Control and coordination
🎯What you need to be able to do
- Describe the features of the endocrine system with reference to ADH, glucagon and insulin, and compare the nervous and endocrine systems.
- Describe the structure and function of sensory and motor neurones, and outline the role of receptor cells.
- Describe how an action potential arises in a sensory neurone, using a chemoreceptor in a taste bud.
- Explain how the resting potential is maintained, what happens during an action potential, and how the resting potential is restored during the refractory period.
- Explain saltatory conduction and the importance of the refractory period in determining impulse frequency.
- Describe the structure and function of a cholinergic synapse, including the role of calcium ions.
- Describe the roles of neuromuscular junctions, the T-tubule system and the sarcoplasmic reticulum, and the ultrastructure of striated muscle.
- Explain the sliding filament model, including troponin, tropomyosin, calcium ions and ATP.
- Describe control and coordination in plants: the Venus fly trap, auxin and gibberellin.
📚The biology
Two coordination systems
The endocrine system consists of glands that secrete hormones directly into the blood, which carries them everywhere; only cells with a complementary receptor respond. ADH, glucagon and insulin (Topic 14) are the syllabus’s examples.
- Nervous — electrical impulses along neurones; very fast; travels to a specific target; effect is short-lived; effectors are muscles or glands.
- Endocrine — chemical messengers in the blood; slower; potentially widespread; effect is longer-lasting; effectors are target cells with receptors.
Neurones
A sensory neurone carries impulses from a receptor to the central nervous system; its cell body lies to one side of the axon, on a branch. A motor neurone carries impulses from the CNS to an effector; its cell body is at one end with many dendrites. Intermediate neurones connect the two. Many axons are wrapped in a myelin sheath of Schwann cells, with gaps called nodes of Ranvier.
Receptor cells detect a stimulus and convert its energy into an electrical response — they are transducers. In a chemoreceptor of a taste bud: a chemical binds to a receptor protein in the membrane, which opens channels so that sodium ions enter; the cell depolarises, producing a receptor potential; if this reaches threshold, calcium channels open, calcium enters, and neurotransmitter is released onto the sensory neurone, which then generates an action potential.
Resting potential
The inside of the axon is about −70 mV relative to the outside. It is maintained by:
- Sodium–potassium pumps, which use ATP to move 3 Na+ out for every 2 K+ in, so more positive charge leaves than enters;
- the membrane being much more permeable to K+ than to Na+, so potassium leaks back out down its gradient, taking positive charge with it;
- negatively charged proteins inside the axon that cannot leave.
Action potential
- Depolarisation. A stimulus opens some voltage-gated sodium channels. Na+ enters, making the inside less negative. If the potential reaches the threshold of about −55 mV, many more sodium channels open — a positive feedback — and the potential rises rapidly to about +40 mV.
- Repolarisation. Sodium channels close; voltage-gated potassium channels open, so K+ leaves and the inside becomes negative again.
- Hyperpolarisation. Potassium channels are slow to close, so a little too much K+ leaves and the potential briefly falls below −70 mV.
- Recovery. The sodium–potassium pump restores the original ion distribution and the resting potential.
Action potentials are all-or-nothing: below threshold nothing happens; at or above it, the size of the action potential is always the same. A stronger stimulus is therefore coded not by a bigger impulse but by a higher frequency of impulses, and by more neurones firing.
The refractory period
Immediately after an action potential the sodium channels are inactivated and cannot reopen, so no further action potential can be generated for a short time. Two consequences:
- it sets an upper limit on impulse frequency, and so on the maximum stimulus intensity that can be coded;
- it ensures impulses travel in one direction only, because the region just behind cannot be re-excited, and it keeps them discrete rather than merging.
Saltatory conduction
In a myelinated axon the myelin sheath is an electrical insulator, so ions cannot cross the membrane except at the nodes of Ranvier. The local currents therefore flow from node to node and the action potential jumps between them — saltatory conduction. Since the membrane is depolarised only at the nodes rather than along its whole length, transmission is much faster (and uses less ATP, since fewer ions must be pumped back).
The cholinergic synapse
- An action potential arrives at the presynaptic knob.
- Voltage-gated calcium channels open and Ca2+ enters.
- Calcium causes vesicles of acetylcholine to fuse with the presynaptic membrane and release the transmitter into the synaptic cleft by exocytosis.
- Acetylcholine diffuses across and binds to receptors on the postsynaptic membrane.
- Sodium channels open, Na+ enters, and if threshold is reached a new action potential is generated.
- Acetylcholinesterase in the cleft hydrolyses acetylcholine, and the products are reabsorbed and resynthesised using ATP. Without this the postsynaptic neurone would fire continuously.
Synapses ensure one-way transmission — vesicles are only on the presynaptic side and receptors only on the postsynaptic side.
Muscle: structure
A muscle fibre contains many myofibrils, divided along their length into sarcomeres between Z discs. Each sarcomere contains thin actin filaments anchored to the Z discs and thick myosin filaments in the middle.
- I band — actin only, appears light.
- A band — the full length of the myosin, including where actin overlaps it; appears dark.
- H zone — the middle of the A band, myosin only, no overlap.
The fibre membrane (sarcolemma) folds inwards as T-tubules that carry the action potential deep into the fibre, and the sarcoplasmic reticulum that surrounds each myofibril stores calcium ions.
Muscle: the sliding filament model
- An action potential arrives at the neuromuscular junction, acetylcholine is released, and an action potential spreads over the sarcolemma and down the T-tubules.
- The sarcoplasmic reticulum releases Ca2+ into the sarcoplasm.
- Ca2+ binds to troponin, changing its shape so that it moves tropomyosin away from the myosin-binding sites on the actin.
- Myosin heads bind to actin, forming cross-bridges.
- The heads tilt (the power stroke), pulling the actin past the myosin towards the centre of the sarcomere; ADP and phosphate are released.
- ATP binds to the myosin head, causing it to detach from actin.
- ATP is hydrolysed, and the energy released returns the head to its upright position, ready to bind further along. The cycle repeats while calcium is present.
- When stimulation stops, Ca2+ is actively pumped back into the sarcoplasmic reticulum, tropomyosin covers the binding sites again, and the muscle relaxes.
ATP is needed twice over: for detachment of the head, and for repumping calcium. This is why rigor mortis occurs — no ATP means the heads cannot detach.
Control and coordination in plants
The Venus fly trap. Sensory hairs on the lobes of the modified leaves are bent by an insect. Bending generates a receptor potential; if a hair is touched twice, or two hairs are touched, within a short interval, an action potential is triggered and spreads across the lobes. This causes a rapid loss of turgor in cells on the inner surface and a gain on the outer, together with acid-induced wall loosening and rapid cell expansion, so the lobes snap shut. Requiring two stimuli prevents the trap closing on a raindrop.
Auxin. Auxin promotes elongation growth by stimulating proton pumping into the cell wall. The resulting low pH activates enzymes that loosen the bonds between cellulose microfibrils, so the wall becomes more plastic and the cell expands as water enters by osmosis.
Gibberellin in barley. On germination, the embryo produces gibberellin, which diffuses to the aleurone layer and switches on genes for amylase. Amylase is secreted into the endosperm and hydrolyses the stored starch to maltose, which is absorbed by the embryo and used for respiration and growth. The gene control mechanism — gibberellin causes the breakdown of DELLA protein repressors, releasing transcription factors — belongs to Topic 16.
✏️Worked example
(a) The sarcomere consists of the A band in the middle with half an I band at each end — each I band is shared between two adjacent sarcomeres, so within one sarcomere you see two half-I-bands. So
Hence a complete I band is 1.2 µm (and each half within this sarcomere is 0.6 µm).
(b) The sarcomere shortens by \( 2.8 - 2.2 = 0.6\ \mu\text{m} \).
- A band: unchanged at 1.6 µm. The A band is defined by the length of the myosin filaments, and myosin does not change length.
- H zone: 0.4 − 0.6, which cannot be negative — the actin filaments have met in the middle and the H zone has closed completely, so it is 0 µm (in practice the overlap begins and the zone disappears).
- I band: 1.2 − 0.6 = 0.6 µm. The whole of the shortening comes out of the I band, since that is the only region of actin not already overlapping myosin.
(c) During contraction the myosin heads bind to actin forming cross-bridges, and the power stroke pulls the actin filaments past the myosin towards the centre of the sarcomere. Neither filament shortens; they slide. The Z discs are therefore drawn closer together and the sarcomere shortens.
Since the A band is the full length of the myosin, and myosin has not changed, the A band is unchanged. The I band is the region containing actin only, and as actin slides further in, more of it overlaps myosin, so the I band shortens. The H zone is the region of myosin with no actin overlapping it, and as actin advances from both ends it too shortens, closing entirely when the actin filaments meet.
📝Practise
Work through these, then reveal the answer. Each question targets a different objective from the list above.
1. Explain how the resting potential of −70 mV is established and maintained.
2. Explain why an action potential is described as all-or-nothing, and how the intensity of a stimulus is coded.
3. Describe transmission across a cholinergic synapse and explain the role of calcium ions and of acetylcholinesterase.
4. Explain how myelination increases the speed of conduction.
5. Describe the roles of ATP in muscle contraction and explain why rigor mortis occurs.
6. Compare the nervous and endocrine systems in terms of the nature of the signal, speed, distribution and duration of effect.
🔗Go deeper — other people’s work
These are external resources, not mine. If one stops working, tell me and everything above it on this page still stands.
- Any interactive action potential simulator — blocking the sodium or potassium channels and watching the trace change makes the two phases separate cleanly in your mind
- Electron micrographs of relaxed and contracted sarcomeres side by side — the constant A band is convincing only when you have seen it
- Slow-motion footage of a Venus fly trap closing, with commentary on the two-touch requirement — a memorable anchor for plant action potentials