A neurone is a specialised cell built for one job: carrying electrical impulses quickly over long distances. Think of a neurone a bit like an electrical cable with a control box at one end — the "cable" part (the axon) carries the signal, while the "control box" (the cell body) contains the nucleus and keeps the cell alive.

Every neurone — no matter its type — shares three basic features:

• A long fibre called an axon, which carries the impulse.
• A cell body containing the nucleus and other organelles.
• An axon terminal at the end, covered in nerve endings that connect to other neurones — this is what lets neurones form networks.

Many neurones are also myelinated — wrapped in a fatty insulating layer made of Schwann cells. Between each Schwann cell there's a tiny gap called a node of Ranvier. This matters hugely for speed — more on that in Topic 4.

The Three Types of Neurone

The nervous system exists to do one thing well: detect a change and react to it fast. Every response — from blinking to pulling your hand off a hot stove — follows the same basic route:

Reflexes: Fast, Automatic, Unconscious

A reflex is a response that happens without conscious thought — automatic and rapid, which minimises damage to the body. Crucially, you become aware of a reflex only after it's already happened, because the information takes longer to reach the conscious parts of your brain than it does to trigger the muscle. That's the whole point — speed over deliberation.

A reflex arc is the pathway impulses take from receptor to effector without involving conscious regions of the brain. There are two flavours, depending on where the relay neurone sits:

Spinal Reflexes (e.g. pulling your foot off a pin)

The spinal cord has two tissue types worth knowing:

• Grey matter — contains the cell bodies of motor neurones AND relay neurones.
• White matter — contains long, myelinated axons carrying information up and down the cord.

Cranial Reflexes (e.g. the pupil reflex)

Same idea, but the relay neurone is up in the brain rather than the spinal cord.

Here's the concept that trips up more students than any other in this chapter, so let's slow right down. A nerve impulse is not electricity flowing through a wire. Instead, it's a travelling wave of reversed charge across the neurone's membrane — a bit like a Mexican wave rippling down a stadium, except the "wave" here is a temporary flip in electrical charge that moves along the axon.

Resting Potential (≈ −70 mV)

When a neurone is not transmitting an impulse, the inside of the axon is always more negative than the outside. This charge difference — the resting potential — sits at about −70 mV. The membrane is said to be polarised.

Two things create and maintain this:

1. Sodium-potassium pumps actively transport (using ATP) 3 Na⁺ ions out for every 2 K⁺ ions in. This unequal exchange builds up concentration gradients for both ions.
2. Unequal membrane permeability: the membrane is much less permeable to Na⁺ than to K⁺. So K⁺ leaks back out through potassium channels faster than Na⁺ can leak back in. Net result: more positive charge accumulates outside than inside → negative resting potential.

Action Potential (rises to ≈ +30 mV)

To fire an impulse, the membrane must be depolarised — meaning the potential difference reverses.

1. A stimulus opens a small number of sodium channels. Na⁺ floods in down its concentration gradient (remember: much more Na⁺ outside due to the pumps).
2. This makes the inside less negative. If it reaches the threshold potential (around −55 mV), many more voltage-gated sodium channels swing open — a rapid, self-amplifying influx of Na⁺.
3. The membrane flips to about +30 mV — this reversal is the action potential, and the membrane is now depolarised.
4. About 1 millisecond later, sodium channels close and voltage-gated potassium channels open. K⁺ rushes out, making the inside negative again — this is repolarisation.
5. Potassium channels are a little slow to close, so the membrane briefly dips below −70 mV — a state called hyperpolarisation. This period is the refractory period: the membrane can't fire again yet, which is what forces the impulse to travel in one direction only and keeps action potentials as discrete, separate events.
6. Sodium-potassium pumps then restore resting potential, ready to fire again.

Propagation — How the Impulse Actually Travels

Once triggered, the action potential doesn't stay in one spot. Sodium ions that flooded in diffuse sideways along the inside of the axon into the next section of membrane, depolarising it in turn and triggering a fresh action potential there. This repeats down the whole axon — a wave of depolarisation. It can only travel forwards because the section just behind it is still in its refractory period (hyperpolarised) and can't be re-triggered.

In an unmyelinated axon, depolarisation has to happen along the entire length of the membrane, section by section — slow going. Myelin changes the game.

The myelin sheath (Schwann cells) acts as an electrical insulator — sodium and potassium simply can't diffuse across the membrane where myelin covers it. So action potentials can only occur at the exposed gaps: the nodes of Ranvier.

Instead of rippling continuously, the impulse effectively "jumps" from node to node — this is saltatory conduction (from the Latin saltare, "to leap"). Local circuits of current flow through the axon's cytoplasm under the insulated sections, depolarising the membrane only when it reaches the next node.

Neurones don't physically touch each other — there's always a tiny gap called the synaptic cleft between the presynaptic neurone (with its bulbous synaptic knob) and the postsynaptic neurone. Since electrical impulses can't "jump" across this gap, the signal has to switch to a chemical messenger — a neurotransmitter — for the crossing.

Step-by-Step: Synaptic Transmission

1. An action potential arrives at the presynaptic membrane, depolarising it.
2. This opens voltage-gated calcium channels; Ca²⁺ diffuses INTO the synaptic knob.
3. The calcium influx causes vesicles full of neurotransmitter (e.g. acetylcholine, ACh) to move to the presynaptic membrane and fuse with it, releasing their contents by exocytosis.
4. Neurotransmitter diffuses across the synaptic cleft and binds to specific receptor proteins on the postsynaptic membrane.
5. This binding opens associated sodium channels; Na⁺ diffuses into the postsynaptic cell.
6. If enough neurotransmitter binds (i.e. threshold is reached), a new action potential is generated in the postsynaptic neurone.
7. The neurotransmitter is then broken down (e.g. ACh by the enzyme acetylcholinesterase) so the signal doesn't keep firing indefinitely.

Why Synapses Matter — Not Just "Relay Points"

Because so much of nervous transmission depends on synapses, drugs that tweak synaptic events can have huge effects on the brain and body. Broadly, drugs can either increase or decrease transmission — and the chapter gives you five named examples, each acting by a different mechanism. Learn the mechanism, not just the name!

The eye is packed with photoreceptors — specialised receptor cells that generate an electrical impulse when stimulated by light. Light enters through the pupil, gets bent by the lens (shape controlled by ciliary muscles via suspensory ligaments), and is focused onto the fovea — a region of the retina.

Rods vs Cones

Action potentials generated by photoreceptors travel to the brain via the optic nerve, which exits the eye at the blind spot — a region with no photoreceptors at all (hence the name).

⚠️ The Tricky Bit: How Rod Cells Actually Work

This is genuinely one of the most counter-intuitive ideas in the whole chapter, so let's be very explicit about it. Rod cells work "backwards" compared to a normal neurone. Instead of firing an action potential when depolarised, they trigger an action potential in the neighbouring bipolar neurone when they are hyperpolarised — i.e., in the light, not the dark!

In the dark:

• Sodium ions are actively pumped out of the rod cell, building a concentration gradient.
• Because sodium channels are open, Na⁺ diffuses back in — the cell is (relatively) depolarised.
• The depolarised rod cell keeps releasing an inhibitory neurotransmitter at its synapse with the bipolar neurone.
• This inhibitory neurotransmitter prevents an action potential in the bipolar neurone → no impulse sent to the optic nerve.

In the light:

• Light bleaches rhodopsin (breaks it into retinal + opsin).
• This causes the sodium channels to close — Na⁺ can no longer diffuse back in, but the pumps keep pumping it out.
• The inside of the rod cell becomes increasingly negative — it becomes hyperpolarised.
• The hyperpolarised rod cell stops releasing the inhibitory neurotransmitter.
• With the "brakes" removed, the bipolar neurone is now free to generate an action potential → impulse sent to the optic nerve!

Responding to stimuli costs energy — so it would be wasteful for an animal to keep reacting to something that turns out to be harmless every single time. Habituation is the process by which an animal learns not to respond to a repeated stimulus that has no negative consequence.

Examples: not noticing a smell after a while, wild animals losing their fear of humans after repeated harmless contact. If the stimulus then changes (e.g. a constant background sound suddenly gets louder), the nervous system responds to it again — habituation is stimulus-specific, not a general "switching off."

The Mechanism — It's All About the Synapse

Habituation happens because of changes at the synapse, not because receptors stop working:

1. Fewer calcium ions enter the presynaptic neurone when an impulse arrives.
2. This means less neurotransmitter is released into the synaptic cleft.
3. Fewer receptors on the postsynaptic membrane are activated → fewer sodium channels open.
4. Not enough Na⁺ enters → the postsynaptic membrane doesn't reach threshold potential.
5. No action potential is generated → the impulse never reaches the effector → no response.

Investigating Habituation — The Snail Practical

A classic experiment: repeatedly touch a snail's head gently with a damp cotton bud, and time how long it takes to re-emerge and fully extend its eye-stalks each time. As the snail habituates, this re-emergence time should get progressively shorter.

• Keep the same surface, same soft object, and same touch location every time (control variables).
• Wait for full eye-stalk extension each time to use a consistent end-point.
• Plot touch number (x-axis) against re-emergence time (y-axis) — expect a downward trend.
• Animal welfare: return snails to their exact original location, handle gently and quickly, avoid high temperatures or dry conditions.

Zooming all the way out, the entire human nervous system splits into two divisions:

A nerve is simply a bundle of neurones. Sense organs cluster receptor cells together — for example, photoreceptors in the eye, chemoreceptors on the tongue, pressure receptors in the skin and blood vessels.