The Nerve Impulse, the Myelin Sheath, and Saltatory Conduction (OCR A-Level Biology A): Revision Notes

The Nerve Impulse, the Myelin Sheath, and Saltatory Conduction

The resting potential

Neurones generate and transmit electrical impulses, a highly specialised function that requires significant adaptation. Even when inactive, neurones maintain constant electrical activity. The 'resting' neurone maintains an ionic imbalance across its cell membrane, creating what is known as a resting potential.

Resting potential is the electrical potential difference across a neurone membrane when the cell is not transmitting an impulse. This value is approximately $-70 \, \text{mV}$, meaning the outside of the membrane is positively charged relative to the inside.

Establishing the resting potential

The resting potential depends on the distribution of sodium ions (Na⁺) and potassium ions (K⁺) across the membrane. Two types of membrane proteins are involved:

• Channel proteins that allow ions to diffuse through
• Carrier proteins that function as sodium-potassium pumps

The sodium-potassium pump is a carrier protein that actively transports ions using ATP. Importantly, it does not exchange ions equally: the pump moves three sodium ions out for every two potassium ions in. This unequal exchange has several consequences:

• More positive ions accumulate outside the membrane, creating an electrochemical gradient
• Sodium ion concentration becomes higher outside, establishing a concentration gradient for sodium
• Potassium ion concentration becomes higher inside, establishing a concentration gradient for potassium

At rest, sodium channels are closed, preventing sodium ions from following their concentration gradient back into the cell. Potassium channels, although technically closed, are very 'leaky', allowing potassium ions to diffuse back out down their concentration gradient. The positive potassium ions move outward despite the electrochemical gradient pulling them toward the negative interior, because the concentration gradient effect is much stronger.

The overall result is an equilibrium state with more positive charge outside the membrane than inside, and a steep concentration gradient for sodium ions (high outside, low inside). This resting potential remains stable until a stimulus disrupts it.

Scientists consider that membrane permeability differences cause the resting potential. The membrane is much more permeable to potassium ions than sodium ions. The sodium-potassium pump primarily creates the necessary concentration gradients, though it also directly affects membrane potential through its unequal ion exchange.

The action potential

A nerve impulse begins when the resting potential converts into an action potential. This involves a rapid sequence of electrical changes triggered by a stimulus, which may be an electrical impulse from another neurone or a chemical change near the membrane.

Threshold potential and depolarisation

When stimulated, voltage-gated sodium channels begin opening. Both the sodium concentration gradient (high outside) and the electrochemical gradient (positive outside, negative inside) favour sodium entry. Once these channels open, sodium ions flood into the neurone, raising the membrane potential from $-70 \, \text{mV}$.

If the stimulus raises the membrane potential to approximately $-55 \, \text{mV}$, this triggers wholesale opening of sodium channels, and sodium ions pour into the neurone. This demonstrates positive feedback: opening some channels causes a membrane potential rise, which opens more channels, causing further potential increases. The $-55 \, \text{mV}$ value that triggers this cascade is the threshold potential. Stimuli that fail to reach threshold will not generate an action potential.

Once threshold is reached, so much sodium enters that the membrane potential reverses completely. The inside becomes more positive than the outside, reaching approximately $+30 \, \text{mV}$. This reversal is called depolarisation, and it creates the electrical impulse that travels down the neurone.

Repolarisation

At around $+30 \, \text{mV}$, sodium channels close and voltage-gated potassium channels open. Potassium ions then move out of the cell, driven by:

• The potassium concentration gradient (higher inside)
• The electrochemical gradient (now positive inside due to sodium entry)

This potassium efflux brings the potential difference back down toward resting level, a process called repolarisation.

Hyperpolarisation

Voltage-gated potassium channels remain open until the membrane potential reaches approximately $-80 \, \text{mV}$ — lower than the resting potential. This temporary 'overshoot' is termed hyperpolarisation.

Although the potential difference now resembles resting potential, the ionic distribution differs: excess sodium remains inside and excess potassium outside. The sodium-potassium pump and continued potassium leakage through channels restore the original resting state.

The refractory period

The refractory period is the time span during which the neurone cannot respond to a second stimulus. During this period, the voltage-gated sodium channels are recovering and cannot open again. The neurone must fully restore its resting potential and ionic balance before conducting another impulse.

Summary of action potential stages

Stage	Inside membrane	Outside membrane	Potential	Sodium-potassium pump	Voltage-gated sodium channels	Voltage-gated potassium channels
Resting	High K⁺, low Na⁺	Low K⁺, high Na⁺	$-70 \, \text{mV}$	Working	Closed	Closed but leaking
Depolarisation	High K⁺, high Na⁺	Low K⁺, decreasing Na⁺	$-70 \, \text{mV}$ to $+30 \, \text{mV}$	Working	Open	Closed but leaking
Repolarisation	Decreasing K⁺, high Na⁺	Increasing K⁺, relatively low Na⁺	$+30 \, \text{mV}$ to $-70 \, \text{mV}$	Working	Closing or closed	Open
Hyperpolarisation	Decreasing K⁺, Na⁺ starting to decrease	Low K⁺, Na⁺ increasing	$-70 \, \text{mV}$ to $-80 \, \text{mV}$	Working	Closed	Closing

The action potential in one region of the neurone acts as a stimulus for the adjacent membrane section, causing the impulse to propagate along the axon.

The all-or-nothing principle

Individual neurones cannot produce impulses of varying magnitude. This follows the all-or-nothing principle: if a stimulus reaches threshold, the neurone fires a full action potential; if the stimulus remains below threshold, no impulse occurs.

Larger stimuli do not create larger impulses. Instead, the neurone transmits information about stimulus intensity through impulse frequency — stronger stimuli cause more frequent action potentials.

The myelin sheath and saltatory conduction

Many neurones possess axons covered by a myelin sheath, produced by Schwann cells wrapped around the axon. Most neurones lack myelin, however. Non-myelinated neurones are found in the grey matter of the central nervous system, typically where axons are short and impulses travel limited distances.

Function of the myelin sheath

The myelin sheath provides electrical insulation for the axon due to its lipid content. However, the gaps in this insulation — the nodes of Ranvier — are the key functional elements.

Action potentials create 'local circuits' in the axon that depolarise adjacent membrane sections. This occurs only in the forward direction because the refractory period prevents backward propagation. The process also involves attraction between oppositely charged ions on either side of the membrane in neighbouring regions.

In non-myelinated axons, impulses travel continuously along the entire axon, depolarising each section sequentially. In myelinated axons, the insulating myelin prevents depolarisation in covered regions. The action potential therefore 'jumps' from one node of Ranvier to the next.

Saltatory conduction

This 'jumping' transmission is called saltatory conduction (from the Latin saltare, meaning to jump or leap). Saltatory conduction produces much faster impulse transmission.