describe and explain the rapid transmission of an impulse in a myelinated neurone with reference to saltatory conduction

Control and Coordination in Mammals – Saltatory Conduction

1. The Neuron – Basic Signalling Unit

• Structure

  • Soma (cell body) – contains nucleus, Nissl bodies and most organelles.
  • Dendrites – specialised for receiving graded potentials from other neurons or sensory receptors.
  • Axon – long, thin process that carries the nerve impulse away from the soma.
  • Axon terminals (synaptic boutons) – release neurotransmitter into the synaptic cleft.

• Resting membrane potential (RMP)

  • Typical value ≈ –70 mV (inside negative).
  • Established by the Na⁺/K⁺‑ATPase (3 Na⁺ out, 2 K⁺ in) and the differential permeability of the membrane (high K⁺ conductance, low Na⁺ conductance).

• Key ion‑channel types

  • Leak channels – set the RMP.
  • Voltage‑gated Na⁺ channels – open rapidly when the membrane reaches threshold (≈ –55 mV).
  • Voltage‑gated K⁺ channels – open more slowly, repolarise the membrane.
  • Voltage‑gated Ca²⁺ channels – at the terminal, trigger neurotransmitter release.

• Action potential (AP) – phases

  1. Depolarisation – Na⁺ influx, membrane potential rises to ≈ +30 mV.
  2. Repolarisation – K⁺ efflux restores negativity.
  3. After‑hyperpolarisation – brief period of membrane potential more negative than the RMP.

• Refractory periods

  • Absolute refractory period – Na⁺ channels are inactivated; no new AP can be generated.
  • Relative refractory period – some Na⁺ channels have recovered; a stronger stimulus can evoke an AP.

2. Synaptic Transmission (Brief Overview)

1. AP reaches the axon terminal → voltage‑gated Ca²⁺ channels open.
2. Ca²⁺ influx causes synaptic vesicles to fuse with the presynaptic membrane.
3. Neurotransmitter is released into the synaptic cleft.
4. Binding to postsynaptic receptors produces an excitatory (EPSP) or inhibitory (IPSP) graded potential.
5. If the summed graded potentials reach threshold at the axon hillock, a new AP is generated.

3. Propagation of the Impulse – Continuous vs. Saltatory Conduction

4. Structure of a Myelinated Neurone

• Axon – cylindrical cable that carries the impulse.
• Myelin sheath

  • Formed by Schwann cells (PNS) or oligodendrocytes (CNS).
  • Multiple tightly‑wrapped layers of lipid‑rich membrane.
  • Functions as an electrical insulator: ↑ membrane resistance (Rₘ) and ↓ membrane capacitance (Cₘ).

• Nodes of Ranvier

  • Gaps ≈ 1 µm long where the axolemma is exposed.
  • Very high density of voltage‑gated Na⁺ (≈ 1 500 µm⁻²) and K⁺ channels.

• Internodes

  • Myelinated segments between two nodes.
  • Typical length 100–200 µm in peripheral nerves; up to 1–2 mm in large motor fibres.

5. Mechanism of Saltatory Conduction

1. At a node, the incoming depolarising current opens voltage‑gated Na⁺ channels → a local AP is generated.
2. The rapid change in membrane potential creates an electric field that drives current longitudinally down the axoplasm.
3. Myelin’s high Rₘ prevents current from leaking across the membrane; its low Cₘ means the membrane charges and discharges very quickly.
4. The axial current reaches the next node before the voltage on the intervening internode falls below threshold.
5. When the depolarising current at the next node reaches ≈ –55 mV, Na⁺ channels open and a new AP is regenerated.
6. The process repeats, giving the appearance that the impulse “jumps’’ from node to node.

5.1 Electrical‑circuit (cable) model

The axon can be represented as a series of resistors and capacitors:

• Rₘ – membrane resistance (Ω·cm²); increased ≈ 100‑fold by myelin.
• Cₘ – membrane capacitance (µF·cm⁻²); reduced ≈ 100‑fold by myelin.
• Rᵢ – internal (axoplasmic) resistance (Ω·cm); inversely proportional to the square of the axon diameter.
• L – length of an internode (cm).

The time constant τ = RₘCₘ and the space constant λ = √(Rₘ / Rᵢ). For a myelinated fibre the conduction velocity can be approximated by:

\$\$

v \;\approx\; \frac{L}{\sqrt{Rm Cm}}

\$\$

Because myelin raises Rₘ and lowers Cₘ, the denominator becomes much smaller, so the velocity increases dramatically.

5.2 Worked example – estimating velocity

Calculate the expected conduction speed for a peripheral motor axon with the following typical values:

• Axon diameter = 10 µm → internal resistance Rᵢ ≈ 0.1 Ω·cm.
• Myelin thickness = 5 µm → effective membrane resistance Rₘ ≈ 5 × 10⁴ Ω·cm².
• Membrane capacitance Cₘ ≈ 1 µF·cm⁻² (unmyelinated) ÷ 100 ≈ 0.01 µF·cm⁻² (myelinated).
• Internode length L = 1 mm = 0.1 cm.

Step 1 – time constant

\$\$

\tau = Rm Cm = (5\times10^{4}\,\Omega\!\cdot\!{\rm cm}^2)(0.01\times10^{-6}\,{\rm F}\!\cdot\!{\rm cm}^2)

= 5\times10^{-4}\,{\rm s}

\$\$

Step 2 – velocity

\$\$

v \approx \frac{L}{\sqrt{\tau}} = \frac{0.1\,{\rm cm}}{\sqrt{5\times10^{-4}\,{\rm s}}}

\approx \frac{0.1}{0.0224}\,{\rm cm\,s^{-1}}

\approx 4.5\,{\rm m\,s^{-1}} \;(\text{≈ 45 m s}^{-1})

\$\$

Experimental values for similar fibres are 50–120 m s⁻¹, confirming that the simple model captures the correct order of magnitude.

5.3 Limits on internode length – the “safety factor”

• If L is too long, the axial current decays before the next node reaches threshold → conduction fails.
• Optimal internode length ≈ 100–150 times the axon diameter; beyond this the safety factor (depolarising current / threshold) drops below 1.

6. Factors Influencing Conduction Velocity

7. Clinical Relevance – Demyelinating Disorders

• Multiple sclerosis (MS) – Autoimmune loss of CNS myelin → ↓ Rₘ, ↑ Cₘ → slowed or blocked conduction, producing muscle weakness, visual disturbances and coordination problems.
• Guillain‑Barré syndrome (GBS) – Peripheral demyelination → markedly slowed peripheral reflexes, loss of sensation and reversible paralysis if remyelination occurs.
• Both conditions illustrate why myelin is essential for rapid, energy‑efficient signalling.

8. Integration with Reflex Arcs and Neuro‑endocrine Control

• Reflex arc – Sensory receptor → afferent (myelinated) neuron → spinal integration centre → efferent (myelinated) motor neuron → effector muscle. Saltatory conduction in both afferent and efferent fibres ensures the whole response occurs within a few milliseconds.
• Neuro‑endocrine pathways – Hypothalamic neurons fire APs that travel via myelinated axons to the median eminence. The rapid signal triggers release of releasing hormones into the portal circulation, allowing the pituitary to secrete target hormones within seconds.

9. Syllabus Alignment – Cambridge International AS & A‑Level (Topic 15: Control and Coordination)

10. Summary – Key Take‑aways for the Exam

• Myelin insulates the axon, increasing membrane resistance (Rₘ) and decreasing capacitance (Cₘ).
• Voltage‑gated Na⁺ channels are clustered at the Nodes of Ranvier; these are the only sites where the AP is regenerated.
• During saltatory conduction the depolarising current travels rapidly inside the axoplasm and “jumps’’ from node to node.
• Conduction velocity ≈ L / √(RₘCₘ); therefore larger internodes, thicker myelin and larger axon diameter all increase speed.
• Fast saltatory conduction underpins rapid reflexes, coordinated movement and swift neuro‑endocrine responses.
• Demyelinating diseases (MS, GBS) illustrate the functional importance of myelin – loss of insulation leads to slowed or blocked impulses.