Control and coordination

Every objective in this topic is printed under "A Level subject content" in the 9700 syllabus, so all of it is A Level and none of it is AS. It is examined on Paper 4. Paper 1 is the AS multiple-choice paper and does not reach this topic, so no multiple-choice practice on this site is tagged to it.

Note the spelling: the syllabus prints "coordination", with no hyphen.

Syllabus points

15.1 Control and coordination in mammals

• Describe the features of the endocrine system with reference to the hormones ADH, glucagon and insulin (see 14.1).
• Compare the features of the nervous system and the endocrine system.
• Describe the structure and function of a sensory neurone and a motor neurone and state that intermediate neurones connect sensory neurones and motor neurones.
• Outline the role of sensory receptor cells in detecting stimuli and stimulating the transmission of impulses in sensory neurones.
• Describe the sequence of events that results in an action potential in a sensory neurone, using a chemoreceptor cell in a human taste bud as an example.
• Describe and explain changes to the membrane potential of neurones, including: how the resting potential is maintained; the events that occur during an action potential; how the resting potential is restored during the refractory period.
• Describe and explain the rapid transmission of an impulse in a myelinated neurone with reference to saltatory conduction.
• Explain the importance of the refractory period in determining the frequency of impulses.
• Describe the structure of a cholinergic synapse and explain how it functions, including the role of calcium ions.
• Describe the roles of neuromuscular junctions, the T-tubule system and sarcoplasmic reticulum in stimulating contraction in striated muscle.
• Describe the ultrastructure of striated muscle with reference to sarcomere structure using electron micrographs and diagrams.
• Explain the sliding filament model of muscular contraction including the roles of troponin, tropomyosin, calcium ions and ATP.

15.2 Control and coordination in plants

• Describe the rapid response of the Venus fly trap to stimulation of hairs on the lobes of modified leaves and explain how the closure of the trap is achieved.
• Explain the role of auxin in elongation growth by stimulating proton pumping to acidify cell walls.
• Describe the role of gibberellin in the germination of barley (see 16.3).

Two coordination systems, compared

The endocrine system works by releasing hormones from endocrine glands directly into the blood. Hormones travel everywhere but affect only target cells, which are the cells carrying the right receptor. ADH, insulin and glucagon are the three the syllabus asks you to know, and they are covered in topic 14.

The examinable point is that speed and precision go together. A neurone delivers its signal down a defined path to a defined effector, so it is quick and specific. A hormone is broadcast, so it is slower and more diffuse, but it can reach every cell in the body at once, which is exactly what a signal like growth or metabolic rate needs.

Neurones

A sensory neurone carries impulses from a receptor to the central nervous system. Its cell body sits in a swelling part-way along, off to one side, with a long dendron carrying impulses towards the cell body and a shorter axon carrying them on.

A motor neurone carries impulses from the central nervous system to an effector. Its cell body is in the central nervous system, with many short dendrites and one long axon running out to the muscle or gland.

Intermediate neurones, also called relay neurones, connect sensory neurones to motor neurones and lie wholly within the central nervous system.

A myelin sheath, formed from Schwann cells wrapped many times around the axon, insulates most of the length. The gaps between Schwann cells are the nodes of Ranvier.

Sensory receptors

A receptor cell is a transducer: it converts one form of energy, the stimulus, into an electrical signal. Light, heat, pressure and chemicals all end up as the same currency.

Take a chemoreceptor cell in a taste bud. The sequence is:

1. A chemical in food binds to a receptor protein on the cell surface membrane of the receptor cell.
2. This opens sodium ion channels, so sodium ions diffuse in.
3. The inside of the cell becomes less negative. This depolarisation is the receptor potential, and, unlike an action potential, its size varies with the strength of the stimulus.
4. If the receptor potential is large enough, voltage-gated calcium ion channels open and calcium ions enter.
5. Calcium ions cause vesicles of neurotransmitter to fuse with the membrane and release their contents onto the sensory neurone.
6. If the resulting depolarisation of the sensory neurone reaches threshold, an action potential is generated and travels to the brain.

A stronger stimulus does not make a bigger action potential. It makes more action potentials per second, and it recruits more receptor cells. That is how intensity is encoded, and it is a favourite question.

The resting potential

At rest the inside of an axon is about -70 mV relative to the outside. Two things maintain it:

• Sodium-potassium pumps actively transport three sodium ions out for every two potassium ions in, using ATP. That alone makes the outside slightly more positive.
• The membrane is far more permeable to potassium than to sodium at rest, because many potassium channels are open and almost all sodium channels are closed. Potassium therefore leaks back out down its concentration gradient, leaving the inside negative.

So the resting potential is mostly a potassium equilibrium, held in place by a pump that keeps the gradients topped up. A question that asks why a metabolic poison abolishes the resting potential is asking about the ATP the pump needs.

The action potential

1. Depolarisation. A stimulus opens a few voltage-gated sodium channels. Sodium enters, the inside becomes less negative, and if the membrane reaches the threshold of about -55 mV, many more voltage-gated sodium channels open. This is positive feedback, and it is why the response is all-or-nothing: below threshold nothing happens; at threshold the full response follows.
2. Peak. The potential overshoots to about +40 mV. Sodium channels then close automatically, a process called inactivation.
3. Repolarisation. Voltage-gated potassium channels open, and potassium ions leave down their electrochemical gradient, restoring the negative inside.
4. Hyperpolarisation. The potassium channels are slow to close, so too much potassium leaves and the potential undershoots to about -80 mV.
5. Recovery. The channels close and the sodium-potassium pump restores the original ion distribution and the resting potential.

Worked example. A membrane goes from -70 mV to +40 mV at the peak.

change in potential = 40 - (-70) = 110 mV

and if that takes 1.0 ms, the mean rate of change is

110 / 1.0 = 110 mV ms⁻¹

The refractory period and impulse frequency

Immediately after an action potential the sodium channels are inactivated, so no new action potential can be produced. This is the refractory period, lasting a few milliseconds. It does three important things:

• It makes the impulse travel in one direction only, because the stretch of membrane just behind cannot fire again.
• It keeps action potentials discrete rather than merging into one another.
• It sets an upper limit on frequency. If the refractory period is 2 ms, the maximum frequency is 1000 / 2 = 500 impulses per second.

Since intensity is coded as frequency, the refractory period sets the ceiling on how intense a stimulus the nervous system can distinguish.

Saltatory conduction

In a myelinated neurone the myelin is an insulator, so ions cannot cross the membrane where it is wrapped. Depolarisation can therefore only occur at the nodes of Ranvier, and local circuits carry the current from one node to the next, so the action potential appears to jump from node to node. The Latin verb is saltare, to leap.

The gain is large. A myelinated human neurone conducts at up to about 120 m s⁻¹, against a few metres per second for an unmyelinated one of the same diameter. It also uses less ATP, because far less of the membrane has to be repolarised and pumped back.

Two other factors raise conduction speed: a greater axon diameter, which lowers resistance to the flow of ions along the axon, and a higher temperature, up to the point at which proteins denature.

The cholinergic synapse

A synapse is a junction between two neurones with a gap, the synaptic cleft, about 20 nm across. Cholinergic means the transmitter is acetylcholine.

1. An action potential arrives at the presynaptic membrane.
2. Voltage-gated calcium ion channels open and calcium ions diffuse into the presynaptic knob.
3. Calcium ions cause synaptic vesicles to move to and fuse with the presynaptic membrane, releasing acetylcholine into the cleft by exocytosis.
4. Acetylcholine diffuses across the cleft and binds to receptors on the postsynaptic membrane. Those receptors are also sodium ion channels, and binding opens them.
5. Sodium ions enter, depolarising the postsynaptic membrane. If threshold is reached, a new action potential is generated.
6. Acetylcholinesterase in the cleft hydrolyses acetylcholine to choline and ethanoate, which are taken back into the presynaptic knob and reassembled using ATP.

Why bother with a gap at all? Because the gap buys control:

• One-way transmission, since vesicles are only on one side and receptors only on the other.
• Summation. Several small depolarisations, either from several synapses at once (spatial summation) or from one synapse firing repeatedly (temporal summation), can add up to reach threshold when none alone would.
• Filtering out low-level noise, since a weak stimulus never reaches threshold.
• Divergence and convergence, allowing one neurone to signal many, or many to signal one.

Step 6 matters more than it looks. If acetylcholine were not destroyed it would keep binding, and the postsynaptic neurone would fire continuously. Some insecticides and nerve agents work by inhibiting acetylcholinesterase, which is why they cause uncontrolled muscle contraction.

From nerve to muscle

A neuromuscular junction works exactly like a cholinergic synapse, except the postsynaptic membrane belongs to a muscle fibre. Acetylcholine binds, the sarcolemma depolarises, and the action potential spreads.

• T-tubules are inward folds of the sarcolemma running deep into the fibre. They carry the action potential to the centre of the fibre, so all the myofibrils are stimulated at nearly the same instant rather than only those at the surface.
• The action potential in a T-tubule causes the sarcoplasmic reticulum, a specialised endoplasmic reticulum wrapped round each myofibril, to release stored calcium ions into the sarcoplasm.

Those calcium ions are the trigger for contraction.

Striated muscle ultrastructure

A muscle fibre is a multinucleate cell packed with myofibrils. Each myofibril is a chain of sarcomeres, and the sarcomere is the repeating unit responsible for the striped appearance.

• Z line to Z line is one sarcomere.
• The I band is light and contains thin filaments (actin) only.
• The A band is dark and spans the whole length of the thick filaments (myosin), including the region where thin filaments overlap them.
• The H zone is the middle of the A band, where there are thick filaments only.
• The M line runs down the centre of the H zone.

Thin filaments are actin, with tropomyosin wound round them and troponin attached at intervals. Thick filaments are myosin, each molecule with a tail and a globular head that can bind actin and can hydrolyse ATP.

The sliding filament model

The filaments do not shorten. They slide past one another, and the sarcomere shortens because the overlap increases.

1. At rest, tropomyosin covers the myosin binding sites on actin, so no cross-bridges can form.
2. Calcium ions released from the sarcoplasmic reticulum bind to troponin, which changes shape and pulls tropomyosin aside, exposing the binding sites.
3. Myosin heads bind to actin, forming cross-bridges.
4. The power stroke: each head tilts, pulling the thin filament towards the centre of the sarcomere. ADP and phosphate are released.
5. ATP binds to the myosin head, which causes it to detach from actin.
6. The head hydrolyses the ATP and uses the energy to return to its upright position, ready to bind again further along the actin.
7. While calcium ions remain, the cycle repeats many times a second, and the sarcomere shortens.

When stimulation stops, calcium ions are actively pumped back into the sarcoplasmic reticulum, tropomyosin covers the binding sites again, and the muscle relaxes.

What happens to each band tells you whether a student has understood the model:

The A band is fixed because it is the length of the thick filaments, and the thick filaments do not change length.

ATP is needed for the power stroke cycle, for pumping calcium back into the sarcoplasmic reticulum, and for the sodium-potassium pumps of the sarcolemma. Rigor mortis follows from the same mechanism: with no ATP, myosin heads cannot detach, and the muscle stays locked.

Control and coordination in plants

Plants have no nervous system, yet two of the responses here are fast enough to look like one.

The Venus fly trap

Each lobe of the modified leaf carries sensitive hairs. When an insect bends a hair, the hair cells are deformed and an action potential, a receptor potential leading to a wave of depolarisation, spreads across the lobe.

The trap requires two stimulations within about 30 seconds, either two hairs touched or one touched twice. That requirement is a filter against wasting a closure on a raindrop, and the plant is in effect remembering the first touch for half a minute.

Closure itself is a change in turgor and wall properties. The action potential causes cells in the midrib to lose or gain water rapidly, so the lobes flip from a convex to a concave shape and the trap snaps shut in a fraction of a second, with the marginal hairs interlocking to form a cage.

Auxin and elongation growth

Auxin, made in the shoot tip, causes cells just behind the tip to elongate. The mechanism is called acid growth:

1. Auxin binds to receptors and causes ATP-powered proton pumps in the cell surface membrane to move hydrogen ions out into the cell wall.
2. The wall becomes more acidic, at around pH 5.
3. That low pH activates expansins, enzymes that loosen the bonds between cellulose microfibrils.
4. The wall becomes more plastic, so the turgor pressure inside the cell stretches it, and water entering by osmosis lengthens the cell.

Because auxin accumulates on the shaded side of a shoot, the cells there elongate more and the shoot bends towards the light. That is phototropism explained at the level of a pump and a pH.

Gibberellin and germinating barley

In a barley grain, the embryo produces gibberellin on absorbing water. Gibberellin diffuses to the aleurone layer surrounding the starchy endosperm and switches on the genes for amylase. The amylase is secreted into the endosperm and hydrolyses starch to maltose, which is absorbed by the embryo and used for respiration and growth.

The gene-switching mechanism is set out in topic 16: gibberellin causes the breakdown of DELLA protein repressors, which otherwise block the transcription factors that promote transcription.

Common mistakes

• Saying a stronger stimulus produces a larger action potential. It produces a higher frequency of identical action potentials.
• Describing the resting potential as being caused only by the sodium-potassium pump, without the differential permeability to potassium.
• Saying potassium ions enter during repolarisation. They leave.
• Saying myelin makes the impulse travel faster by conducting it. Myelin is an insulator; the speed comes from depolarisation only occurring at the nodes.
• Forgetting that calcium ions, not sodium ions, trigger vesicle fusion at the presynaptic membrane.
• Leaving out acetylcholinesterase, so the synapse in the answer never resets.
• Confusing the roles of troponin and tropomyosin. Calcium binds troponin; tropomyosin is what moves aside.
• Saying the filaments contract or shorten. They slide.
• Claiming the A band shortens during contraction. It does not.
• Saying ATP provides the energy for the power stroke directly. ATP binding causes detachment, and its hydrolysis re-cocks the head.
• Treating the Venus fly trap as a nervous response involving neurones. It uses action potentials in plant cells and changes in turgor, with no nerves at all.
• Saying auxin makes cells divide faster in phototropism. It makes them elongate.