You are viewing a free preview of this lesson.
Subscribe to unlock all 8 lessons in this course and every other course on LearningBro.
This lesson is mapped to AQA 7402 Section 3.6.2 — Nervous coordination / neurones (refer to the official AQA specification document for exact wording). The nervous system is the body's high-speed signalling network: it detects changes in the internal and external environment, integrates that information in the central nervous system, and triggers rapid, coordinated responses by skeletal muscle and glands. Unlike the endocrine system — which uses bloodborne chemical messengers that act over seconds to days — the nervous system operates in milliseconds, using specialised electrically-excitable cells called neurones. A withdrawal of the hand from a hot pan is complete in around 200 ms; a sprinter's reaction to a starter's pistol takes a similar interval. None of this would be possible without the structural specialisations covered in this lesson.
The architecture of the neurone — long, thin, electrically insulated, electrochemically polarised — represents one of the most striking adaptations in animal biology. The squid giant axon work associated with Hodgkin and Huxley in the mid-twentieth century (paraphrased here as their reconstruction of the action potential from voltage-clamp ionic-current measurements) supplied the experimental basis for everything that follows in the next three lessons. Sir Charles Sherrington's framework of the nervous system as an integrative network of excitatory and inhibitory inputs — rather than a simple wire-by-wire telegraph — remains the conceptual scaffold AQA examiners expect at A* level.
Key Definition: A neurone is a specialised cell adapted for the rapid transmission of electrical impulses (action potentials) from one part of the body to another.
The mammalian nervous system is divided into two main parts:
The PNS is further subdivided:
graph TD
A["Nervous system"] --> B["CNS<br/>brain + spinal cord"]
A --> C["PNS<br/>cranial + spinal nerves"]
C --> D["Somatic<br/>voluntary skeletal muscle"]
C --> E["Autonomic<br/>involuntary visceral"]
E --> F["Sympathetic<br/>fight or flight"]
E --> G["Parasympathetic<br/>rest and digest"]
style B fill:#27ae60,color:#fff
style C fill:#3498db,color:#fff
style F fill:#e74c3c,color:#fff
style G fill:#16a085,color:#fff
This top-down view is the scaffold you should sketch at the start of any nervous-system question. The somatic / autonomic and sympathetic / parasympathetic distinctions are returned to in detail in lesson 5 of this course.
There are three main types of neurone, each with a distinct role and structure:
| Feature | Sensory Neurone | Relay Neurone | Motor Neurone |
|---|---|---|---|
| Direction of impulse | Receptor → CNS | Within CNS | CNS → Effector |
| Cell body position | Off to one side (dorsal root ganglion) | Within CNS | Within CNS (ventral horn) |
| Axon length | Long dendron, short axon | Short axon | Long axon |
| Myelinated? | Usually yes | Usually no | Usually yes |
| Typical conduction speed | 30–120 m s⁻¹ (myelinated) | Local, ~0.5 m s⁻¹ | 30–120 m s⁻¹ (myelinated) |
A motor neurone has the following key structures:
graph LR
A["Dendrites<br/>receive EPSPs / IPSPs"] --> B["Cell body<br/>nucleus, ER, ribosomes"]
B --> C["Axon hillock<br/>trigger zone"]
C --> D["Myelinated axon<br/>saltatory conduction"]
D --> E["Axon terminal<br/>synaptic vesicles, Ca²⁺ channels"]
E --> F["Neuromuscular junction<br/>skeletal muscle"]
style C fill:#e67e22,color:#fff
style D fill:#3498db,color:#fff
style E fill:#27ae60,color:#fff
Many neurones in the PNS are myelinated — they are surrounded by a fatty, insulating layer called the myelin sheath.
Exam Tip: Be precise with terminology. The myelin sheath is formed by Schwann cells (PNS) or oligodendrocytes (CNS). The gaps between Schwann cells are nodes of Ranvier. The impulse "jumps" between nodes — this is saltatory conduction. A common A* discriminator is naming the saltatory mechanism as local current flow between adjacent nodes rather than literal physical jumping — the depolarisation at one node spreads passively through the axoplasm to the next.
Several factors influence how quickly an action potential travels along a neurone:
| Factor | Effect on Speed | Explanation |
|---|---|---|
| Myelination | Increases speed | Saltatory conduction means the impulse jumps between nodes of Ranvier; axoplasmic current flows over longer distances per regeneration event |
| Axon diameter | Larger diameter = faster | Less resistance to ion flow in the axoplasm (analogous to a thicker wire). Squid giant axons (~1 mm diameter) achieve ~25 m s⁻¹ unmyelinated; this is why squid evolved giant axons to drive escape jets |
| Temperature | Higher temperature = faster (up to ~40 °C in mammals) | Increased kinetic energy of ions and faster opening kinetics of voltage-gated channels; above ~45 °C, channel proteins denature and conduction fails |
The squid giant axon strategy and the vertebrate myelination strategy are alternative evolutionary solutions to the same problem: how to conduct quickly without making every axon a millimetre thick. Myelination is the more space-efficient solution and enabled the dense vertebrate CNS.
A reflex arc is the simplest nerve pathway, enabling a rapid, involuntary response to a stimulus. The pathway is:
Stimulus → Receptor → Sensory neurone → Relay neurone (in CNS) → Motor neurone → Effector → Response
A fuller treatment of reflex arcs — including the crossed extensor reflex that maintains balance — is covered in lesson 5 of this course.
Multiple sclerosis (MS) is an autoimmune disease in which the immune system attacks and destroys the myelin sheath surrounding neurones in the CNS. Loss of myelin disrupts saltatory conduction, slowing or blocking nerve impulse transmission. Symptoms include muscle weakness, loss of coordination, numbness, visual disturbances (optic neuritis), and cognitive fatigue. MS provides a "natural experiment" demonstrating that myelin is required for normal CNS function — an A* response can deploy this clinical detail to evaluate the importance of saltatory conduction.
Guillain-Barré syndrome is a PNS counterpart, where the immune system attacks Schwann-cell myelin, producing flaccid paralysis that ascends from the limbs. Recovery occurs over weeks as Schwann cells re-myelinate the spared axons.
This content sits in AQA 7402 Section 3.6.2 — nervous coordination (refer to the official AQA specification document for exact wording). It is examined on Paper 2 (3.5–3.8 content) and synoptically on Paper 3. Always handle the nervous system at three levels: cellular (neurone structure, ion channels), circuit (reflex arc, integration at synapses), system (CNS / PNS organisation; somatic vs autonomic).
This lesson connects to:
Neurone-structure questions split AO marks predictably:
| AO | Typical share | Earned by |
|---|---|---|
| AO1 (knowledge) | 50–60% | Naming neurone types, identifying labelled diagram structures, defining saltatory conduction |
| AO2 (application) | 30–40% | Linking structural features (myelination, diameter, dendrite branching) to function (speed, integration) |
| AO3 (analysis / evaluation) | 10–20% | Evaluating evolutionary trade-offs; using clinical evidence (MS, Guillain-Barré) to test the role of myelin |
Reward language includes "saltatory conduction depends on the high density of voltage-gated Na⁺ channels at the node of Ranvier", "myelin reduces capacitance of the internodal membrane", "the cell body is in the dorsal root ganglion off the main path of the impulse". Mark-loss patterns include calling the myelin sheath a "fat" or "covering" without specifying lipid composition / Schwann-cell origin, conflating Schwann cells with oligodendrocytes (location matters), and treating reflex arcs as if they never involve the brain (the brain is informed in parallel even when it does not initiate the response).
Question (6 marks): Describe how the structure of a myelinated motor neurone is adapted for the rapid transmission of nerve impulses.
Mark scheme decomposition:
| Mark | AO | Awarded for |
|---|---|---|
| 1 | AO1 | Long axon allows impulses to be transmitted over long distances without relay synapses |
| 2 | AO1 | Myelin sheath formed by Schwann cells, acts as electrical insulator |
| 3 | AO1 | Nodes of Ranvier expose the axon membrane at regular intervals |
| 4 | AO2 | Saltatory conduction — action potential "jumps" between nodes |
| 5 | AO2 | High density of voltage-gated Na⁺ channels at nodes / large axon diameter reduces internal resistance |
| 6 | AO3 | Synthesis: cumulative effect is conduction speeds up to ~120 m s⁻¹; metabolic cost is reduced because only nodal regions repolarise |
Split: AO1 = 3, AO2 = 2, AO3 = 1.
A motor neurone has a long axon that carries impulses from the spinal cord to the effector. The axon is surrounded by a myelin sheath made of Schwann cells which act as insulation. Between the Schwann cells are gaps called nodes of Ranvier. At the nodes, sodium ions can move across the membrane, so the action potential jumps from node to node. This is called saltatory conduction and makes the impulse faster. The axon also has a large diameter which makes it faster too because there is less resistance. Without myelin, the impulse would have to depolarise the whole length of the membrane, which would take longer. So myelinated neurones are adapted to send impulses quickly.
Examiner commentary: M1 long axon, M1 myelin / Schwann, M1 nodes of Ranvier, M1 saltatory conduction. Around 4/6. The candidate omits the mechanism of why myelin speeds conduction (it reduces depolarisation events / metabolic cost) and never reaches the AO3 synthesis. A typical mid-band response that names structures but stops short of explaining cause.
The motor neurone exemplifies the principle that structure dictates conduction velocity. Its long axon — up to a metre in human lower-limb motor neurones — allows direct transmission from the ventral horn of the spinal cord to the target muscle fibre, avoiding intermediate synapses that would impose ~0.5–1 ms delays each. The axon is wrapped by concentric layers of Schwann-cell plasma membrane, the myelin sheath, which functions as a lipid-bilayer electrical insulator: ion exchange across the internodal membrane is essentially abolished, and membrane capacitance is reduced, so local currents flow further before dissipating.
At regular ~1 mm intervals, nodes of Ranvier expose the axon membrane to extracellular fluid. These nodes carry an exceptionally high density of voltage-gated Na⁺ channels (~1,200 µm⁻²), so depolarising current arriving from the previous node rapidly triggers a new action potential. The impulse therefore appears to "jump" from node to node — saltatory conduction — at up to 120 m s⁻¹ in large mammalian axons, around fifty times faster than in unmyelinated axons of comparable diameter.
A large axon diameter complements this strategy by reducing axoplasmic resistance to current flow. The cumulative effect is twofold: rapid transmission essential for reflex protection and coordinated movement, and reduced metabolic cost because only nodal regions, not the entire internode, must restore ion gradients after each impulse. The evolutionary alternative — invertebrate giant axons up to 1 mm wide — achieves comparable speed but at vastly greater anatomical cost.
Examiner commentary: Full 6/6. M1 long axon with delay analysis, M1 myelin and capacitance, M1 nodes and channel density, M1 saltatory conduction quantified, M1 axon diameter, M1 (AO3) evolutionary synthesis comparing myelination with invertebrate giant axons. The quantitative anchors (1 mm internodes, 1,200 µm⁻² channel density, 120 m s⁻¹) and the explicit "structure dictates velocity" framing are the moves that secure the top band.
Pedagogical observations — not fabricated statistics:
Subtle errors that distinguish A from A*:
Question: Compare the structure and function of sensory and motor neurones. Explain how each structure is adapted to its function in the reflex arc.
Indicative content (AO1 = 3, AO2 = 4, AO3 = 2):
| Element | AO |
|---|---|
| Sensory neurone: carries impulses from receptor to CNS (afferent) | AO1 |
| Motor neurone: carries impulses from CNS to effector (efferent) | AO1 |
| Sensory: long dendron + short axon; cell body off to one side (dorsal root ganglion) | AO1 |
| Motor: many short dendrites + long axon; cell body within CNS (ventral horn) | AO1 |
| Both myelinated, both with dense voltage-gated Na⁺ channels at nodes of Ranvier | AO2 |
| Cell body of sensory neurone is off the impulse path — does not delay conduction | AO2 |
| Motor neurone receives convergent input on dendrites; integration at the cell body | AO2 |
| Adaptive value: sensory carries one signal long-distance from periphery; motor integrates many CNS inputs and delivers one signal long-distance to effector | AO3 |
| Synthesis: both architectures support fast long-range conduction (myelination) but the sensory cell-body location and the motor dendritic branching solve different problems | AO3 |
A sensory neurone carries impulses from a receptor to the CNS. It has a long dendron that goes from the receptor toward the cell body, and a short axon that goes from the cell body into the CNS. The cell body is off to one side, in the dorsal root ganglion.
A motor neurone carries impulses from the CNS to an effector like a muscle. It has many short dendrites and one long axon that goes from the CNS to the muscle. The cell body is in the CNS.
Both types of neurone have a myelin sheath made of Schwann cells, with nodes of Ranvier between the Schwann cells. The myelin sheath insulates the axon and the nodes have voltage-gated sodium channels, so the impulse can jump from node to node (saltatory conduction). This makes the impulse travel faster.
The differences in structure suit the function: the sensory neurone only needs to carry one signal from the receptor, so a simple long dendron is enough. The motor neurone receives signals from many other neurones, so it has many dendrites to collect those inputs.
Examiner commentary: M1 sensory function, M1 motor function, M1 sensory structure, M1 motor structure, M1 myelin / nodes, M1 saltatory conduction, M1 architectural difference linked to function. Around 7/9.
Sensory and motor neurones share a common cellular architecture — a cell body with a nucleus and rough ER, a myelinated axon with nodes of Ranvier, and an excitable membrane bearing voltage-gated Na⁺ and K⁺ channels — but they differ in their dendritic, axonal, and cell-body geometries in ways that exactly match their roles in the reflex arc.
Sensory (afferent) neurones carry impulses unidirectionally from a peripheral receptor to the dorsal horn of the spinal cord. The structural signature is a long dendron running from the receptor toward the cell body and a short axon running from the cell body into the CNS. The cell body sits in the dorsal root ganglion, off the main impulse path — the impulse propagates through a T-junction at the cell body. This unusual geometry minimises conduction delay (the impulse does not need to pass through the cell body) and explains why sensory neurones have one of the fastest conduction velocities in the body (Ia afferents reach ~80 m s⁻¹).
Motor (efferent) neurones carry impulses from the ventral horn of the spinal cord to a peripheral effector (skeletal muscle for somatic motor neurones). The structural signature is many short branching dendrites receiving convergent synaptic inputs from thousands of presynaptic cells, and a long axon terminating at the neuromuscular junction. The dendritic tree is the receiver; the cell body integrates inputs at the axon hillock (the trigger zone); the axon delivers the integrated decision to the effector. Up to a metre of myelinated axon in the lower limb is required to reach the target muscle fibre.
Both architectures share myelination and saltatory conduction because both must conduct rapidly over long distances, but the receiver end differs profoundly: sensory neurones have one peripheral terminal (one receptor); motor neurones have an enormous receptive surface (thousands of synapses on the dendritic tree). The architectural differences reflect a single design principle — structure matches function — and the reflex arc threads them together: one fast input line, one fast output line, joined by an integrator (the relay neurone or direct synapse) in the CNS.
Examiner commentary: Full 9/9. The candidate names the dorsal root ganglion T-junction, partitions the dendritic vs axonal asymmetry, quantifies conduction velocity, and synthesises the "structure matches function" principle.
This lesson underpins Required Practical 10 (factor affecting reflex / response — covered in detail in lesson 7 of this course). Reaction-time measurements rest on the conduction delays introduced by every neurone, synapse, and effector in the reflex chain. Quantitatively, a 200 ms reaction time partitions into ~30 ms sensory-receptor delay, ~50 ms CNS processing, ~50 ms motor conduction, and ~70 ms muscle latency — a useful sanity check for student data.
AQA alignment: This lesson is aligned with the AQA GCE A-Level Biology (7402) specification, Section 3.6.2 — Nervous coordination / neurone structure. For the most accurate and up-to-date information, refer to the official AQA specification document.