Key Idea: Topic C2.1 is chemical signalling: how one cell sends a chemical message that changes the behaviour of another. Every example uses the same three ideas. 1. The signal is a ligand. A signalling molecule that binds a receptor is a ligand, and the receptor's binding site is complementary to it (lock-and-key). Only cells with the matching receptor — the target cells — respond. 2. The chemistry of the signal decides the route. Hydrophilic signals (peptide hormones, neurotransmitters) can't cross the membrane, so they bind a surface receptor and the signal is relayed inside (signal transduction). Lipid-soluble signals (steroids) diffuse straight through and bind receptors inside the cell that switch genes on or off. 3. The response is controlled. Binding is reversible, signals are switched off (broken down or removed), and pathways are held in check by negative feedback. This is a concept/structure topic, so it is tested qualitatively — name the parts and explain the chain, not calculate.
🔑 Chemical signals, ligands & receptors (3.4.1)
Cells communicate using chemical signals. A signalling molecule that binds a receptor is called a ligand. A receptor is a protein whose binding site is complementary in shape and chemistry to one ligand — this lock-and-key fit is the basis of specificity. Because only a cell that carries the matching receptor can respond, that cell is the target cell. Binding is reversible and triggers a response. The same signal can even cause different responses in different cell types, because the response depends on the receptor and machinery each cell type happens to have — not on the signal alone.
The surface-receptor route that ties this topic together. A hydrophilic LIGAND binds a TRANSMEMBRANE receptor on the target cell. The ligand never enters the cell — instead the activated receptor RELAYS the signal inside, making a SECOND MESSENGER (e.g. cyclic AMP) that triggers a CASCADE and a cellular RESPONSE. One ligand → many second-messenger molecules → a big response, so the signal is AMPLIFIED. Steroid hormones skip all of this — they diffuse straight through the membrane instead (see 3.4.4).
🔒 Interactive diagram
Explore the labelled diagram, charts and maps for this topic in study mode.
| Term | What it means |
|---|---|
| Signalling molecule | A chemical released by one cell to communicate with another |
| Ligand | A signalling molecule once it BINDS a receptor (the thing that 'fits') |
| Receptor | A protein with a binding site COMPLEMENTARY in shape and chemistry to one ligand |
| Target cell | A cell that CARRIES the matching receptor — only these cells can respond |
| Specificity | Each receptor fits one ligand (lock-and-key), so a signal only hits its targets |
Key Idea: A signal travels everywhere (e.g. a hormone in the blood reaches every cell), but only cells with the complementary receptor can bind it and respond. That is why the same signal can do different jobs: adrenaline speeds the heart at one receptor and breaks down glycogen in the liver at another — same ligand, different receptor, different response.
Ligand = lock-fitter. The receptor is the lock, the ligand is the key — and only the target cell owns that lock. No matching receptor, no response.
📡 Types of signalling & hormones (3.4.2)
Chemical signalling works over a range of distances: endocrine (hormones travel far in the blood), paracrine (acts locally on nearby cells), autocrine (a cell signals itself), and neurotransmitter (across a synapse to the adjacent cell). Hormones fall into two chemical classes that behave very differently. Peptide / protein hormones (insulin, glucagon, adrenaline) are hydrophilic, so they cannot cross the membrane and must bind a surface receptor. Steroid hormones (oestrogen, testosterone, cortisol) are lipid-soluble, so they diffuse through the membrane and bind receptors inside the cell. The signal's chemistry decides where its receptor sits — that is the key takeaway.
| Mode | Range | How the signal travels |
|---|---|---|
| Endocrine | Long | Hormone carried in the BLOOD to distant target cells |
| Paracrine | Short | Diffuses LOCALLY to nearby cells |
| Autocrine | Self | The cell signals ITSELF (binds its own receptors) |
| Neurotransmitter | Very short | Released across a SYNAPSE onto the adjacent cell |
| Feature | Peptide / protein hormone | Steroid hormone |
|---|---|---|
| Examples | Insulin, glucagon, adrenaline* | Oestrogen, testosterone, cortisol |
| Solubility | Hydrophilic (water-soluble) | Lipid-soluble |
| Crosses the membrane? | No — blocked by the phospholipid bilayer | Yes — diffuses straight through |
| Receptor location | Cell-SURFACE (transmembrane) receptor | INSIDE the cell (cytoplasm / nucleus) |
| Mechanism | Signal transduction → second messenger → cascade | Complex acts as a transcription factor on genes |
| Speed & duration | Fast to start, short-lived | Slower to start, longer-lasting |
Don't memorise which hormone is which — reason from solubility. Water-soluble (peptide) → can't get in → SURFACE receptor → transduction. Lipid-soluble (steroid) → slips through the membrane → INSIDE receptor → gene action. (Adrenaline is amino-acid-derived but hydrophilic, so it acts like the peptide class.)
🔄 Transmembrane receptors & signal transduction (3.4.3)
A hydrophilic ligand cannot cross the bilayer, so it binds a transmembrane receptor (e.g. a G-protein-coupled receptor) on the outside of the cell. Binding activates an intracellular relay that produces a second messenger, such as cyclic AMP (cAMP), inside the cell. The second messenger sets off a cascade of enzyme activations that ends in a cellular response — an enzyme is switched on, or a gene is switched on. The key idea is that the signal is relayed and amplified across the membrane WITHOUT the ligand entering: one ligand → many second-messenger molecules → a big response. Example: adrenaline → cAMP → glycogen broken down to glucose.
| Step | What happens |
|---|---|
| 1. Bind | Hydrophilic ligand binds a TRANSMEMBRANE receptor on the cell surface |
| 2. Activate | The receptor changes shape and activates an intracellular relay |
| 3. Second messenger | A small molecule (e.g. cyclic AMP) is made INSIDE the cell |
| 4. Cascade | The second messenger switches on a chain of enzymes — the signal is AMPLIFIED |
| 5. Response | An enzyme is activated (or a gene switched on) → the cellular response |
Key Idea: A tiny amount of hormone can produce a huge effect because each step multiplies: one ligand activates a receptor, which makes many second-messenger molecules, each of which switches on many enzymes. This is how a faint signal becomes a strong, fast response.
🧬 Intracellular receptors & gene activation (3.4.4)
Lipid-soluble signals — steroid hormones and thyroxine — diffuse straight through the plasma membrane and bind intracellular receptors in the cytoplasm or nucleus. The hormone–receptor complex then acts as a transcription factor: it binds DNA and switches specific genes on (or off), changing which proteins the cell makes. Contrast this with the surface route of 3.4.3: intracellular signalling is slower to start but longer-lasting, because it works by changing gene expression. Second-messenger pathways are fast but short-lived. The same big difference — surface vs inside the cell — runs through the whole topic.
| Feature | Surface receptor (peptide) | Intracellular receptor (steroid) |
|---|---|---|
| Where the receptor is | On the cell surface (transmembrane) | In the cytoplasm or nucleus |
| Does the ligand enter? | No — it stays outside | Yes — it diffuses through the membrane |
| What the signal does | Makes a second messenger → enzyme cascade | Forms a complex that acts as a TRANSCRIPTION FACTOR |
| Final effect | Usually changes enzyme activity (fast) | Switches GENES on/off → changes proteins made |
| Speed & duration | Fast, short-lived | Slow to start, long-lasting |
Steroids go inside and reach the DNA. Lipid-soluble → through the membrane → bind a receptor → the complex is a transcription factor → genes on/off → slow but long-lasting. Peptides stay outside and shout through the wall → surface receptor → second messenger → fast but brief.
⚡ Neurotransmitters, receptors & feedback (3.4.5)
Neurotransmitters are chemical signals released at synapses. They diffuse across the synaptic cleft and bind receptors on the postsynaptic membrane, opening ion channels. Whether the result is excitation or inhibition depends on the receptor / channel: opening Na⁺-type channels depolarises (excitatory); opening Cl⁻/K⁺-type channels hyperpolarises (inhibitory). So the same neurotransmitter can be excitatory at one receptor and inhibitory at another — again, the response depends on the receptor, not the signal. Signalling is switched off by re-uptake or enzyme breakdown, keeping each signal brief and repeatable. And whole pathways are held in check by negative feedback: a rising response inhibits further signalling, returning the system to its set point.
| Stage at the synapse | What happens |
|---|---|
| Release | Neurotransmitter is released from the presynaptic terminal into the cleft |
| Diffuse | It diffuses across the synaptic cleft to the postsynaptic membrane |
| Bind | It binds a specific receptor and opens ion channels |
| Excite OR inhibit | Na⁺-type channels → depolarise (excitatory); Cl⁻/K⁺-type → hyperpolarise (inhibitory) |
| Switch off | It is removed by re-uptake or enzyme breakdown, so the signal is brief and repeatable |
Key Idea: This is the unifying idea of the topic. A signal is just a molecule — what it does is decided by which receptor it meets. So the same neurotransmitter can excite one neuron and inhibit another, and the same hormone can do different jobs in different tissues.
Release → diffuse → bind → respond → switch off. And negative feedback = No! — a strong response damps down its own signalling so the system never runs away.
✍️ Worked examples
IB-style question — why steroid and peptide hormones use different receptors
Oestrogen binds a receptor inside its target cells, whereas insulin binds a receptor on the cell surface. Explain this difference and its consequence for how each hormone acts. [4]
Model answer:
Solubility of each hormone. Oestrogen is a steroid and is lipid-soluble, so it can diffuse through the phospholipid membrane; insulin is a peptide hormone and is hydrophilic, so it cannot cross the membrane.
Where each receptor must be. Because oestrogen gets inside, its receptor is intracellular (cytoplasm/nucleus); because insulin is stuck outside, its receptor is a transmembrane (surface) receptor.
How each acts. The oestrogen–receptor complex acts as a transcription factor, switching genes on/off and changing the proteins made; insulin acts through a surface receptor that triggers signal transduction inside the cell.
The consequence. The steroid route is slower to start but longer-lasting (it changes gene expression); the peptide route is fast but short-lived. (1 mark each: solubility difference / receptor location follows from it / oestrogen = gene action vs insulin = transduction / speed–duration consequence.)
Oestrogen is lipid-soluble so it diffuses in and binds an intracellular receptor; the complex acts as a transcription factor changing gene expression (slow, long-lasting). Insulin is hydrophilic so it binds a surface receptor and acts via signal transduction (fast, short-lived).
IB-style question — adrenaline and signal transduction
Adrenaline cannot enter liver cells, yet it causes large amounts of glucose to be released from them. Explain how this is possible. [4]
Model answer:
Binding at the surface. Adrenaline is hydrophilic, so it binds a transmembrane receptor on the outside of the liver cell without entering it.
Make a second messenger. The activated receptor triggers an intracellular relay that produces a second messenger inside the cell, such as cyclic AMP (cAMP).
Cascade and amplification. cAMP sets off an enzyme cascade; because one ligand → many cAMP molecules → many activated enzymes, the signal is hugely amplified.
The response. The cascade activates the enzymes that break glycogen down to glucose, which is released — a large response from a small signal that never crossed the membrane. (1 mark each: surface receptor, no entry / second messenger e.g. cAMP / cascade amplifies / glycogen → glucose response.)
Adrenaline binds a surface receptor (it can't enter); this makes a second messenger (cAMP) inside the cell, which triggers an amplifying enzyme cascade that breaks glycogen down to glucose — so a small external signal gives a large response without the hormone entering the cell.
IB-style question — one neurotransmitter, two responses
The same neurotransmitter is excitatory at one synapse but inhibitory at another. Explain how this is possible, and how the signal is kept brief. [3]
Model answer:
The response depends on the receptor. The neurotransmitter itself does not carry an 'excite' or 'inhibit' label; the effect depends on the receptor / ion channel it binds on the postsynaptic membrane.
Excitatory vs inhibitory. At a receptor that opens Na⁺-type channels the membrane depolarises (excitatory); at one that opens Cl⁻/K⁺-type channels it hyperpolarises (inhibitory).
Keeping it brief. The neurotransmitter is quickly removed by re-uptake or broken down by an enzyme, so the signal stops and the synapse can fire again. (1 mark: response set by receptor; 1 mark: Na⁺ excite vs Cl⁻/K⁺ inhibit; 1 mark: removal/breakdown switches it off.)
The effect is decided by the postsynaptic receptor, not the neurotransmitter: opening Na⁺-type channels excites (depolarises), opening Cl⁻/K⁺-type channels inhibits (hyperpolarises). The signal is kept brief because the neurotransmitter is removed by re-uptake or enzyme breakdown.
✅ Quick self-check
Tap each card to check yourself.
What is a ligand, and what makes a receptor specific? A ligand is a signalling molecule that binds a receptor. The receptor's binding site is complementary in shape and chemistry to one ligand (lock-and-key), so only cells with the matching receptor — the target cells — respond.
Name the four modes of chemical signalling by distance. Endocrine (hormone in the blood, long range), paracrine (local diffusion to nearby cells), autocrine (a cell signals itself), and neurotransmitter (across a synapse to the adjacent cell).
How do peptide and steroid hormones differ in receptor location and action? Peptide hormones are hydrophilic, can't cross the membrane, bind surface receptors and act via signal transduction (fast, short-lived). Steroids are lipid-soluble, diffuse in, bind intracellular receptors, and the complex acts as a transcription factor on genes (slow, long-lasting).
What is signal transduction, and why does it amplify the signal? A surface receptor binds a hydrophilic ligand and relays the signal inside by making a second messenger (e.g. cAMP) that triggers an enzyme cascade. One ligand makes many second messengers, each activating many enzymes — so a small signal gives a large response without the ligand entering.
How can one signal cause different responses? The response depends on the RECEPTOR, not the signal. The same neurotransmitter excites at a Na⁺-channel receptor and inhibits at a Cl⁻/K⁺-channel receptor; the same hormone does different jobs in tissues with different receptors.
How are chemical signals kept under control? Binding is reversible; signals are switched off by removal or breakdown (e.g. neurotransmitter re-uptake or enzyme breakdown); and whole pathways are regulated by negative feedback — a rising response inhibits further signalling, returning the system to its set point.
Exam Tips
- Master idea: a signal is a ligand that binds a complementary receptor; only target cells (with the matching receptor) respond — this is specificity.
- Reason from solubility: hydrophilic (peptide) → can't cross → SURFACE receptor → transduction; lipid-soluble (steroid) → diffuses in → INTRACELLULAR receptor → gene action.
- Signal transduction chain: ligand binds transmembrane receptor → second messenger (e.g. cAMP) → enzyme cascade → response. The ligand never enters the cell, and the cascade AMPLIFIES the signal.
- Steroid/intracellular route: the hormone–receptor complex acts as a transcription factor, switching genes on/off — slower to start but longer-lasting than the surface route.
- Speed vs duration is a favourite contrast: surface = fast & short-lived; intracellular/gene = slow & long-lasting.
- At a synapse: release → diffuse → bind → excite or inhibit → switch off. Whether it excites or inhibits depends on the receptor/ion channel, NOT the neurotransmitter.
- The same signal can give different (even opposite) responses because the response depends on the receptor a cell carries.
- Control: binding is reversible, signals are removed/broken down, and pathways are regulated by negative feedback (a rising response inhibits further signalling).