Cells talk by chemistry. Hormones, neurotransmitters, second messengers — the same toolbox at every scale.
Every sub-topic below feeds at least one of these questions.
How do cells distinguish between the many different signals that they receive?
What interactions occur inside animal cells in response to chemical signals?
An extra 14 sub-topics for HL — same syllabus, deeper mechanism.
Receptors as proteins with binding sites for specific signalling chemicals
Cell signalling by bacteria in quorum sensing
Hormones, neurotransmitters, cytokines and calcium ions as examples of functional categories of signalling chemicals in animals
Chemical diversity of hormones and neurotransmitters
Localized and distant effects of signalling molecules
Differences between transmembrane receptors in a plasma membrane and intracellular receptors in the cytoplasm or nucleus
Initiation of signal transduction pathways by receptors
Transmembrane receptors for neurotransmitters and changes to membrane potential
Transmembrane receptors that activate G proteins
Mechanism of action of epinephrine (adrenaline) receptors
Transmembrane receptors with tyrosine kinase activity
Intracellular receptors that affect gene expression
Effects of the hormones oestradiol and progesterone on target cells
Regulation of cell signalling pathways by positive and negative feedback
Cells communicate by sending chemical signals (ligands) that bind to receptor proteins with matching shape and chemistry.
Receptor proteins have specific binding sites. The signalling chemical is called a ligand. The ligand binds; the receptor changes shape; a cellular response is triggered. This is the central logic of all cell signalling — bacterial to mammalian.
Quorum sensing lets bacteria regulate behaviour according to population density — using the concentration of their own released signals as an indicator.
This marine bacterium releases an autoinducer. When density is high enough (e.g. inside a squid's light organ), autoinducer binds LuxR receptors → triggers expression of the luciferase enzyme → light is produced. A single bacterium isolated in seawater doesn't glow — it would be wasteful. A dense population in a light organ glows brightly.
Each category serves a different role, from short-range to whole-body, from milliseconds to days.
Secreted by endocrine glands into the bloodstream. Travel anywhere in the body. Act on cells that have the matching receptor. Chemical diversity: amines (epinephrine), peptides (insulin), steroids (oestradiol).
Released by neurons into synapses; diffuse across to receptors on the postsynaptic cell. Local action only. Diverse chemistry: amino acids, peptides, amines, even gases like NO.
Coordinate immune cell behaviour — activation, proliferation, migration. Example: interleukin-2 stimulates T cell proliferation.
Ca²⁺ stored in the SR/ER. Released into cytoplasm in response to other signals; triggers muscle contraction, neurotransmitter release, gene expression changes.
Why so many different chemicals? Natural selection has favoured any signalling molecule that gave an advantage; and the wide range of cellular roles needed required diverse messengers — different solubilities, different binding properties, different timescales.
Hormones travel; neurotransmitters don't. Both reach the right target — by very different routes.
Endocrine gland secretes into blood → hormone circulates everywhere → only cells with the matching receptor respond. Slow (seconds to minutes), wide-reaching, long-lasting.
Neuron releases into the synapse → diffuses across the ~20 nm gap → binds receptors on the postsynaptic cell. Fast (milliseconds), highly localised, brief.
Hydrophilic ligands can't cross the membrane — their receptors must be on the outside. Hydrophobic ligands can — their receptors sit inside the cell.
Binding site is on the outside; hydrophilic. Hydrophobic middle region anchors the receptor in the bilayer. Inner end communicates with the cytoplasm. Used by polar ligands: peptide hormones, neurotransmitters.
Hydrophobic binding sites for hydrophobic ligands that have crossed the membrane. Used by steroid hormones.
Binding doesn't directly do anything — it initiates a sequence of intracellular reactions (the transduction pathway) that ends in a cellular response.
Pathways usually amplify the original signal — one ligand-receptor binding can trigger thousands of downstream events. Specificity is preserved because each receptor activates only its specific cascade.
Neurotransmitter binding to receptor often directly opens ion channels, changing the membrane potential and triggering an action potential.
Example: acetylcholine binds to nicotinic acetylcholine receptors at a neuromuscular junction. The receptor is a ligand-gated Na⁺ channel. Binding opens it → Na⁺ flows into the postsynaptic cell → membrane depolarises → action potential triggered.
G protein-coupled receptors trigger intracellular cascades by activating G proteins, which then produce a second messenger like cAMP.
When epinephrine (adrenaline) binds to its G protein-coupled receptor on a liver cell:
Crucially, the cascade amplifies: one epinephrine molecule → many cAMP molecules → many activated kinases → huge release of glucose. A trace of hormone produces a major cellular response.
A different class of transmembrane receptor with built-in enzymatic activity. Insulin's receptor is the canonical example.
Tyrosine kinase receptors phosphorylate tyrosine residues — adding a phosphate group. When two receptors meet a ligand (insulin), they pair up as a dimer and phosphorylate each other's tyrosine residues. These phosphorylated tyrosines become docking sites for intracellular signalling proteins → cascade begins.
In response to insulin, the cascade triggers translocation of GLUT4 glucose transporters to the plasma membrane → glucose enters the cell → blood glucose falls.
Hydrophobic steroid hormones cross the plasma membrane and bind intracellular receptors. The complex enters the nucleus and acts as a transcription factor.
Examples: Oestradiol and progesterone act on uterine cells during the menstrual cycle. Oestradiol triggers proliferation of the endometrium; progesterone maintains it for pregnancy. Both work through this gene-expression route — which is why their effects build up slowly compared to neurotransmitters.
Signalling pathways are regulated by feedback. Two opposite kinds.
The response counteracts the original signal. Keeps a variable near a setpoint. Most homeostatic loops (blood glucose, body temperature, pH) work this way.
The response amplifies the signal — producing a sharp, decisive change. Less common; reserved for processes that need to happen quickly and completely. Example: the LH surge that triggers ovulation; oxytocin release during labour.
If you can't define one of these in a sentence, that's where to revise next.
“What patterns exist in communication in biological systems?”
“In what ways is negative feedback evident at all levels of biological organization?”