Cambridge International AS & A Level Biology 9700: Control and coordination – Revision Notes

These revision notes cover topic 15, Control and coordination, of the Cambridge International AS & A Level Biology 9700 syllabus for examination in 2025, 2026 and 2027: section 15.1 (outcomes 1–12) and section 15.2 (outcomes 1–3). This is A Level content, examined on Paper 4 alongside AS knowledge, and it may set the context for Paper 5. For full explanations and worked examples, use the control and coordination study guide.

Also useful: the control and coordination practice questions, the Cambridge A Level Biology hub, the printable 9700 checklist and the free A Level diagnostic. ADH, insulin and glucagon are covered in depth in the homeostasis revision notes.

Key definitions

Term	What to write
Resting potential	The potential difference across the membrane of a neurone at rest, about −70 mV (inside negative)
Action potential	A rapid depolarisation and repolarisation of the membrane, reaching about +40 mV
Threshold	The potential that must be reached for an action potential to start
Refractory period	The time after an action potential when another cannot be generated
Saltatory conduction	Action potentials occurring only at nodes of Ranvier, so the impulse jumps from node to node
Receptor potential	Change in membrane potential of a receptor cell caused by a stimulus
Sarcomere	The unit of striated muscle between two Z lines
Target cell	A cell with receptors for a particular hormone

15.1.1–15.1.2 Endocrine vs nervous

	Nervous	Endocrine
Signal	Action potentials; chemicals at synapses	Hormones
Route	Neurones	Blood
Speed	Fast	Slower
Duration	Short	Longer
Effect	Localised	Often widespread

Endocrine glands are ductless. Examples: ADH (collecting ducts), glucagon (liver), insulin (liver and muscle).

15.1.3–15.1.5 Neurones and receptors

• Sensory neurone: receptor → CNS; cell body in a ganglion outside the CNS; long dendron.
• Motor neurone: CNS → effector; cell body in the CNS; long axon, many dendrites.
• Intermediate neurones link sensory to motor neurones in the CNS.
• Receptor cells convert a stimulus into a receptor potential; above threshold → action potentials in the sensory neurone. Stronger stimulus → higher frequency, same size.

Taste bud chemoreceptor: method in steps

1. Na⁺ diffuses in through Na⁺ channels → depolarisation.
2. Voltage-gated Ca²⁺ channels open → Ca²⁺ in.
3. Vesicles release neurotransmitter onto the sensory neurone.
4. Threshold reached → action potential to the brain.

15.1.6–15.1.8 Membrane potentials

 +40 mV |        /\
        |       /  \
    0   |------/----\----------------------
        |     /      \
 −55 mV |....x........\....... threshold
 −70 mV |___/          \      ____ resting
        |               \____/  hyperpolarisation
          stimulus  Na⁺ in  K⁺ out   refractory period

Stage	Channels	Ion movement
Resting	Na⁺–K⁺ pump (3 Na⁺ out, 2 K⁺ in); K⁺ leak channels	K⁺ diffuses out more than Na⁺ leaks in
Depolarisation	Voltage-gated Na⁺ open	Na⁺ in
Repolarisation	Na⁺ close; voltage-gated K⁺ open	K⁺ out
Hyperpolarisation	K⁺ channels slow to close	Extra K⁺ out
Recovery	Pump and leak channels	Resting potential restored

Refractory period does three things: keeps impulses discrete, makes them travel one way, and sets the maximum frequency (maximum frequency = 1 ÷ refractory period in seconds).

Saltatory conduction: myelin (Schwann cells) insulates; channels concentrated at nodes of Ranvier; local circuits between nodes; faster than in unmyelinated axons.

15.1.9 Cholinergic synapse: method in steps

1. Action potential arrives at the presynaptic knob.
2. Voltage-gated Ca²⁺ channels open; Ca²⁺ diffuses in.
3. Vesicles fuse with the presynaptic membrane; ACh released by exocytosis.
4. ACh diffuses across the cleft; binds to receptors on the postsynaptic membrane.
5. Ligand-gated Na⁺ channels open; Na⁺ in; depolarisation; action potential if threshold reached.
6. Acetylcholinesterase hydrolyses ACh → choline + ethanoic acid; choline recycled to the knob.

15.1.10–15.1.12 Muscle

From nerve to contraction

motor neurone → neuromuscular junction (ACh) → sarcolemma depolarised
  → T-tubules carry depolarisation inward → sarcoplasmic reticulum releases Ca²⁺

Bands during contraction

Shortens	Stays the same
Sarcomere (Z to Z), I band, H zone	A band; lengths of actin and myosin filaments

Sliding filament: method in steps

1. Ca²⁺ binds troponin → troponin changes shape.
2. Tropomyosin moves, exposing binding sites on actin.
3. Myosin heads bind → cross-bridges.
4. Power stroke: ADP + Pi released; actin pulled towards the M line.
5. ATP binds → myosin head detaches.
6. ATP hydrolysed → head re-cocked.
7. Relaxation: Ca²⁺ actively pumped back into the sarcoplasmic reticulum.

15.2 Plants

Response	Key points
Venus fly trap (15.2.1)	Hairs bent → receptor potential; repeated stimulation within a short time → action potential across lobes; rapid change in cell turgor flips lobes from convex to concave → trap closes
Auxin (15.2.2)	Stimulates proton pumps → H⁺ into cell wall → wall acidified → expansins loosen cellulose → water in by osmosis → cell elongates
Gibberellin (15.2.3)	Embryo releases gibberellin → aleurone layer → DELLA proteins broken down → amylase gene transcribed → amylase hydrolyses starch in endosperm → maltose for the embryo

Worked reminders

Reading an action potential trace. Mark the resting level (about −70 mV), the threshold, the peak and the dip below resting. Name the ion and the direction for each section: rising = Na⁺ in; falling = K⁺ out; dip = K⁺ channels slow to close. Quote values with units and signs.

A drug that blocks presynaptic Ca²⁺ channels. Ca²⁺ cannot enter the knob, so vesicles do not fuse with the presynaptic membrane and no ACh is released. The postsynaptic membrane is not depolarised, so no action potential starts in the next neurone or muscle fibre. Follow the chain one link at a time.

A muscle fibre with no ATP. Myosin heads stay bound to actin, because ATP is needed to detach them, and Ca²⁺ cannot be pumped back into the sarcoplasmic reticulum. The muscle stays rigid instead of relaxing.

Why myelinated axons conduct faster. Ions cross the membrane only at the nodes of Ranvier, so depolarisation happens only there. Local circuits stretch from node to node and the action potential jumps between them, instead of passing along every part of the membrane.

Stronger stimulus on a receptor. The action potentials stay the same size (all-or-nothing); their frequency rises, up to the limit set by the refractory period.

Must-know distinctions

• Voltage-gated (open with a change in potential: Na⁺ and K⁺ on the axon, Ca²⁺ at the knob) vs ligand-gated (open when ACh binds: postsynaptic Na⁺ channels).
• Depolarisation (inside less negative) vs repolarisation (back towards negative) vs hyperpolarisation (more negative than resting).
• Receptor potential (graded) vs action potential (all-or-nothing).
• T-tubules (carry depolarisation) vs sarcoplasmic reticulum (stores and releases Ca²⁺).
• Troponin (binds Ca²⁺) vs tropomyosin (blocks binding sites).
• Auxin (elongation by acid wall loosening) vs gibberellin (germination by releasing gene transcription).

Quick self-test

1. State two features of the endocrine system.
2. Where is the cell body of a sensory neurone?
3. Which ion enters a taste-bud chemoreceptor cell when it detects salt?
4. The membrane potential rises from −70 mV to +35 mV. Calculate the change.
5. Which channels open during repolarisation?
6. A neurone’s refractory period is 4 ms. Calculate the maximum impulse frequency.
7. Explain why impulses cannot travel backwards along an axon.
8. State the role of calcium ions in the presynaptic knob.
9. A sarcomere measures 33 mm on a micrograph at ×15 000. Calculate its actual length in µm.
10. A sarcomere shortens from 2.5 µm to 2.0 µm; the A band is 1.6 µm. Find the total length of I band in the sarcomere before and after.
11. Which protein does Ca²⁺ bind to in a muscle fibre?
12. How does auxin make cell walls more extensible?

Answers

1. Any two: ductless glands; hormones carried in the blood; act on target cells with receptors; slower, longer-lasting effects.
2. In a ganglion outside the CNS (part-way along the neurone).
3. Sodium ions (Na⁺).
4. 35 − (−70) = 105 mV.
5. Voltage-gated K⁺ channels.
6. 1 ÷ 0.004 = 250 impulses per second (250 Hz).
7. The membrane behind the action potential is in its refractory period, so it cannot be depolarised again straight away.
8. Ca²⁺ enters through voltage-gated channels and causes vesicles to fuse with the presynaptic membrane, releasing ACh by exocytosis.
9. 33 000 µm ÷ 15 000 = 2.2 µm.
10. Before: 2.5 − 1.6 = 0.9 µm; after: 2.0 − 1.6 = 0.4 µm (the A band does not change).
11. Troponin.
12. It stimulates proton pumps, so H⁺ is pumped into the wall; the low pH loosens links between cellulose microfibrils.

Where marks are usually lost

• Saying the inside becomes “negative” during repolarisation or hyperpolarisation, instead of “more negative” or “negative again”.
• Mixing up which channels are voltage-gated and which are ligand-gated.
• Leaving out Ca²⁺ entry and exocytosis at the synapse.
• Writing “membrane” without saying presynaptic or postsynaptic.
• Saying the A band shortens, or that the filaments shorten.
• Saying ATP is needed for myosin to attach; it is needed to detach and re-cock the head.
• Confusing troponin and tropomyosin.
• Describing auxin as causing cell division rather than elongation by acidifying the cell wall.
• Forgetting to convert ms to s before calculating frequency.

Official syllabus

Cambridge International AS & A Level Biology 9700 syllabus for examination in 2025, 2026 and 2027 (Version 1), published by Cambridge University Press & Assessment (Cambridge International Education). Topic 15 Control and coordination: sections 15.1 Control and coordination in mammals and 15.2 Control and coordination in plants.