Nervous coordination

In a nutshell

Nerve cells (neurones) carry information as fast, brief electrical signals. This subtopic is how they do it: how a neurone holds a resting potential, how a stimulus flips that into an action potential that travels along the axon, and how the signal is passed on chemically at a synapse.

The signal itself is electrical, but every gap between one neurone and the next (or between a neurone and a muscle) is crossed by a chemical neurotransmitter, and that is where most exam marks are won and lost.

Assumed knowledge: Transport across cell membranes, Stimuli and receptors.

Core content

The myelinated motor neurone

A motor neurone carries impulses from the central nervous system (CNS) to an effector (a muscle or gland). You need its structure:

• Cell body: contains the nucleus; sits in the CNS.
• Dendrites (dendrons): carry impulses towards the cell body.
• Axon: a long fibre carrying the impulse away from the cell body to the effector.
• Myelin sheath: a fatty, insulating layer made of Schwann cells wrapped around the axon.
• Nodes of Ranvier: gaps in the myelin sheath where the axon membrane is exposed.
• Axon terminals: the endings that form synapses with the effector.

The resting potential

The resting potential is the potential difference across the axon membrane when the neurone is not conducting an impulse. It is about -70 mV, meaning the inside of the axon is negative relative to the outside. A membrane in this state is polarised.

It is set up and maintained by two things working together:

1. The sodium-potassium pump actively transports 3 Na⁺ ions out of the axon for every 2 K⁺ ions in, using ATP. This moves the ions against their concentration gradients and leaves more positive ions outside than inside.
2. The membrane is more permeable to potassium ions than to sodium ions. K⁺ ions therefore diffuse back out through open K⁺ channels, while very few Na⁺ ions diffuse back in.

The net effect: positive ions build up outside faster than inside, so the inside stays negative at about -70 mV.

The action potential

An action potential is a brief reversal of the potential difference across the axon membrane: the inside momentarily becomes positive (about +40 mV) relative to the outside. It is produced by a rapid change in membrane permeability to Na⁺ and K⁺ ions.

The stages, in order:

1. Resting potential: membrane polarised at -70 mV.
2. Depolarisation: a stimulus opens some voltage-gated Na⁺ channels; Na⁺ ions diffuse in, making the inside less negative. If the threshold (about -55 mV) is reached, more voltage-gated Na⁺ channels open, so more Na⁺ ions enter. This is positive feedback, and it drives the inside to about +40 mV.
3. Repolarisation: the Na⁺ channels close and voltage-gated K⁺ channels open, so K⁺ ions diffuse out, making the inside negative again.
4. Hyperpolarisation: K⁺ channels are slow to close, so slightly too many K⁺ ions leave and the potential overshoots to about -80 mV.
5. Return to resting potential: the K⁺ channels close and the sodium-potassium pump restores the original ion distribution, ready for the next impulse.

The all-or-nothing principle

An action potential only fires if the stimulus is large enough to reach the threshold. Below threshold, nothing happens; at or above it, a full-sized action potential is always produced.

A bigger stimulus does not give a bigger action potential. A more intense stimulus is instead signalled by a higher frequency of action potentials (and by more neurones firing).

Still don't get it? · the all-or-nothing principle

Think of a light switch, not a dimmer. Pressing the switch softly does nothing at all; press it past the click and the light comes fully on. Pressing harder does not make the light brighter, it is already fully on.

Step by step:

1. A weak (sub-threshold) stimulus lets a little Na⁺ in, but not enough to reach the threshold, so the voltage-gated Na⁺ channels do not all open and the membrane slides back to rest. No action potential.
2. Once the threshold is crossed, positive feedback takes over: open channels let Na⁺ in, which opens more channels, which lets more Na⁺ in. The membrane always shoots to the same +40 mV.
3. So every action potential is the same size, whatever the stimulus. Intensity is coded by how often impulses fire, not how big they are.

In the exam: a stimulus below threshold gives no action potential; at or above threshold gives an action potential of the same (maximal) size, and a stronger stimulus increases the frequency of impulses.

Passage of the impulse along the axon

When one region depolarises, the Na⁺ ions that entered spread sideways along the inside of the axon. This depolarises the adjacent region to threshold, opening its Na⁺ channels, so the action potential is regenerated further along. The impulse therefore travels as a wave of depolarisation.

• In a non-myelinated axon, this happens along the whole length of the membrane, so it is relatively slow.
• In a myelinated axon, the myelin insulates the membrane and stops ion movement except at the nodes of Ranvier. Depolarisation and the action potential occur only at the nodes, and the impulse jumps from node to node. This is saltatory conduction, and it is much faster.

The refractory period

Straight after an action potential there is a short refractory period during which the membrane cannot be depolarised again, because the voltage-gated Na⁺ channels are closed or inactivated (and the membrane is hyperpolarised, so a greater stimulus would be needed).

Its importance:

• It makes impulses discrete (separate), because each region must recover before it can fire again.
• It ensures the impulse travels in one direction only, because the region behind the action potential is still refractory and cannot be re-stimulated.
• It limits the frequency of impulses, setting a maximum number per second.

Factors affecting the speed of conductance

The structure of a synapse

A synapse is the junction between two neurones. The tiny gap between them is the synaptic cleft. The neurone before the cleft is the presynaptic neurone (ending in a swollen synaptic knob); the one after it is the postsynaptic neurone.

• The synaptic knob contains many mitochondria and synaptic vesicles filled with a neurotransmitter.
• The presynaptic membrane has voltage-gated calcium ion channels.
• The postsynaptic membrane has receptors complementary to the neurotransmitter, linked to sodium ion channels.

A cholinergic synapse is one that uses acetylcholine (ACh) as its neurotransmitter. These are found in the CNS and at neuromuscular junctions.

Transmission across a cholinergic synapse

Learn this as a numbered chain: an "explain" question here is marked by the number of correct linked points.

1. An action potential arrives at the synaptic knob and depolarises the presynaptic membrane.
2. This opens voltage-gated calcium ion channels, and Ca²⁺ ions diffuse into the synaptic knob.
3. The Ca²⁺ ions cause synaptic vesicles to move to and fuse with the presynaptic membrane, releasing acetylcholine into the synaptic cleft by exocytosis.
4. Acetylcholine diffuses across the synaptic cleft.
5. It binds to receptors on the postsynaptic membrane.
6. This opens sodium ion channels, so Na⁺ ions diffuse into the postsynaptic neurone, depolarising the postsynaptic membrane.
7. If enough Na⁺ ions enter to reach the threshold, a new action potential is generated in the postsynaptic neurone.
8. Acetylcholinesterase in the cleft breaks acetylcholine down (into choline and ethanoic acid), so the Na⁺ channels close and the membrane is not continuously depolarised. The products are reabsorbed into the presynaptic knob and acetylcholine is resynthesised using ATP.

Why transmission is unidirectional

An impulse can only cross a synapse in one direction, from presynaptic to postsynaptic, because:

• the neurotransmitter is only made, stored and released by the presynaptic neurone, and
• the receptors are only on the postsynaptic membrane.

Summation

A single impulse often releases too little neurotransmitter to reach threshold. Summation adds up several small amounts so that threshold is reached and the postsynaptic neurone fires.

• Temporal summation: one presynaptic neurone fires repeatedly in quick succession, so neurotransmitter builds up until threshold is reached.
• Spatial summation: several presynaptic neurones release neurotransmitter onto one postsynaptic neurone at the same time, and their effects add together.

Inhibitory synapses

Some synapses make the postsynaptic neurone less likely to fire. Here the neurotransmitter opens chloride ion (Cl^-) channels (and potassium ion channels), so Cl^- ions move in and K⁺ ions move out. The inside of the postsynaptic membrane becomes more negative than the resting potential (hyperpolarised), so more Na⁺ ions than usual would be needed to reach threshold, making an action potential less likely.

Still don't get it? · how an inhibitory synapse blocks the impulse

Think of the high jump. To score, the jumper has to clear the bar. An inhibitory synapse does not touch the jumper, it just raises the bar so the same jump no longer clears it.

Step by step:

1. Normally the resting membrane sits at -70 mV and only has to climb to about -55 mV (threshold) to fire.
2. The inhibitory neurotransmitter opens Cl^- channels (Cl^- in) and K⁺ channels (K⁺ out). Both make the inside more negative, say -80 mV. That is hyperpolarisation: the bar has been raised.
3. From -80 mV the membrane now has much further to climb, so far more Na⁺ ions must enter to reach threshold. An excitatory input that would normally have fired the neurone now fails.

The mark-scheme sentence: the inside becomes more negative / hyperpolarised, so more sodium ions are needed to reach threshold, making depolarisation / an action potential less likely.

Comparing a cholinergic synapse and a neuromuscular junction

A neuromuscular junction (NMJ) is the synapse between a motor neurone and a skeletal muscle fibre. The sequence of events is essentially the same (ACh released, diffuses across, binds receptors, opens Na⁺ channels), but the two differ in what they connect and how they behave.

Similarities: both use acetylcholine, both have receptors only on the postsynaptic membrane, both are unidirectional, and both use acetylcholinesterase to break the neurotransmitter down.

Predicting the effect of drugs on a synapse

You are not asked to recall named drugs, but you must use information given to predict what a drug does. Work from where it acts in the sequence:

• A drug that is complementary to the receptor and mimics the neurotransmitter binds and opens the Na⁺ channels, so it triggers more action potentials (an agonist).
• A drug that blocks the receptor (complementary, so it competes with the neurotransmitter) stops the neurotransmitter binding, so fewer or no action potentials are produced.
• A drug that inhibits acetylcholinesterase means ACh is not broken down, so it stays bound and causes continuous depolarisation / repeated action potentials.
• A drug that blocks the calcium ion channels stops Ca²⁺ entering the knob, so vesicles do not fuse and no neurotransmitter is released.

Worked examples

Model answer, 5 marks: "Describe how a nerve impulse is transmitted across a cholinergic synapse."

The marks come from distinct, correctly ordered points. Aim for five of these:

1. Action potential causes calcium ion channels to open and Ca²⁺ ions diffuse into the synaptic knob.
2. Vesicles fuse with the presynaptic membrane and release acetylcholine (by exocytosis).
3. Acetylcholine diffuses across the synaptic cleft.
4. Acetylcholine binds to receptors on the postsynaptic membrane.
5. Sodium ion channels open and Na⁺ ions enter, depolarising the membrane; if threshold is reached an action potential is produced.

Notice what the marks depend on: "calcium ions", "diffuse into the knob", "vesicles fuse with the membrane" (not "cross the cleft"), "binds to receptors", and Na⁺ ions entering (not just "channels open").

Calculation: maximum frequency of impulses from the refractory period.

A neurone has a refractory period of 4 ms. The maximum frequency of impulses is one impulse per refractory period.

Step 1, convert the refractory period to seconds:

$4 \text{ ms} = 4 \times 10^{-3} \text{ s} = 0.004 \text{ s}$

Step 2, take the reciprocal to get impulses per second:

$\text{maximum frequency} = \frac{1}{0.004} = 250 \text{ s}^{-1}$

So the neurone can carry at most 250 impulses per second. The mark that most students drop is the ms to s conversion: forgetting it gives an answer 1000 times too small.

Common exam mistakes

• Writing "sodium" or "potassium" instead of "sodium ions" or "potassium ions". Examiners reject the unqualified element; the mark needs the word ions (or the symbol Na⁺ / K⁺).
• Not stating the direction of ion movement. "Sodium ions enter the membrane" is ambiguous; say Na⁺ ions move into the axon (or out of it).
• Saying "channels open" without adding that ions then diffuse in or out. Both halves are needed.
• For the resting potential, calling the pump "diffusion", or saying K⁺ ions enter. At rest K⁺ ions diffuse out, and the pump uses active transport.
• For repolarisation, writing "the pump restores it". Repolarisation is K⁺ channels opening and K⁺ ions leaving; the pump only resets the ion balance afterwards.
• Treating a bigger stimulus as a bigger action potential. A sub-threshold stimulus gives no action potential; above threshold every action potential is the same size (all-or-nothing). Intensity is coded by frequency.
• On the refractory period, writing that it "stops the impulse going backwards" when asked why a greater stimulus is needed. The relevant point is that Na⁺ channels are closed / inactivated and the membrane is hyperpolarised.
• Describing saltatory conduction as just "jumps node to node" with no mention that myelin insulates the membrane, and not comparing it to the non-myelinated axon where the whole membrane depolarises.
• Saying speed depends on the "diameter of the axon membrane". It is the axon's diameter; a wider axon has less resistance to ion flow.
• Writing that vesicles cross the synaptic cleft. Vesicles fuse with the presynaptic membrane; it is the neurotransmitter that diffuses across.
• Saying calcium ions "cross the membrane" or enter the cleft. Ca²⁺ ions enter the synaptic knob by facilitated diffusion.
• Using "active site" or "enzyme-substrate" language for a receptor. A receptor is not an enzyme; the neurotransmitter is complementary to and binds the receptor.
• For inhibition, not saying the inside becomes more negative (hyperpolarised) and that more Na⁺ ions are then needed to reach threshold.
• Using "messages" or "signals" instead of impulses.
• Forgetting the ms to s conversion in frequency or speed calculations.

Key definitions

• Resting potential: the potential difference across the axon membrane when the neurone is not conducting an impulse (about -70 mV, inside negative relative to outside).
• Action potential: a temporary reversal of the potential difference across the axon membrane, so the inside briefly becomes positive relative to the outside.
• Depolarisation: the influx of sodium ions that makes the inside of the axon less negative / positive.
• Repolarisation: the efflux of potassium ions that restores the negative charge inside the axon.
• Threshold: the membrane potential that must be reached for an action potential to be generated.
• All-or-nothing principle: a stimulus at or above the threshold always produces an action potential of the same size; a stimulus below the threshold produces none.
• Refractory period: the period after an action potential during which the axon membrane cannot be depolarised, because the voltage-gated sodium ion channels are closed or inactivated.
• Saltatory conduction: transmission in a myelinated axon in which the action potential jumps from one node of Ranvier to the next.
• Synapse: the junction between two neurones, across which a neurotransmitter diffuses.
• Cholinergic synapse: a synapse that uses acetylcholine as its neurotransmitter.
• Temporal summation: several impulses from one presynaptic neurone arrive in quick succession, releasing enough neurotransmitter to reach threshold.
• Spatial summation: several presynaptic neurones release neurotransmitter onto one postsynaptic neurone at the same time, together reaching threshold.

Specification

3.6.2.1 Nerve impulses

• I can describe the structure of a myelinated motor neurone.
• I can explain how the resting potential is established, in terms of differential membrane permeability, electrochemical gradients and the movement of sodium ions and potassium ions.
• I can explain how changes in membrane permeability cause depolarisation and generate an action potential.
• I can state and apply the all-or-nothing principle.
• I can describe the passage of an action potential along non-myelinated and myelinated axons.
• I can explain the nature and importance of the refractory period in producing discrete impulses and limiting impulse frequency.
• I can explain how myelination and saltatory conduction, axon diameter and temperature affect the speed of conductance.

3.6.2.2 Synaptic transmission

• I can describe the detailed structure of a synapse and of a neuromuscular junction.
• I can describe the sequence of events at a cholinergic synapse in enough detail to explain unidirectionality, temporal and spatial summation, and inhibition.
• I can compare transmission across a cholinergic synapse and across a neuromuscular junction.
• I can use given information to predict and explain the effects of drugs on a synapse.

Related notes

• Stimuli, internal and external
• Skeletal muscles and contraction
• Homeostasis
• Transport across cell membranes