Neurons are specialised signalling cells

A neuron is a nervous system cell that sends information as electrical impulses along projections from its cell body. At the cell level, this answers the guiding question: neurons generate and move electrical signals because their membranes maintain ion gradients, then rapidly change membrane voltage.

A nerve impulse is an electrical signal that travels along a neuron when the distribution of charged ions changes across the plasma membrane. It is electrical, but not in the way a wire is electrical. Electrons are not flowing along the cell; in neurons, the moving charged particles are mainly ions.

A neuron has a cell body, a region of cytoplasm that contains the nucleus and much of the cell’s metabolic machinery. Nerve fibres of different lengths project from it. An axon is a long, usually single nerve fibre that conducts impulses away from the cell body. Dendrites are shorter, often branched nerve fibres that receive signals and conduct impulses towards the cell body.

Here, structure fits function very neatly. Dendrites give the neuron a large receiving surface, the axon gives it a long conducting pathway, and the cell body keeps the living cell running so both can work. The neuron’s shape is not just decorative — it is the form needed for rapid communication between distant parts of an animal body.

Membrane potential and polarization

A membrane potential is a voltage difference across a plasma membrane, caused by charged particles being distributed unequally on the two sides. In neurons, the inside of the membrane is usually negative compared with the outside.

Membrane polarization describes a membrane when its two sides have different net charges. A resting neuron is polarized: the cytoplasm just inside the axon membrane is more negative than the extracellular fluid.

A resting potential is the membrane potential of a neuron when it is not transmitting an impulse. A typical value is about $-70\ \text{mV}$. The minus sign matters: it shows that the inside of the neuron is negative relative to the outside.

How the resting potential is generated

A sodium–potassium pump is a membrane transport protein that uses energy from ATP to move sodium ions out of the neuron and potassium ions into the neuron against their concentration gradients. In each cycle, three $Na^+$ are pumped out and two $K^+$ are pumped in. Since more positive charge leaves than enters, the pump helps make the inside negative.

The pump also builds concentration gradients. $Na^+$ becomes more concentrated outside the neuron, while $K^+$ becomes more concentrated inside. These gradients matter because diffusion will later drive rapid ion movement during impulses.

The resting potential is negative for three linked reasons:

• the sodium–potassium pump exports more positive charge than it imports;
• the membrane is more permeable to $K^+$ than to $Na^+$, so $K^+$ leaks out more readily than $Na^+$ leaks in;
• large negatively charged proteins and other organic anions remain inside the neuron.

ATP, then, is not used to “make the impulse” directly. It is used to maintain the ion gradients and resting conditions that make impulses possible.

Action potentials are brief voltage changes

An action potential is a rapid, all-or-nothing change in membrane potential that travels along a nerve fibre. “All-or-nothing” means that once the triggering level is reached, a full action potential occurs; a half-sized action potential is not the normal outcome.

There are two main phases in an action potential. Depolarization is a change in membrane potential where the inside becomes less negative and may become positive. Repolarization is the return of membrane potential towards the negative resting state after depolarization.

A nerve impulse is electrical because positively charged ions move across the axon membrane. When $Na^+$ moves into a region of axon, the inside becomes less negative; when $K^+$ moves out, negativity is restored. This is not electron flow, and it is not a chemical diffusing all the way down the axon. The impulse is a travelling pattern of membrane voltage change.

Propagation along the fibre

To propagate a signal is to transmit it onwards from one region to the next. When one patch of nerve fibre depolarizes, ion movement near that patch helps trigger depolarization in the neighbouring patch. So the action potential moves along the fibre.

In a functioning nervous system, impulses normally move in one direction along a neuron: from receiving regions towards the output end. The arrangement of synapses and the brief refractory period after depolarization both help maintain this one-way traffic.

Diameter and myelination affect speed

A nerve impulse doesn’t always travel at the same speed. The structure of the nerve fibre matters a lot. Wider axons conduct faster than narrower axons because a larger diameter gives lower internal resistance to ion movement. That explains why a giant axon in a squid can conduct much faster than a small non-myelinated fibre.

A giant axon is an unusually wide axon that allows rapid impulse conduction by reducing resistance inside the nerve fibre. Squid giant axons are non-myelinated but very wide, so they can coordinate fast escape responses. Small non-myelinated fibres are much slower.

Myelin is a lipid-rich insulating layer wrapped around some axons by glial cells. Myelinated fibres conduct faster than non-myelinated fibres of similar diameter because action potentials are generated only at gaps in the myelin, rather than continuously along the whole membrane.

Correlation skills in this topic

A correlation is a statistical association between two variables. A positive correlation is an association in which the dependent variable tends to increase as the independent variable increases. A negative correlation is an association in which the dependent variable tends to decrease as the independent variable increases.

In neural signalling, conduction speed is usually positively correlated with axon diameter: larger diameter, faster conduction. The guide also gives the example that conduction speed can be negatively correlated with animal size in some datasets.

The correlation coefficient, $r$, is a dimensionless statistic that indicates the direction and strength of a linear association between two variables. Values close to $+1$ show a strong positive correlation; values close to $-1$ show a strong negative correlation; values close to $0$ show little or no linear correlation.

The coefficient of determination, $R^2$, is a dimensionless statistic that estimates the proportion of variation in the dependent variable explained by variation in the independent variable. If

then an $R^2$ value of $0.64$ means 64% of the variation in the dependent variable is explained by the fitted linear relationship.

For this topic, a scatter graph is the natural choice: axon diameter on the x-axis and conduction speed on the y-axis. You can then judge the trend by eye and use $r$ and $R^2$ to support the description mathematically.

Chemical synapses connect neurons to other cells

A synapse is a junction where a neuron communicates with another cell by releasing a chemical signal across a narrow gap. In this topic, synapse means chemical synapse; electrical synapses are not required here.

Synapses can link one neuron to another. They also occur between sensory receptor cells and neurons, and between neurons and effector cells. An effector cell is a cell, such as a muscle fibre or gland cell, that carries out a response after receiving a signal.

The presynaptic neuron is the neuron that releases the chemical signal into the synapse. The postsynaptic cell receives that chemical signal; it may be another neuron, a muscle fibre or a gland cell.

A neurotransmitter is a chemical messenger released by a presynaptic neuron that diffuses across the synaptic cleft and binds to receptors on the postsynaptic cell. The synaptic cleft is the narrow fluid-filled gap between the presynaptic and postsynaptic membranes.

A typical synapse transmits in one direction only. Vesicles containing neurotransmitter sit on the presynaptic side, while receptors that detect the neurotransmitter are on the postsynaptic side. This asymmetry answers the second guiding question neatly: neurons interact with other cells by converting an electrical signal into a chemical signal, then often back into an electrical response in the next cell.

Calcium links depolarization to secretion

When an action potential reaches the end of the presynaptic neuron, the presynaptic membrane depolarizes. Calcium channels open, so $Ca^{2+}$ enters the synaptic knob from the extracellular fluid.

$Ca^{2+}$ then works as an intracellular signalling ion. Here, a signalling chemical is a substance that causes a change in cell activity by binding to or activating target proteins. Inside the presynaptic ending, $Ca^{2+}$ makes vesicles containing neurotransmitter move to the presynaptic membrane and fuse with it.

The neurotransmitter leaves the cell by exocytosis, a process in which a vesicle fuses with the plasma membrane and releases its contents outside the cell. Learn the sequence in order: action potential arrives $\to$ presynaptic membrane depolarizes $\to$ $Ca^{2+}$ enters $\to$ vesicles fuse $\to$ neurotransmitter is released into the synaptic cleft.

From neurotransmitter binding to an EPSP

An excitatory postsynaptic potential is a small depolarization of the postsynaptic membrane that makes an action potential more likely. It’s often shortened to EPSP. The key idea is simple: the postsynaptic membrane gets pushed upwards towards threshold.

Once released, neurotransmitter molecules diffuse across the synaptic cleft. The gap is tiny, so diffusion happens quickly. They then bind to transmembrane receptor proteins in the postsynaptic membrane. In many cases, this binding opens ion channels, allowing positively charged ions to enter the postsynaptic cell.

Acetylcholine is the required example. Acetylcholine is a neurotransmitter used at many synapses, including neuromuscular junctions between motor neurons and muscle fibres. When acetylcholine binds to its receptor, an ion channel opens in the receptor and lets positive ions, especially $Na^+$, diffuse into the postsynaptic cell. The membrane potential becomes less negative, producing an EPSP.

At a neuromuscular junction, this EPSP can trigger an action potential in the muscle fibre, leading towards contraction. At neuron-to-neuron synapses, the EPSP helps determine whether the postsynaptic neuron reaches threshold.

The neurotransmitter cannot stay in the cleft indefinitely. Acetylcholine is rapidly broken down by acetylcholinesterase, so the postsynaptic membrane is not continuously stimulated. Quick removal helps regulate biological signals: they need to start, be transmitted, and then switch off.

Voltage-gated channels and threshold

A voltage-gated ion channel is a membrane channel that opens or closes when the membrane potential changes. During an action potential, voltage-gated $Na^+$ channels and voltage-gated $K^+$ channels do not open at the same time.

A threshold potential is the membrane potential needed to open enough voltage-gated $Na^+$ channels to begin an action potential. In many neurons, it is around $-50\ \text{mV}$, compared with a resting potential near $-70\ \text{mV}$.

Once threshold is reached, voltage-gated $Na^+$ channels open. $Na^+$ then diffuses into the axon down its electrochemical gradient, so the membrane depolarizes quickly, often reaching about $+30\ \text{mV}$. This is positive feedback: $Na^+$ entry causes depolarization, depolarization opens more $Na^+$ channels, and more $Na^+$ enters.

After a very short time, $Na^+$ channels close or become inactivated. Voltage-gated $K^+$ channels open, allowing $K^+$ to diffuse out of the axon. As positive charge leaves the inside, the membrane repolarizes. If $K^+$ channels remain open slightly too long, the membrane may briefly become more negative than the resting potential; this is often called hyperpolarization or an undershoot.

The all-or-nothing nature of the nerve impulse shows regulation clearly: small disturbances below threshold are corrected back towards resting potential, but once threshold is crossed, the channel sequence runs as a full action potential.

Local currents move the wave along

A local current is a short-distance movement of ions near a depolarized region of membrane that changes the membrane potential of neighbouring regions. Local currents show why an action potential moves along the axon instead of sitting in one spot.

When one patch of axon depolarizes, $\mathrm{Na}^+$ has entered that region. Inside the axon, $\mathrm{Na}^+$ diffuses from the depolarized region into the adjacent region, which is still at resting potential. Outside the axon, $\mathrm{Na}^+$ moves in the opposite direction, completing local circuits of ion movement.

These local currents make the neighbouring membrane less negative. If that region reaches threshold, voltage-gated $\mathrm{Na}^+$ channels open there, generating a new action potential. The region that depolarized just before is in its refractory state, so the wave normally keeps moving forwards rather than reversing.

An action potential, then, is not one packet of ions racing from one end of an axon to the other. It is a self-renewing wave: each region of membrane triggers the next region by local ion movement.

Reading voltage traces as cellular events

An oscilloscope trace shows voltage plotted against time, so it can be used to track changes in membrane potential. In neural signalling, the y-axis gives membrane potential, usually in millivolts, while the x-axis gives time, often in milliseconds.

At rest, the trace sits as a near-horizontal line at the resting potential. During an action potential, it forms a sharp spike: the rising phase shows depolarization as $Na^+$ enters; the falling phase shows repolarization as $K^+$ leaves; a dip below the resting potential shows hyperpolarization.

When interpreting an oscilloscope trace, match each part of the line to the cellular event that causes it. Don’t just describe the shape. A steep upward line shows rapid opening of voltage-gated $Na^+$ channels; the peak marks the point where $Na^+$ entry no longer dominates; the downward line shows $K^+$ efflux restoring the negative internal charge.

You can measure the number of impulses per second from the trace. Count the action potential spikes in a known time interval, then convert the value to per second. For example, if a trace shows 5 spikes in 0.25 s, the firing frequency is $20\ \text{impulses }\ s^{-1}$.

Jumping from node to node

A node of Ranvier is a gap in the myelin sheath. At this gap, the axon membrane is exposed to extracellular fluid and has many ion channels and pumps. In myelinated fibres, voltage-gated $Na^+$ channels, voltage-gated $K^+$ channels and sodium–potassium pumps are clustered at these nodes.

Saltatory conduction is the propagation of an action potential along a myelinated axon from one node of Ranvier to the next. The name comes from “jumping”, which is a useful image, but don’t take it too literally: local currents still flow through the axon between nodes.

Myelin works as electrical insulation. Under the myelin, few ions cross the axon membrane, so action potentials are not regenerated at every tiny patch of membrane. Instead, local currents carry depolarization rapidly to the next node. There, the high density of channels allows threshold to be reached and a new action potential to form.

This is a strong structure–function example: myelin wraps the axon, while regularly spaced nodes allow much faster impulse transmission without needing an enormous axon diameter.

Outside chemicals can alter synapses

An exogenous chemical is a substance that enters an organism from an external source and affects biological processes. At a synapse, an outside chemical can either block transmission or make it stronger, depending on where it acts.

Neonicotinoids are synthetic insecticides that bind to nicotinic acetylcholine receptors in insect nervous systems. Once they occupy these receptors, normal acetylcholine signalling is disrupted. In the required IB example, neonicotinoids block synaptic transmission, causing paralysis and death of insects.

This selectivity matters, both biologically and environmentally. Neonicotinoids are especially effective in insects because of receptor differences and the importance of cholinergic transmission in insect nervous systems. Their use has also raised concern about effects on non-target insects such as pollinators.

Cocaine is an exogenous psychoactive drug that blocks reuptake of dopamine at synapses. Reuptake is the removal of a neurotransmitter from the synaptic cleft by transport back into the presynaptic neuron. If dopamine reuptake is blocked, dopamine stays in the synaptic cleft for longer, so postsynaptic receptors are stimulated more than usual.

The two examples work in different ways: neonicotinoids block receptor-mediated transmission at acetylcholine synapses; cocaine prolongs neurotransmitter action by blocking reuptake.

Not every synapse excites

An inhibitory neurotransmitter is a neurotransmitter that makes the postsynaptic neuron less likely to fire an action potential. It has the opposite effect to an excitatory neurotransmitter.

An inhibitory postsynaptic potential is a small hyperpolarization of the postsynaptic membrane, moving the membrane potential further from threshold. You’ll often see it shortened to IPSP.

Hyperpolarization is a change in membrane potential where the inside of the cell becomes more negative than it is at rest. When the membrane becomes more negative, threshold is harder to reach, so firing is inhibited.

One common way to produce an IPSP is to open channels that let negative ions, such as $Cl^-$, enter the postsynaptic neuron, or to increase $K^+$ exit. Either way, the postsynaptic membrane becomes more negative.

The key contrast is simple: acetylcholine at many synapses opens channels that allow positive ions in, producing an EPSP; inhibitory neurotransmitters open or influence channels so that the postsynaptic membrane becomes hyperpolarized, producing an IPSP.

Postsynaptic neurons integrate many inputs

Summation means combining several postsynaptic potentials to decide whether the postsynaptic neuron reaches threshold. In the brain especially, a single neuron may receive input from hundreds or thousands of presynaptic neurons.

One EPSP often isn’t enough to trigger an action potential. Several EPSPs can add together when they arrive close together in time or at nearby regions of the postsynaptic neuron. If the combined depolarization reaches threshold, the postsynaptic neuron fires an action potential.

IPSPs are part of the same calculation, but they push the membrane potential the other way. They hyperpolarize the postsynaptic membrane or reduce some of the depolarizing effect of EPSPs. Whether the neuron fires depends on the balance between excitatory and inhibitory input.

At the output, the result is all-or-nothing: after integration, the postsynaptic neuron either reaches threshold and fires an action potential, or it does not. This is one of the neatest examples of biological regulation in the topic. Many graded inputs are integrated, but the final axon response is a binary event.

Free nerve endings detect damaging stimuli

A free nerve ending is the exposed terminal region of a sensory neuron that detects stimuli without being enclosed in a specialised capsule. In the skin, some free nerve endings detect pain.

Pain-detecting nerve endings contain ion channels that open when a stimulus is damaging or could cause damage. Examples include high temperature, acid and certain chemicals such as capsaicin from chilli peppers.

Once these channels open, positively charged ions enter the ending of the sensory neuron. The membrane depolarizes. If threshold is reached, action potentials are generated and travel along the sensory neuron towards the central nervous system.

Pain itself is not entirely “in the skin”. Skin receptors begin the nerve impulses, but the brain perceives pain when it processes those impulses. Keep the distinction clear: receptors detect stimuli; the nervous system interprets the signals.

Consciousness as an emergent property

Consciousness is a state of awareness that comes from brain activity, including awareness of sensations, thoughts and surroundings. It’s hard to define neatly, but we can still talk about it in biological terms.

An emergent property is a property of a system that comes from interactions among its parts and is not shown by the parts individually. One neuron is not conscious. A network of interacting neurons in the brain can produce consciousness.

This links to a final theme-C idea: interaction and interdependence can create new properties at higher levels of organization. Individual neurons exchange electrical and chemical signals; neural circuits process information; conscious awareness emerges from the interaction of many such circuits.

Sleep and general anaesthesia show that consciousness can change with brain state. We do not yet have a complete cellular explanation of consciousness, and pretending that we do would be misleading. The syllabus point is narrower: consciousness is not located in one isolated neuron; it is a property that emerges from the coordinated activity of many neurons.