3.6.2 Nervous coordination

Neurones carry electrical impulses along axons polarised at a resting potential of −70 mV. A stimulus that reaches threshold triggers an all-or-nothing action potential that propagates as a wave of ion movement. Between neurones the signal crosses chemical synapses. The heart runs on its own pacemaker, modulated by the medulla.

The resting potential is maintained at −70 mV by the sodium-potassium pump.

Neurones are specialised cells built to carry electrical impulses. The body of the neurone houses the nucleus and the metabolic machinery; dendrites carry impulses toward the body; the axon carries impulses away. Many axons are wrapped in a myelin sheath formed by Schwann cells, with periodic gaps at the nodes of Ranvier.

1. The **sodium-potassium pump** uses **ATP** in **active transport** to move **three sodium ions out** of the axon for every **two potassium ions in**. The asymmetric stoichiometry sends more positive charge out than is returned, contributing directly to the charge imbalance.
2. **Potassium ion** channels are predominantly open at rest, so potassium ions leak out by facilitated diffusion down their concentration gradient, carrying positive charge with them.
3. **Sodium ion** channels are predominantly closed at rest, preventing sodium ions from leaking back in. The net result is a stable polarised state: the inside of the axon sits at approximately **−70 mV** relative to the outside.

Write the full term: sodium ions, potassium ions. Dropping ions caps the answer at 1 of 3. If you cite pump stoichiometry, it must be three out, two in; wrong numbers lose the mark even when the rest of the answer is correct.

The action potential is depolarisation, repolarisation, and brief hyperpolarisation, all-or-nothing.

An action potential is initiated when a stimulus depolarises the membrane to about −55 mV, the threshold value. From threshold, voltage-gated sodium ion channels open, and a self-reinforcing wave of depolarisation drives the interior potential to about +40 mV.

1. **Depolarisation.** Voltage-gated **sodium ion channels** open at **threshold** (about −55 mV). **Sodium ions** diffuse into the axon down the concentration gradient, and the interior potential rises sharply to about **+40 mV**.
2. **Repolarisation.** Sodium ion channels close; voltage-gated **potassium ion channels** open. **Potassium ions** diffuse out of the axon down the concentration gradient, removing positive charge, and the interior potential falls back toward −70 mV.
3. **Hyperpolarisation.** Potassium ion channels close slightly late. Continued outflow of potassium ions briefly drops the interior potential below −70 mV; the membrane is now **more negative than the resting potential**.
4. The **sodium-potassium pump** and the leakage channels re-establish the **−70 mV resting potential**, and the membrane is ready to fire again once the refractory period ends.

Hyperpolarisation is continued potassium ion outflow. Write more negative than the resting potential. Don't write sodium ions leave during hyperpolarisation; sodium ions do not exit the axon at this stage.

Write impulse or action potential. Signal and message are both rejected; either disqualifies the first credited mark.

Action potentials propagate by local current; myelinated axons use saltatory conduction for speed.

In an unmyelinated axon, the action potential propagates by local current. Sodium ions that have entered at the depolarised region diffuse laterally inside the membrane and depolarise the adjacent region, opening its voltage-gated sodium ion channels. The wave moves forward continuously. Continuous propagation is relatively slow, around 0.5 to 10 m/s.

Write electrical insulation for myelin. Thermal insulation is rejected; the myelin's role is to prevent ion movement across the internodal membrane, not to retain heat.

Reaction time exceeds the time predicted from pure nerve conduction speed because of additional components: synaptic transmission delay at each synapse, sensory transduction time at the receptor, and muscle contraction time. Citing factors that affect conduction speed itself, such as temperature or axon diameter, scores zero on reaction-time questions; reaction time and conduction speed are distinct.

The cholinergic synapse transmits the signal as Ca²⁺-triggered acetylcholine release.

A synapse is the junction between two neurones, or between a neurone and an effector. At a chemical synapse, the signal crosses the gap (the synaptic cleft) in chemical form, via a neurotransmitter. The cholinergic synapse uses acetylcholine and is the AQA standard model.

1. An **action potential** arrives at the **presynaptic membrane** of the **synaptic knob** and depolarises it. **Voltage-gated calcium ion channel proteins** in the synaptic knob membrane open.
2. **Calcium ions diffuse into the synaptic knob** down the electrochemical gradient. The rise in intracellular calcium causes synaptic vesicles loaded with **acetylcholine** to **fuse with** the presynaptic membrane, releasing acetylcholine into the cleft by exocytosis.
3. **Acetylcholine diffuses across the synaptic cleft** by simple diffusion down its concentration gradient. The cleft is narrow (about 20 nm) so the crossing is rapid, even though no active mechanism drives it.
4. **Acetylcholine binds to receptors on the postsynaptic membrane.** The receptors have **binding sites** complementary to acetylcholine. Binding causes **sodium ion channels** in the postsynaptic membrane to open.
5. **Sodium ions diffuse into the postsynaptic neurone** down the concentration gradient. If the resulting depolarisation reaches the threshold, a new action potential is generated and propagates onward.

On step 1, write synaptic knob for the location of calcium ion entry. Not the synapse, not presynaptic membrane alone, and not carrier proteins. Channel proteins is the correct phrase; carrier proteins is rejected.

On step 2, vesicles fuse with the presynaptic membrane. They do not release themselves, and they do not travel across the cleft. Acetylcholine is released by exocytosis through the fused opening.

On step 4, receptors have binding sites, not active sites. Active site is for enzymes only. Naming an active site on a postsynaptic receptor is rejected.

1. **Fewer calcium ions** diffuse into the synaptic knob; the calcium-channel signal that triggers vesicle fusion is reduced or absent.
2. **Fewer vesicles fuse** with the presynaptic membrane, so **less acetylcholine** is released into the synaptic cleft by exocytosis.
3. **Less acetylcholine** diffuses across the cleft, so a smaller quantity reaches the postsynaptic membrane in any given window of time.
4. **Less acetylcholine binds** to receptors on the postsynaptic membrane, so fewer sodium ion channels open in response.
5. **Fewer sodium ions diffuse** into the postsynaptic neurone, so the depolarisation does not reach threshold and **fewer action potentials** are generated.

On any inhibitor or blockade question, every step requires no, fewer, or less. Describing normal transmission positively under blockade conditions caps the answer at mark tariff minus one.

Synapses enforce unidirectionality, allow summation, and can be inhibitory via chloride ions.

Beyond simple signal transmission, chemical synapses perform several functions that arise from the structural and chemical asymmetry of the synapse. They enforce one-way signal flow, integrate multiple inputs through summation, and can be inhibitory as well as excitatory.

1. **Chloride ions diffuse into the postsynaptic neurone** through chloride ion channels opened by the inhibitory neurotransmitter binding to its receptors.
2. The inside of the postsynaptic neurone becomes **more negative**, producing **hyperpolarisation**. The membrane is now further from threshold than it was before.
3. **More sodium ions are required to reach threshold**, so depolarisation to action potentials becomes less likely. Potassium ions are not involved here. **Calcium ions are not the inhibitory ion**; calcium is an explicit reject in this context.

The neuromuscular junction is a specialised cholinergic synapse onto skeletal muscle.

The neuromuscular junction (NMJ) is the synapse between a motor neurone and a skeletal muscle fibre. The mechanism is the same cholinergic chain, with acetylcholine as the neurotransmitter. The postsynaptic cell is the muscle fibre; the postsynaptic membrane is the sarcolemma, the muscle cell membrane (muscle alone is too imprecise).

1. **Acetylcholinesterase is inhibited**, so **acetylcholine is not broken down** in the synaptic cleft after binding to its receptors.
2. **Acetylcholine accumulates in the synaptic cleft** as it continues to be released by the synaptic knob but is no longer being hydrolysed.
3. **More acetylcholine binds to the remaining functional receptors** on the postsynaptic membrane, so depolarisation reaches threshold and **action potentials are generated** in the muscle fibre once again.

Cardiac conduction is myogenic; the medulla modulates heart rate via the autonomic nervous system.

The heart is myogenic: it generates its own rhythmic electrical excitation independently of neural input. The SAN (sinoatrial node) in the wall of the right atrium is the pacemaker. Autonomic input from the medulla modulates the pacemaker's rate.

1. **Chemoreceptors** in the carotid arteries, the aorta, and the medulla detect **rising carbon dioxide** in the blood (and the associated falling pH). Chemoreceptors detect carbon dioxide, not oxygen.
2. Chemoreceptors send a **higher frequency of impulses** to the cardiac centre of the medulla, signalling that the blood needs to clear excess carbon dioxide more quickly.
3. The medulla increases **sympathetic output** via the **accelerator nerve** to the SAN; heart rate rises, blood flows through the lungs faster, and carbon dioxide is expelled. The baroreceptor pathway mirrors this: rising blood pressure increases **parasympathetic output** via the **vagus nerve**, lowering heart rate.

Key terms

• presynaptic
• depolarisation
• action potential
• threshold
• acetylcholine
• postsynaptic membrane
• synaptic knob
• hyperpolarisation
• neurotransmitter
• active transport
• electrical insulation
• receptor