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Spec Mapping — OCR H420 Module 5.1.3 — Neuronal communication, content statements covering the role of myelin in the transmission of nerve impulses, including the comparison of conduction velocities in myelinated and non-myelinated neurones (refer to the official OCR H420 specification document for exact wording). The mechanism of saltatory conduction is the highest-value AO2 content in the entire module and is required for any A* answer on nervous transmission speed.
Speed matters. A gazelle escaping a cheetah cannot afford to wait 500 ms while nerve impulses meander from its retina to its leg muscles. Evolution has produced an elegant solution: myelinate the axon, insulating it so that action potentials regenerate at discrete nodes rather than propagating continuously. This lesson explores how myelination is achieved, how it accelerates conduction, and why it matters clinically.
The biophysical story has a clear scientific lineage. Louis-Antoine Ranvier (1878) described the gaps in myelin that now bear his name. Alan Hodgkin & Andrew Huxley (1952 Nobel-prize work, paraphrased) gave the ionic explanation of the action potential on the squid giant axon — an unmyelinated axon — and recognised that the same biophysics, applied to a myelinated geometry with active regeneration confined to nodes, would predict a dramatic speed-up. Ichiji Tasaki (1939) and Andrew Huxley & Robert Stämpfli (1949) demonstrated saltatory conduction directly using extracellular recording electrodes placed along a frog myelinated axon, showing that active regions corresponded to nodes and intermodal segments remained electrically silent (paraphrase). Modern computational neuroscience reconstructs the same picture in molecular detail, but the underlying explanation is the one you will learn here.
Key Definitions:
- Myelin sheath — a multilayered wrap of Schwann cell membrane that insulates an axon.
- Schwann cell — a glial cell of the peripheral nervous system that forms myelin.
- Nodes of Ranvier — short gaps (~1 μm) between adjacent Schwann cells where the axon membrane is exposed.
- Saltatory conduction — the "jumping" of action potentials from one node of Ranvier to the next, greatly increasing conduction velocity.
In the peripheral nervous system, a single Schwann cell wraps itself around a short segment of axon (~1 mm). It does this by extending a flap of plasma membrane, then rotating around the axon many times — up to 100 layers in the thickest axons. Because each Schwann cell lies alongside only one small stretch of axon, thousands are needed to myelinate a long motor neurone.
Between each pair of neighbouring Schwann cells is a small exposed region of axon membrane called a node of Ranvier, typically 1–2 μm long and spaced roughly every 1 mm. At the node, voltage-gated Na⁺ and K⁺ channels are densely packed; elsewhere along the axon, under the myelin, these channels are absent because the membrane is physically insulated.
Myelin is rich in lipid (about 80% lipid, 20% protein) and is therefore an excellent electrical insulator. Current flow across the axon membrane (i.e. ion movement) can only occur where the membrane is exposed — at the nodes of Ranvier. Under a myelinated segment, no ion movement takes place. This has two consequences:
The upshot is that the action potential effectively jumps from node to node, reaching the next node in a fraction of the time it would take to propagate continuously.
| Type of axon | Typical diameter | Typical speed | Example |
|---|---|---|---|
| Unmyelinated (small) | 1 μm | 0.5–2 m s⁻¹ | Many sympathetic post-ganglionic neurones |
| Unmyelinated (giant squid) | 500 μm | ~25 m s⁻¹ | Escape reflex of squid |
| Myelinated (mammalian) | 5–20 μm | 10–120 m s⁻¹ | Motor neurones, sensory neurones |
Two features determine conduction speed:
Myelination allows mammalian neurones to achieve extraordinary speed with a diameter of just 10–20 μm — a huge saving in space and metabolic cost compared with the giant axons needed in molluscs.
"Saltatory" comes from the Latin saltare, meaning "to leap". Action potentials do not literally teleport — they appear at each node in sequence, one after another, regenerated by voltage-gated Na⁺ channels. Between nodes, the electrical disturbance travels passively (local-circuit current) and very quickly, because it is a simple electrical event rather than a series of ion channels opening. The wave of depolarisation propagates continuously along the axon; what is discrete is the active regeneration. In the strict sense, only the regeneration "jumps" between nodes — charge flow itself is continuous along the cytoplasm.
flowchart LR
A["Node 1<br/>Action potential"] -->|Passive current flow under myelin| B["Node 2<br/>Depolarises to threshold"]
B -->|New action potential| C["Node 3<br/>Depolarises to threshold"]
C -->|...| D[Next node]
| Property | Myelinated mammalian axon | Unmyelinated axon |
|---|---|---|
| Geometry | Wrapped in spirally-coiled Schwann-cell membrane; ~100 layers; nodes of Ranvier every ~1 mm | Bare axolemma with continuously distributed Na⁺/K⁺ channels |
| Voltage-gated Na⁺ channel distribution | Concentrated at nodes (~2000 μm⁻²) | Spread along entire axon membrane (~100 μm⁻²) |
| Mechanism | Active regeneration at nodes + passive spread between → saltatory | Continuous AP propagation by sequential channel opening |
| Typical conduction speed | 10–120 m s⁻¹ | 0.5–25 m s⁻¹ |
| Axon diameter needed for fast conduction | Small (5–20 μm) is sufficient | Must be huge (giant squid axon ~500 μm) to match modest speeds |
| Energy cost per AP | Low (only nodal membrane pumps) | High (entire axon length pumps) |
| Effect of demyelination | Slows or blocks conduction (e.g. multiple sclerosis) | Not applicable — no myelin to lose |
| Biological role | Most vertebrate sensory/motor neurones | Vertebrate C-fibre pain, autonomic post-ganglionic, invertebrate axons |
Saltatory conduction is not only faster — it is also much more energetically efficient. Each action potential involves Na⁺ entering the cell and K⁺ leaving; the Na⁺/K⁺ pump must then restore gradients using ATP. In a myelinated axon, only the membrane at the nodes takes part in the ion exchange, so only a small fraction of the membrane needs active pumping. In an unmyelinated axon, the whole axon membrane does, consuming far more ATP.
Myelination is not complete at birth. In humans, major motor tracts continue to myelinate through childhood and adolescence — one reason that young children are less coordinated than adults. The corticospinal tract (motor cortex to spinal cord) is one of the last to fully myelinate, finishing in the early twenties. This pattern of staggered myelination roughly tracks the developmental sequence of motor skills — gross motor control matures before fine motor control because the corresponding tracts myelinate at different rates.
Multiple sclerosis (MS) is the most important demyelinating disease. In MS, the immune system attacks and destroys myelin around axons in the CNS (oligodendrocyte myelin in this case, not Schwann-cell myelin). As myelin is lost, conduction slows or fails altogether. Symptoms depend on which tracts are affected and may include blurred vision (optic nerve demyelination → optic neuritis), muscle weakness (corticospinal tract), loss of balance (cerebellar tracts), numbness (sensory tracts), and fatigue. OCR does not require detailed knowledge of MS, but understanding its basis is an excellent test of whether you truly grasp the role of myelin.
Guillain-Barré syndrome is the peripheral analogue: auto-immune destruction of Schwann-cell myelin in peripheral nerves. Onset is typically rapid, weakness progressing from the feet upwards over days. Most patients recover as Schwann cells re-myelinate the affected segments — peripheral myelin regenerates better than central myelin, a long-standing puzzle that is the subject of ongoing research into oligodendrocyte biology and central remyelination therapeutics.
The node of Ranvier is packed with molecular machinery:
OCR students are not expected to know all the molecular detail, but knowing that Na⁺ channels cluster at the nodes is essential.
| Neurone | Diameter (μm) | Myelinated? | Speed (m s⁻¹) |
|---|---|---|---|
| Motor neurone (α) | 15 | Yes | 80–120 |
| Touch sensory neurone (Aβ) | 10 | Yes | 30–70 |
| Fast pain (Aδ) | 3 | Thin myelin | 5–30 |
| Slow pain, temperature (C fibres) | 1 | No | 0.5–2 |
This explains the two waves of pain you feel when you stub your toe: a sharp fast wave carried by Aδ fibres, followed a second or two later by a throbbing dull wave carried by unmyelinated C fibres.
In an exam, the question often asks you to explain why myelinated axons conduct faster. A high-mark answer must include all of: (1) myelin insulates the axon so ions only flow at nodes of Ranvier; (2) the action potential jumps from node to node — saltatory conduction; (3) this is faster than continuous propagation along an unmyelinated membrane; (4) it is also more energy-efficient. Just saying "the impulse jumps" is a one-mark answer at best.
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