point positive enter through the membrane at this point; they do not travel along the axon from behind.
6 Conduction speeds were measured in three nerve fibres. Fibre P (a squid giant axon) is non-myelinated, 500 µm in diameter, and conducts at 25 m s⁻¹. Fibre Q is non-myelinated, 1 µm in diameter, and conducts at 1 m s⁻¹. Fibre R is myelinated, 10 µm in diameter, and conducts at 60 m s⁻¹. Which conclusion is supported by these data?
Answer and reasoning
Myelin speeds up fibre R because the myelin sheath itself conducts the electrical current along the length of the fibre. — A student who thinks myelin is a conductor picks this. In fact myelin is an insulator; it speeds conduction by restricting action potentials to the nodes, and the data say nothing about myelin conducting.
Diameter has no effect on speed, so the difference between P and Q must be caused by the type of animal they came from. — A student who thinks only myelination matters picks this. In fact P and Q differ only in diameter and their speeds differ 25-fold, which is direct evidence that diameter affects speed.
Fibre R must come from a larger animal than fibre P, because larger animals conduct nerve impulses faster. — A student who assumes speed scales with body size picks this. In fact conduction speed is negatively correlated with animal size, and the data give no information about the animals' sizes.
Speed rises with diameter in non-myelinated fibres, and myelination lets a narrow fibre conduct faster than a much wider one. — P and Q are both non-myelinated and the wider one is far faster, showing the positive correlation between diameter and speed. R is fifty times narrower than P yet faster, showing that myelination increases speed more than a large diameter does.
7 Across a range of animal species, the correlation coefficient between body size and nerve impulse conduction speed was r = −0.85. What does this value show?
Answer and reasoning
A weak correlation, because a negative coefficient shows a smaller effect than a positive one would. — A student who reads the minus sign as meaning 'weak' picks this. In fact the sign gives the direction only; a magnitude of 0.85 is a strong correlation whichever sign it carries.
A strong negative correlation: speed tends to fall as body size rises, and R² is about 0.72. — The sign of r shows the direction (negative: speed falls as size rises) and the magnitude shows the strength (0.85 is close to 1, so strong). The coefficient of determination is (−0.85)² = 0.7225, so about 72% of the variation in speed is explained by body size.
That an increase in body size is the direct cause of slower impulses in the larger species. — A student who treats correlation as causation picks this. In fact a correlation coefficient measures association; it cannot show that body size causes the difference in speed.
That about 85% of the variation in conduction speed is explained by the variation in body size. — A student who uses r as the proportion explained picks this. In fact that proportion is R² = 0.85² = 0.72, so about 72%.
8 Why can a signal pass in only one direction across a synapse?
Answer and reasoning
Electric current can only cross the cleft from the more positive presynaptic membrane to the more negative postsynaptic one. — A student who thinks the impulse crosses the cleft electrically picks this. In fact no current crosses the cleft; a chemical neurotransmitter carries the signal.
Calcium ions can only diffuse across the cleft from the presynaptic side, because that is where they are concentrated. — A student who thinks calcium is the messenger across the cleft picks this. In fact calcium ions enter the presynaptic neuron and act inside it; they do not cross the cleft.
Carrier proteins in the cleft actively transport the neurotransmitter towards the postsynaptic membrane only. — A student who thinks neurotransmitter is pumped across the cleft picks this. In fact it diffuses through the fluid in the cleft; there are no carrier proteins in the cleft itself.
Only the presynaptic neuron stores neurotransmitter in vesicles, and only the postsynaptic membrane has receptors for it. — The two sides of a synapse are structurally different. Neurotransmitter can be released only from the presynaptic membrane, and it can act only where there are receptors, which are on the postsynaptic membrane, so the signal is one-way.
9 What is the role of calcium ions in the release of neurotransmitter from a presynaptic neuron?
Answer and reasoning
Depolarization of the presynaptic membrane opens calcium channels; calcium ions enter and signal vesicles to fuse with the membrane. — When an action potential depolarizes the presynaptic membrane, calcium ions are taken up into the neuron. Inside the neuron they act as a signalling chemical that causes vesicles of neurotransmitter to fuse with the presynaptic membrane, releasing it into the cleft.
Calcium ions are released from the presynaptic neuron and diffuse across the cleft, where they then depolarize the postsynaptic membrane. — A student who confuses calcium with the neurotransmitter picks this. In fact calcium ions move into the presynaptic neuron and act inside it; the neurotransmitter is what crosses the cleft.
Calcium ions have no role, because neurotransmitter simply diffuses out through the presynaptic membrane when an impulse arrives. — A student who assumes release is passive diffusion picks this. In fact neurotransmitter is stored in vesicles and released by exocytosis, which is triggered by calcium ion entry.
Calcium ions provide the energy for carrier proteins to pump the neurotransmitter across the synaptic cleft to its postsynaptic receptors. — A student who thinks neurotransmitter is actively transported across the cleft picks this. In fact it diffuses across the cleft; calcium ions are a signal for release, not an energy source.
10 Calcium ions were removed from the fluid around a synapse. When the presynaptic neuron was stimulated, action potentials still reached the presynaptic terminal, but no response was recorded in the postsynaptic neuron. What does this result show?
Answer and reasoning
Calcium ions are the chemical that normally crosses the cleft and stimulates the postsynaptic neuron to respond. — A student who thinks calcium is the messenger across the cleft picks this. In fact the result is explained by calcium acting inside the presynaptic neuron to trigger release of the neurotransmitter, which is what crosses the cleft.
Entry of calcium ions is needed for neurotransmitter to be released, but not for the impulse to reach the terminal. — The action potential arrived normally, so calcium is not needed for conduction along the axon. Transmission failed at the synapse, which is explained by calcium ions being required to enter the terminal and signal the vesicles to release neurotransmitter.
The neurotransmitter should have diffused out regardless, so the postsynaptic receptors must have been damaged. — A student who thinks release is passive diffusion cannot explain the result and blames the receptors. In fact release requires calcium ion entry, so removing calcium prevents release; nothing else need have changed.
Calcium ions are needed to power the active transport of neurotransmitter across the cleft to the postsynaptic membrane. — A student who thinks neurotransmitter is pumped across the cleft picks this. In fact neurotransmitter diffuses across the cleft; calcium ions are the signal for its release from vesicles.
11 A motor neuron forms a neuromuscular junction with a skeletal muscle fibre. Which statement about acetylcholine at this junction is correct?
Answer and reasoning
It is found only at neuromuscular junctions, because synapses between two neurons use different neurotransmitters. — A student who has met acetylcholine only at the neuromuscular junction picks this. In fact acetylcholine is used at many types of synapse, including many between neurons.
It cannot be involved here, because synapses form only between two neurons and the muscle fibre is stimulated electrically. — A student who does not classify the neuromuscular junction as a synapse picks this. In fact it is a synapse between a neuron and an effector cell, and acetylcholine is its neurotransmitter.
It passes through the membrane into the muscle fibre and triggers contraction directly from inside the cell. — A student who thinks the neurotransmitter enters the postsynaptic cell picks this. In fact acetylcholine binds to receptors on the outside of the muscle fibre membrane and does not enter it.
It is the same neurotransmitter used at many synapses between neurons, and here it binds to receptors on the muscle fibre membrane. — Acetylcholine exists in many types of synapse, including synapses between neurons and neuromuscular junctions. At the neuromuscular junction it binds to transmembrane receptors on the muscle fibre, depolarizing it and generating an excitatory postsynaptic potential.
12 Which sequence of events produces depolarization and then repolarization during an action potential? HL
Answer and reasoning
Voltage-gated sodium channels open at threshold and sodium ions enter; these channels then close and voltage-gated potassium channels open, so potassium ions leave. — When the threshold potential is reached, voltage-gated sodium channels open and sodium ions diffuse in, depolarizing the membrane to about +30 mV. The sodium channels then close and voltage-gated potassium channels open; potassium ions diffuse out and the membrane repolarizes.
Voltage-gated potassium channels open at threshold and potassium ions enter; these then close and voltage-gated sodium channels open, so sodium ions leave. — A student who has the two ions swapped picks this. In fact sodium ions enter to depolarize the membrane and potassium ions leave to repolarize it; the concentration gradients make the reverse impossible.
Voltage-gated sodium channels open at threshold and sodium ions enter; the sodium–potassium pump then actively pumps the sodium ions back out to repolarize the membrane. — A student who assigns repolarization to the pump picks this. In fact repolarization is caused by potassium ions leaving through voltage-gated channels; the pump is far too slow and only restores the gradients afterwards.
Sodium channels open in proportion to the stimulus, with no threshold, and the size of the action potential then matches the strength of the stimulus applied. — A student who forgets the threshold picks this. In fact voltage-gated sodium channels open only when threshold is reached, and the action potential is then always the same size.
13 The resting potential of a neuron is −70 mV and its threshold potential is −55 mV. A weak stimulus depolarizes the membrane to −60 mV. What happens next? HL
Answer and reasoning
A small action potential is produced, in proportion to the size of the stimulus that was applied to the membrane. — A student who thinks action potentials are graded picks this. In fact there are no small action potentials: below threshold nothing happens, and at threshold a full-sized one occurs.
The membrane returns to rest: threshold was not reached, so voltage-gated sodium channels stay closed. — −60 mV is less depolarized than the threshold of −55 mV. Voltage-gated sodium channels open only when the threshold potential is reached, so no action potential is produced and the small depolarization fades back to −70 mV.
The membrane has become hyperpolarized, so no action potential can be produced until it recovers to −70 mV. — A student who thinks depolarization means becoming more negative reads −60 mV as hyperpolarization. In fact −60 mV is less negative than −70 mV, so this is a small depolarization, just not enough to reach threshold.
A full action potential is produced, because the voltage-gated channels holding the membrane at −70 mV have been disturbed. — A student who thinks voltage-gated channels maintain the resting potential picks this. In fact those channels are closed at rest and open only at threshold; a depolarization to −60 mV does not reach −55 mV, so they stay shut and the membrane returns to rest.
14 A drug blocks the voltage-gated potassium channels in an axon. Which effect on its action potentials is predicted? HL
Answer and reasoning
Repolarization is unaffected, because the sodium–potassium pump returns the membrane potential to its resting value. — A student who thinks the pump repolarizes the membrane picks this. In fact repolarization is the rapid exit of potassium ions through voltage-gated channels, so blocking them slows repolarization markedly.
Depolarization cannot occur, because potassium ions can no longer enter the axon to make the inside positive. — A student who has the ions swapped picks this. In fact depolarization is caused by sodium ions entering, so blocking potassium channels does not prevent it.
Depolarization occurs normally, but repolarization is much slower, so each action potential lasts longer. — Depolarization depends on voltage-gated sodium channels, which are unaffected. Repolarization depends on potassium ions leaving through voltage-gated potassium channels; with these blocked, the return to the resting potential relies on slower leakage, so the action potential is prolonged.
The resting potential cannot be maintained, so the axon can no longer produce any action potentials at all. — A student who thinks voltage-gated channels maintain the resting potential picks this. In fact these channels are closed at rest; the resting potential depends on the pump and leak channels, so it is maintained and action potentials can still begin.
15 An axon is cooled so that diffusion of ions becomes slower. Which prediction about conduction of impulses along it is correct? HL
Answer and reasoning
Conduction is slower, because local currents take longer to bring each adjacent region of membrane to threshold. — Propagation depends on diffusion of sodium ions inside and outside the axon to reduce the membrane potential of the next region to threshold. Slower diffusion means each region reaches threshold later, so the action potential travels more slowly.
Conduction is slower, because the sodium ions take longer to travel from one end of the axon to the other. — A student who thinks the ions travel the whole length picks this. In fact sodium ions diffuse only to the adjacent region; the delay is in bringing each region to threshold, not in a long journey by the ions.
Conduction is unchanged, because the impulse is carried by electrons, whose movement is not affected by temperature. — A student who thinks of the axon as a wire picks this. In fact the impulse depends on diffusion of ions, which is slowed by cooling.
Conduction is unchanged, because each region is depolarized directly by the one before it without any diffusion of ions. — A student who thinks the depolarization is simply handed on picks this. In fact the link between regions is diffusion of sodium ions, the local current, so slowing diffusion slows conduction.
16 An oscilloscope trace covering 60 ms shows 15 action potentials. What is the frequency of impulses? HL
Answer and reasoning
0.25 impulses per second — A student who divides by 60 without converting milliseconds to seconds picks this. In fact 60 ms is 0.060 s, so the answer is a thousand times larger: 250.
4 impulses per second — A student who divides the time by the number of spikes picks this. In fact 60 ÷ 15 = 4 ms is the interval between impulses; frequency is spikes divided by time in seconds.
250 impulses per second — 60 ms is 0.060 s, so the frequency is 15 ÷ 0.060 = 250 impulses per second. The number of impulses per second is measured from a trace by counting the spikes and dividing by the time covered, in seconds.
15 impulses per second — A student who takes the number of spikes as the frequency picks this. In fact 15 spikes were recorded in only 60 ms, so in a full second there would be 250.
17 Two oscilloscope traces were recorded from the same sensory neuron. With a weak stimulus there were 5 action potentials in 100 ms; with a strong stimulus there were 20 action potentials in 100 ms. In both traces every action potential peaked at +30 mV. What do the traces show? HL
Answer and reasoning
The recording must be faulty, because a stronger stimulus should produce action potentials with a higher peak. — A student who reads spike height as stimulus strength picks this. In fact the peak of an action potential is fixed by the ion gradients and channels; the traces are exactly what is expected.
The stronger stimulus made each impulse travel faster, so more of them reached the electrode in the time available. — A student who thinks stimulus strength affects conduction speed picks this. In fact speed is a property of the fibre; the strong stimulus made the neuron fire more often, not faster.
The neuron fired 5 impulses per second with the weak stimulus and 20 impulses per second with the strong stimulus. — A student who takes the spike count as the frequency picks this. In fact the traces cover only 100 ms, so the frequencies are 50 and 200 impulses per second.
Stimulus strength is coded by the frequency of impulses, while the size of each action potential stays fixed. — The stronger stimulus produced four times as many impulses in the same time (200 per second rather than 50 per second) but no change in the height of the spikes. Action potentials are all-or-nothing, so stimulus strength is conveyed by how often they occur.
18 Which statement explains saltatory conduction in a myelinated nerve fibre? HL
Answer and reasoning
Ion channels and pumps are clustered at the nodes of Ranvier, so action potentials occur only at the nodes and the impulse passes from node to node. — Myelin insulates the fibre between nodes, and the ion pumps and voltage-gated channels are clustered at the nodes of Ranvier. Local currents spread along the insulated section to the next node, which is depolarized to threshold, so the action potential is propagated from node to node.
The myelin sheath conducts the electrical current along the fibre, so the impulse travels through the myelin between the nodes. — A student who thinks myelin is a conductor picks this. In fact myelin is an insulator that prevents ion movement across the covered membrane; the current flows inside and outside the axon, not through the myelin.
Action potentials occur along the entire membrane of the fibre, but the myelin makes each of them develop more quickly. — A student who keeps the non-myelinated mechanism picks this. In fact the myelinated sections lack the clustered channels and do not produce action potentials; only the nodes do.
The nodes of Ranvier are gaps in the insulation where the impulse leaks out, so each node slows the impulse slightly. — A student who sees the nodes as faults in the insulation picks this. In fact the nodes are where the action potential is regenerated, and jumping between them is what makes conduction fast.
19 Why does a myelinated fibre conduct impulses faster than a non-myelinated fibre of the same diameter? HL
Answer and reasoning
Myelin is a good conductor of electricity, so the current flows through it faster than it can flow through the cytoplasm of the axon. — A student who thinks myelin conducts picks this. In fact myelin insulates; the speed comes from restricting action potentials to the nodes.
Depolarization has to occur only at the nodes, so far fewer regions of membrane are depolarized along the length of the fibre. — In a non-myelinated fibre every region of membrane must be brought to threshold in turn. In a myelinated fibre the action potential is propagated from node to node, so only the nodes are depolarized and the impulse covers the same distance in far fewer steps.
A myelinated fibre has fewer nodes than a non-myelinated one, and it is the nodes that slow the impulse down. — A student who sees nodes as obstacles picks this. In fact a non-myelinated fibre has no nodes at all, and the nodes are where the action potential is regenerated, not where it is slowed.
Action potentials form all along the fibre, but each one is generated more quickly beneath the insulating myelin. — A student who assumes myelin just speeds each action potential picks this. In fact no action potentials occur beneath the myelin; they occur only at the nodes.
20 Cocaine binds to the transporter proteins that return dopamine to the presynaptic neuron. What effect does this have at a dopamine synapse? HL
Answer and reasoning
Dopamine cannot bind to its postsynaptic receptors because they are blocked, so the postsynaptic neuron receives less stimulation than normal. — A student who assumes 'blocks' means blocking the receptor picks this. In fact cocaine blocks the transporter, not the receptor, so dopamine binds to the receptors more, not less.
Transmission is inhibited, because any drug that acts at a synapse prevents the postsynaptic neuron from firing. — A student who thinks all synaptic drugs are inhibitory picks this. In fact blocking reuptake increases stimulation of the postsynaptic neuron.
Dopamine remains in the synaptic cleft and continues to bind to postsynaptic receptors, so the postsynaptic neuron is stimulated for longer. — Cocaine blocks reuptake of the neurotransmitter. Dopamine that would normally be removed from the cleft by the transporter proteins stays there, repeatedly binding to receptors on the postsynaptic membrane and prolonging its stimulation.
Dopamine release stops, because dopamine can only leave the presynaptic neuron through the transporter proteins that cocaine has blocked. — A student who thinks neurotransmitter leaves by diffusing through membrane proteins rather than by exocytosis picks this. In fact dopamine is released from vesicles by exocytosis; the transporters only carry it back in, so release continues and dopamine accumulates in the cleft.
21 A postsynaptic neuron has a resting potential of −70 mV and a threshold of −55 mV. At the same moment it receives two excitatory inputs, each producing a +8 mV change, and one inhibitory input producing a −6 mV change. What is the result? HL
Answer and reasoning
An action potential, because the two excitatory inputs alone take the membrane to −54 mV. — A student who thinks inhibitory inputs cannot cancel excitatory ones ignores the −6 mV. In fact all inputs are summed, and the inhibitory hyperpolarization keeps the membrane at −60 mV, below threshold.
No action potential, because the combined change takes the membrane only to −60 mV. — Summation adds the postsynaptic potentials: −70 + 8 + 8 − 6 = −60 mV. This does not reach the threshold of −55 mV, so the all-or-nothing consequence is that no action potential is produced.
Two action potentials, one triggered by each of the two excitatory inputs that arrive. — A student who thinks every excitatory input fires the neuron picks this. In fact a single +8 mV input is far below threshold, and inputs are summed rather than counted.
A small action potential of 10 mV, matching the net change in the membrane potential. — A student who thinks action potentials are graded picks this. In fact action potentials are all-or-nothing; a net depolarization below threshold produces none.
22 Which statement about summation at a postsynaptic neuron is correct? HL
Answer and reasoning
Each impulse arriving from any presynaptic neuron produces its own action potential in the postsynaptic neuron. — A student who pictures a synapse as a one-to-one relay picks this. In fact a single input is usually too small to reach threshold, which is why summation is needed.
Postsynaptic potentials are all-or-nothing, so each one is either a full-sized action potential or nothing at all. — A student who confuses postsynaptic potentials with action potentials picks this. In fact postsynaptic potentials are graded and add together; only the action potential is all-or-nothing.
Postsynaptic potentials from several presynaptic neurons add together, and an action potential results only if threshold is reached. — Multiple presynaptic neurons interact at a postsynaptic neuron. Their excitatory and inhibitory postsynaptic potentials are summed, and the consequence is all-or-nothing: an action potential is produced if the net depolarization reaches threshold and not otherwise.
Inhibitory and excitatory inputs act on separate parts of the membrane and so cannot cancel each other out. — A student who treats excitation and inhibition as independent switches picks this. In fact both change the same membrane potential in opposite directions, so they do cancel.
23 A local anaesthetic blocks the voltage-gated sodium channels in the sensory neurons of a patch of skin. A hot object is then placed on the skin, but no pain is felt. Why? HL
Answer and reasoning
Positive ions still enter the free nerve endings, but no impulses can be propagated to the brain, where pain is perceived. — The heat-sensitive channels in the free nerve endings are opened by the stimulus, not by voltage, so positive ions still enter and threshold may be reached. Without voltage-gated sodium channels, however, no action potentials can be generated or propagated, so nothing reaches the brain and no pain is perceived.
The channels that respond to heat are voltage-gated, so they are blocked too and no positive ions can enter. — A student who thinks every channel in a neuron is voltage-gated picks this. In fact the stimulus-sensitive channels open in response to heat itself; it is the later impulse that is prevented.
The skin is where pain is perceived, and the anaesthetic has stopped the skin from perceiving the heat. — A student who locates perception in the skin picks this. In fact the skin's nerve endings detect; pain is perceived in the brain, which the impulses cannot now reach.
The anaesthetic cools the skin, so the free nerve endings are not exposed to a temperature high enough to respond. — A student who thinks pain-related chemicals act by changing temperature picks this. In fact the anaesthetic acts on ion channels, not on temperature, and the hot object still heats the skin.
24 Why is consciousness described as an emergent property of the brain? HL
Answer and reasoning
It is stored in a particular small group of neurons in the brain that are specialized for consciousness. — A student who expects consciousness to have a location picks this. In fact it is not stored anywhere; it emerges from interactions across very many neurons.
It arises from the interaction of very many neurons and is not a property of any individual neuron. — Emergent properties are consequences of interaction. Consciousness emerges from the interaction of individual neurons in the brain; no single neuron is conscious, and the property cannot be found by studying neurons one at a time.
Each neuron in the brain contributes a small amount of consciousness, and these amounts add up to the whole. — A student who thinks emergent means additive picks this. In fact no neuron is conscious to any degree; the property appears only from the interactions.
It is produced by a single neurotransmitter, which is released throughout the brain whenever a person is awake. — A student who links mental states to single chemicals picks this. In fact consciousness cannot be reduced to one molecule; it emerges from the interaction of neurons.
That was your twenty minutes. Real practice on C2.2 is past-paper questions marked against the mark scheme.
What the exam asks of C2.2
Paper 1A asks you to identify neuron parts, ion movements and the direction of a signal across a synapse. Paper 1B gives oscilloscope traces to interpret, or conduction-speed data with r and R² values to describe and evaluate. Paper 2 uses *describe* and *explain* at SL on the resting potential and synaptic transmission. At HL, expect *explain* on the action potential, propagation, saltatory conduction and summation, and *outline* on neonicotinoids, cocaine and pain: name the channel, the ion, its direction and the change in potential.
Compiled from the IB Biology guide (first assessment 2025, updated May 2026 for 2028) and our question bank · Specialist review in progress. How these pages are made ·
DP Science Cafe