HookYour hand leaves the hot pan before your brain feels a thing
In 1939, two Cambridge physiologists pushed a fine electrode inside a single nerve fibre and, for the first time, watched an action potential happen. Their fibre came from a squid, whose giant axon is so wide — up to a millimetre across — that you can thread a wire straight down it. Alan Hodgkin and Andrew Huxley recorded a nerve at rest sitting at about −70 millivolts inside, then spiking to about +40 millivolts and back within a couple of milliseconds, all driven by sodium and potassium ions crossing the membrane through gated channels. The measurements won them the Nobel Prize in 1963, and they are the very numbers printed on the AQA specification.
Their work explains something you have felt. Your hand leaves a hot pan before you consciously feel the heat, because a reflex runs the loop from skin to spinal cord to muscle in a fraction of a second, without waiting for the brain to decide. Section 3.6 is that whole loop and more — how receptors detect a change, how neurones carry the message at up to a hundred metres a second, how synapses pass it on, how muscles turn it into movement, and how a separate, slower, hormonal system holds your internal conditions steady while all of this happens. It rewards precise sequences and precise numbers, so this is a section to learn as ordered mechanisms rather than loose facts.
ModelResponding to survive: tropisms, taxes, kineses and reflexes
A response that improves survival is favoured by selection, and even organisms with no brain manage them. Plants grow directionally — a tropism — controlled by the hormone IAA (auxin). In a shoot, IAA gathers on the shaded side, where it promotes cell elongation, so the shoot bends toward the light (positive phototropism); gravity is sensed the same way in roots. Simple animals show two contrasting movements. A taxis is a directional response — a woodlouse moving directly away from light is showing negative phototaxis. A kinesis is non-directional: the animal changes its speed and its rate of turning according to intensity, so in dry air a woodlouse moves fast and turns little, while in damp air it slows and turns more, and so tends to end up, and stay, where it is damp.
In animals with nervous systems, the fastest responses are reflexes, which skip conscious thought. The reflex arc runs stimulus → receptor → sensory neurone → intermediate (relay) neurone in the spinal cord → motor neurone → effector → response. Because it does not route through the conscious brain, a reflex is rapid, automatic and protective — pulling away from damage, adjusting posture, or protecting the eye — and its survival value is exactly that it needs no decision.
MechanismReceptors: the Pacinian corpuscle and the retina
A receptor is a biological transducer: it converts the energy of a stimulus into the electrical energy of a nerve impulse, and each type responds only to its own specific stimulus. The Pacinian corpuscle, a pressure receptor deep in the skin, shows the mechanism cleanly. It is a nerve ending wrapped in layers of tissue (lamellae); pressure deforms them, which stretches stretch-mediated sodium ion channels in the membrane; sodium ions rush in, producing a generator potential; and if that reaches threshold, an action potential fires. A greater pressure makes a larger generator potential and a higher frequency of impulses — which is how the intensity of a stimulus is coded.
The retina carries two receptor types with a revealing trade-off. Rod cells are extremely sensitive in dim light because many rods feed into one bipolar neurone (retinal convergence), so their weak signals add together to reach threshold — but that same convergence means the brain cannot tell which rod fired, giving low visual acuity; rods see only in monochrome, using the pigment rhodopsin. Cone cells, concentrated at the fovea, each connect to their own bipolar neurone, giving high acuity and colour vision (three types tuned to red, green and blue), but they need bright light to respond. So we see fine detail and colour by day with cones, and shape and movement at night with rods.
MechanismControlling heart rate: nerves and hormones
The heart sets its own basic rhythm at the sinoatrial node (SAN), but the rate is adjusted to demand by the medulla oblongata in the brain, acting through the autonomic nervous system. Receptors feed it information: chemoreceptors in the aorta and carotid arteries detect a fall in blood pH (a rise in carbon dioxide), and baroreceptors in the same vessels detect blood pressure. When exercise raises carbon dioxide, the chemoreceptors signal the medulla, which sends impulses down the sympathetic (accelerator) nerve to the SAN, speeding the heart; when pressure climbs too high, the parasympathetic (vagus) nerve slows it again.
A second, hormonal route works in parallel and lasts longer: adrenaline, released from the adrenal glands in fear or exertion, binds to the SAN and raises heart rate directly. This is the division of labour that runs through the whole section — nervous control is fast and brief, hormonal control is slower to start but sustained.
MechanismThe nerve impulse: resting and action potentials
At rest, a neurone's inside is about −70 mV relative to outside — the resting potential — maintained by the sodium–potassium pump, which pushes three sodium ions out for every two potassium ions in, and by the membrane being more permeable to potassium leaking back out. The membrane is polarised. A stimulus that reaches threshold opens voltage-gated sodium channels; sodium floods in and the inside shoots to about +40 mV — depolarisation. The sodium channels then close and potassium channels open, potassium leaves, and the membrane repolarises, briefly overshooting (hyperpolarisation) before the pump restores the resting potential.
The spike is all-or-nothing: any stimulus above threshold gives the same size of action potential, and a stronger stimulus is signalled by a higher frequency of impulses, never a taller spike. A refractory period — while the channels reset — prevents a new impulse forming immediately, which keeps impulses discrete and forces them to travel one way. Conduction is faster in myelinated neurones, where the impulse jumps between the gaps in the sheath (nodes of Ranvier) in saltatory conduction, and faster still in wide, warm axons.
How much does myelination buy you? A motor neurone 1.2 m long conducts at about 100 m s⁻¹ when myelinated, so an impulse takes \(t = \dfrac{1.2}{100} = 0.012\ \text{s}\) — roughly 12 milliseconds. The same fibre unmyelinated, conducting at about 1 m s⁻¹, would take \(1.2\ \text{s}\), a hundred times slower. That is why the neurones carrying urgent signals, such as a withdrawal reflex, are heavily myelinated: those saved milliseconds are the difference between a warm pan and a burn.
MechanismSynapses: passing the message on
Where one neurone meets the next there is a gap, the synaptic cleft, and the signal crosses it chemically. When an action potential reaches the synaptic knob, it opens voltage-gated calcium channels; calcium floods in and makes vesicles of the neurotransmitter acetylcholine (ACh) fuse with the membrane and release their contents by exocytosis. ACh diffuses across the cleft and binds to receptors on the postsynaptic membrane, opening sodium channels there; if enough binds, the postsynaptic membrane reaches threshold and a fresh action potential fires. The enzyme acetylcholinesterase then hydrolyses the ACh, switching the response off and freeing the components to be recycled.
Two consequences are heavily examined. Because the receptors sit only on the postsynaptic membrane, transmission is unidirectional. And because a single impulse often releases too little ACh to fire the next neurone, synapses perform summation: several impulses close together in time (temporal), or from several neurones at once (spatial), add up to reach threshold. The neuromuscular junction is a special cholinergic synapse between a motor neurone and a muscle fibre — it works the same way but is always excitatory, and the ACh binds receptors on the muscle's membrane (the sarcolemma) to trigger contraction.
MechanismMuscles: the sliding filament mechanism
Skeletal muscle works in antagonistic pairs — one contracts as its partner relaxes — because muscle can only pull, never push. Inside, muscle fibres are packed with myofibrils striped into repeating units, sarcomeres, built from thin actin and thick myosin filaments. Contraction is the sliding filament mechanism: the filaments themselves do not shorten; they slide past one another, so the sarcomere shortens, its I band and H zone narrow, and its A band stays the same width.
The trigger is calcium. An action potential sweeps along the sarcolemma and down the T-tubules, making the sarcoplasmic reticulum release calcium ions. Calcium binds to troponin, shifting tropomyosin off the binding sites on the actin; myosin heads then attach, forming cross-bridges, and flex in a power stroke that drags the actin along. ATP binds each myosin head to detach it, and is hydrolysed by the head's ATPase to re-cock it for the next stroke. The cycle repeats many times a second while calcium and ATP are present; when nerve stimulation stops, calcium is pumped back, tropomyosin re-covers the sites, and the muscle relaxes. For the first few seconds of intense effort, phosphocreatine stored in the muscle regenerates ATP anaerobically to keep the heads cycling.
ModelHomeostasis and negative feedback
Homeostasis is the maintenance of a stable internal environment within narrow limits, and it matters because cell chemistry is fussy: enzymes have narrow optima for temperature and pH, and cells shrivel or burst if the water potential of the blood drifts. The mechanism is negative feedback: a receptor detects a deviation from the set point, a corrective mechanism reverses it, and the factor returns toward normal.
A subtle but examinable point is that good control uses separate mechanisms for departures in each direction — one process to cool you and a different one to warm you, one hormone to lower blood glucose and another to raise it. Two opposing controls give finer, faster correction than one alone. This contrasts with positive feedback, which amplifies a change rather than reversing it, and so is not a homeostatic mechanism.
MechanismBlood glucose: insulin, glucagon and diabetes
Blood glucose is held near 90 mg per 100 cm³ by two hormones from the islets of Langerhans in the pancreas. When glucose rises, beta cells release insulin, which makes liver and muscle cells take up more glucose (more carrier proteins move into their cell-surface membranes) and convert it to glycogen — glycogenesis — lowering blood glucose. When glucose falls, alpha cells release glucagon, which makes the liver break glycogen back down — glycogenolysis — and make new glucose from other molecules such as glycerol and amino acids — gluconeogenesis — raising blood glucose. Adrenaline reinforces the glucagon side in an emergency.
Glucagon and adrenaline act by the second messenger model: the hormone binds a receptor and activates the enzyme adenylate cyclase, which makes cyclic AMP inside the cell, which activates enzymes that liberate glucose — amplifying the signal without the hormone ever entering the cell. When this control fails you have diabetes. In type 1 the immune system destroys the beta cells, so no insulin is made; it appears early in life and is treated with insulin injections. In type 2 the cells stop responding to insulin (receptor insensitivity), usually later in life and often linked to obesity; it is managed by diet, exercise and drugs. This is the biology behind the discovery that turned type 1 diabetes from a death sentence into a manageable condition — Banting and Best's isolation of insulin in 1921.
MechanismOsmoregulation: the kidney and ADH
The kidney filters the blood and adjusts its water potential, in a working unit called the nephron. First comes ultrafiltration: blood at high pressure in the glomerulus is forced through a basement membrane that holds back cells and large proteins but lets water, glucose, ions and urea through into the tubule. Then selective reabsorption in the proximal convoluted tubule returns all the glucose and much of the water and ions to the blood, using co-transport and a brush border of microvilli. The loop of Henle then sets up a salt gradient in the medulla — its ascending limb pumps sodium and chloride ions out but is impermeable to water, making the surrounding tissue increasingly salty the deeper you go (a countercurrent multiplier).
That gradient is what lets the body concentrate urine. As filtrate passes down the collecting duct through the salty medulla, water leaves by osmosis — but only if the duct is permeable, and that permeability is controlled. Osmoreceptors in the hypothalamus detect a low blood water potential (too little water) and trigger the posterior pituitary to release ADH, which makes the collecting duct insert more water channels (aquaporins), so more water is reabsorbed and a small volume of concentrated urine is produced. Drink too much and ADH falls, the duct closes up, and you make copious dilute urine — negative feedback restoring the blood's water potential either way. Mammals of dry habitats have a very long loop of Henle, building a steeper gradient and the most concentrated urine of all.
DataTwo practicals: choice chambers and a glucose calibration curve — RP10 and RP11
Required practical 10 investigates how an environmental variable changes an animal's movement, using a choice chamber or maze. You create a gradient — humid against dry using damp paper versus a drying agent, or light against dark — introduce small invertebrates such as woodlice or maggots, and after a set time either count how many are in each region (for a taxis) or record their speed and turning (for a kinesis). The independent variable is the condition, the dependent variable is the distribution or the movement, and you control the organisms used, the handling and the time; a distribution can be tested against chance with a chi-squared test. Ethics matter — the animals are handled gently and returned unharmed.
Required practical 11 puts a number on glucose concentration with a colorimetric calibration curve. You make a set of known glucose standards by serial dilution, react each with an excess of Benedict's solution, and measure the colour in a colorimeter (using the complementary filter); plotting the reading against the known concentration gives a calibration curve. An unknown sample — glucose in urine, for a diabetes test — is then read off that curve. It is the quantitative version of the qualitative Benedict's test, and it is how a laboratory turns a colour into a diagnosis.
Read a concentration off a calibration curve. Glucose standards of 0, 2, 4, 6, 8 and 10 mmol dm⁻³ are each heated with an excess of Benedict's solution; the more glucose, the more blue reagent is used up, so the colorimeter absorbance of the remaining blue solution falls steadily as concentration rises. That line is the calibration curve. An unknown urine sample gives an absorbance sitting between the 6 and 8 standards, which reads across to \(7\ \text{mmol dm}^{-3}\). The commonest error is failing to use excess Benedict's: once the reagent runs out at high concentrations the line bends flat, and any reading taken from that region is meaningless.
VocabularyKey terms the mark scheme pays for
TrapsMisconceptions that cost marks
ExamWhat examiners want
This section rewards precise ordered sequences and precise numbers. Learn the reflex arc, the events of the action potential, synaptic transmission and the sliding filament mechanism as strict sequences, and quote the values — about −70 mV at rest, about +40 mV at the peak, three sodium out to two potassium in. Keep the antagonistic pairs straight: sympathetic speeds the heart and parasympathetic slows it; insulin lowers blood glucose and glucagon raises it; ADH is anti-diuretic.
Expect to apply the ideas to unfamiliar contexts — a drug that blocks calcium channels or inhibits acetylcholinesterase, an oscilloscope trace of an action potential, a graph of glucose and insulin after a meal. Read graphs quantitatively (measure the delay, the frequency, the refractory period) and be ready to calculate a conduction speed from distance and time, or read a concentration off a calibration curve. Explain acuity versus sensitivity through retinal convergence, rather than just asserting the difference.
For the required practicals, give the independent, dependent and controlled variables and, for practical 10, the chi-squared test and the ethics of returning animals unharmed. Six-mark answers on homeostasis are marked as a logical line of reasoning: name the receptor, the corrective mechanism and the return to the set point, and stress that separate mechanisms for each direction give finer control. Wherever feedback appears, state explicitly whether it is negative (restores the set point) or positive (amplifies the change). This is heavily synoptic Paper 2 and Paper 3 material — expect it linked back to membranes, ATP and proteins.