AQA A-Level Biology 3.6 Organisms respond to changes in their internal and external environments: deep dive on the nerve impulse, synapses, muscle, homeostasis and the kidney

What section 3.6 actually demands

Section 3.6 is the topic that turns biology into a story about signalling and control. Every sub-topic answers the same underlying question: how does an organism detect a change and bring about a response that keeps it alive or that returns its internal environment to normal? The examiner therefore rewards two linked skills. The first is precise sequence recall of the named processes (the action potential, the cholinergic synapse, the cross-bridge cycle, the ADH feedback loop). The second is application: predicting the effect of a drug, a lesion, or a change in conditions on one of these processes.

This guide knits the seven dot points together so you can see the through-line: a stimulus is detected by a receptor, an electrical impulse is conducted along a neurone, it crosses a synapse, and it triggers an effector such as a muscle or a gland. The same logic of detection and negative-feedback correction runs through blood glucose and water potential control. Master the spine and the detail attaches to it.

Stimuli, responses and the survival value of detection

A stimulus is a detectable change in the internal or external environment; a response is the change it brings about. Responding raises an organism's chance of survival, and AQA frames this at three levels.

Simple mobile organisms use taxes and kineses. A taxis is a directional response, moving the whole body towards (positive) or away from (negative) a directional stimulus, such as a maggot moving away from light. A kinesis is non-directional: the rate of movement and turning change with the intensity of the stimulus, with no preferred direction. Woodlice in dry air move fast and turn little (so leave the dry area) and in humid air slow down and turn often (so stay), accumulating where conditions reduce water loss.

Plants use tropisms, directional growth responses controlled by the auxin indoleacetic acid (IAA). The single fact that unlocks every tropism question is that IAA has opposite effects in shoots and roots: it stimulates cell elongation in shoots but inhibits it in roots. So when IAA accumulates on the shaded or lower side, a shoot bends towards the light (the shaded side elongates more) and a root bends downwards (the lower side elongates less).

Animals with nervous systems use the reflex arc for fast, automatic protection: receptor, sensory neurone, relay neurone, motor neurone, effector. The pathway is short and bypasses conscious processing in the brain, which is exactly why it is fast enough to protect the body from harm before you are aware of the threat.

The nerve impulse: from resting potential to saltatory conduction

The resting potential of about -70 mV is the foundation. Three facts establish it: the sodium-potassium pump moves 3 Na+ out for every 2 K+ in; this builds gradients of high Na+ outside and high K+ inside; and the membrane is more permeable to K+ than Na+, so potassium leaks out faster than sodium leaks in, leaving the inside negative.

An action potential is a brief, all-or-nothing reversal of this potential. A stimulus that depolarises the membrane to the threshold (about -55 mV) opens voltage-gated sodium channels; Na+ floods in and the potential rises to about +40 mV (depolarisation). The sodium channels then close and voltage-gated potassium channels open; K+ leaves and the membrane repolarises, briefly overshooting (hyperpolarisation) before the resting potential is restored.

The all-or-nothing principle is examined relentlessly: above threshold a full, fixed-size action potential is always produced; below threshold, none. A stronger stimulus does not make a bigger action potential, it increases the frequency of action potentials. That is how stimulus intensity is coded.

Three factors speed conduction: myelination, larger axon diameter and higher temperature. Myelination matters most. The myelin sheath insulates the membrane so depolarisation occurs only at the nodes of Ranvier, and the impulse jumps node to node, which is saltatory conduction. The refractory period that follows each action potential ensures the impulse travels in one direction only, separates discrete impulses, and limits their maximum frequency.

Crossing the gap: synaptic transmission

A synapse converts an electrical impulse into a chemical signal and back. At a cholinergic synapse the steps are fixed and must be given in order:

1. The action potential depolarises the presynaptic membrane, opening voltage-gated calcium channels; Ca2+ diffuses in.
2. Calcium triggers synaptic vesicles to fuse with the presynaptic membrane, releasing acetylcholine by exocytosis.
3. Acetylcholine diffuses across the cleft and binds receptors on the postsynaptic membrane.
4. Sodium channels open, Na+ enters and the postsynaptic membrane depolarises; if threshold is reached an action potential is generated.
5. Acetylcholinesterase hydrolyses the acetylcholine, stopping the signal and allowing recycling.

The neuromuscular junction is the same machinery applied to a muscle, with one important difference: it is always excitatory, so it always triggers contraction rather than potentially inhibiting the next cell.

Two features of synapses are favourite exam points. Summation lets sub-threshold inputs add up: spatial summation (several presynaptic neurones firing onto one postsynaptic neurone at once) and temporal summation (one neurone firing repeatedly). And unidirectionality follows simply from structure: only the presynaptic side makes and releases neurotransmitter, and only the postsynaptic side has receptors.

This sub-topic is also where drug application questions live. An agonist mimics or boosts the neurotransmitter; an antagonist blocks the receptor or release; an acetylcholinesterase inhibitor leaves acetylcholine in the cleft, causing continuous stimulation. Read the described mechanism and reason from it.

Receptors as transducers

A receptor is a transducer: it converts a specific stimulus into a generator potential, a small depolarisation that, if it reaches threshold, fires an action potential in the sensory neurone. Receptors are specific to one stimulus type, and a bigger stimulus gives a bigger generator potential.

The Pacinian corpuscle detects changes in pressure. Pressure deforms its lamellae, stretches the membrane, and widens stretch-mediated sodium channels; Na+ enters and produces a generator potential. It responds to change rather than steady pressure.

Rods and cones are the two retinal photoreceptors, and the whole sub-topic turns on their wiring. Many rods connect to one bipolar neurone (retinal convergence), so their generator potentials sum (spatial summation) and let rods work in dim light (high sensitivity), but two close points produce only one impulse so acuity is low, and rhodopsin gives only monochrome vision. Each cone connects to its own neurone, so there is no summation (low sensitivity, needs bright light) but close points are resolved separately (high acuity), and three iodopsin types give colour vision. Rods sit in the periphery; cones cluster at the fovea.

Effectors: skeletal muscle and the sliding filament theory

Muscle is the classic effector. A sarcomere, the repeating unit between two Z lines, contains thin actin and thick myosin filaments. When the muscle contracts the I band and H zone shorten and the Z lines move closer, but the A band stays the same, because the filaments slide rather than shorten.

The sliding filament cycle must be told as a story with calcium and ATP in their roles:

1. Ca2+ is released from the sarcoplasmic reticulum and binds troponin, moving tropomyosin off the binding sites on actin.
2. Myosin heads bind actin, forming cross-bridges.
3. The power stroke bends the heads, pulling actin over myosin and shortening the sarcomere; ADP and Pi are released.
4. ATP binds the myosin head, which detaches.
5. ATPase hydrolyses ATP, recocking the head to repeat the cycle while Ca2+ is present.

ATP is therefore needed for detachment, recocking and pumping Ca2+ back during relaxation, which is why rigor mortis (no ATP after death) locks the cross-bridges.

Slow twitch fibres are aerobic, rich in mitochondria, myoglobin and capillaries, and resist fatigue (endurance, postural muscles). Fast twitch fibres are anaerobic, store glycogen and phosphocreatine for rapid ATP, and fatigue quickly (sprinting, eye muscles).

Homeostasis: negative feedback and blood glucose

Homeostasis maintains a constant internal environment by negative feedback: detect a change, then respond to reverse it. Using separate mechanisms to raise and to lower a factor gives finer control.

Blood glucose is the worked example. The islets of Langerhans in the pancreas contain beta cells (secrete insulin when glucose is high) and alpha cells (secrete glucagon when glucose is low). Insulin lowers glucose by increasing glucose uptake (more transporter proteins), promoting glycogenesis, and raising respiration. Glucagon raises glucose by glycogenolysis (breaking glycogen down) and gluconeogenesis (making glucose from non-carbohydrate sources). Keep the three liver processes distinct: glycogen-esis makes glycogen, glycogeno-lysis breaks it, gluconeo-genesis makes new glucose.

Glucagon and adrenaline act through the second messenger model: the hormone binds a membrane receptor, activates adenylate cyclase, which converts ATP to cyclic AMP (cAMP); cAMP activates an enzyme cascade that carries out glycogenolysis. Learn this as a named chain.

Diabetes is the application. Type 1 is a failure to make insulin (beta cells destroyed), treated with insulin injections. Type 2 is insulin resistance (receptors stop responding), managed by diet, weight loss and exercise. In both, untreated high blood glucose exceeds the kidney's reabsorptive capacity, so glucose appears in the urine.

Osmoregulation: the nephron and ADH

The kidney both excretes urea and osmoregulates by controlling the water potential of the blood. The nephron runs: Bowman's capsule (glomerulus), proximal convoluted tubule, loop of Henle, distal convoluted tubule, collecting duct.

Ultrafiltration happens in the Bowman's capsule: because the efferent arteriole is narrower than the afferent, glomerular hydrostatic pressure is high and forces small molecules through the basement membrane, while proteins and cells stay in the blood. Selective reabsorption in the proximal convoluted tubule recovers all glucose and amino acids by co-transport with sodium (active transport), aided by microvilli and many mitochondria; water follows by osmosis.

The loop of Henle is a countercurrent multiplier. The ascending limb is impermeable to water and actively pumps ions out into the medulla, lowering its water potential; the descending limb is permeable to water, which leaves by osmosis. The opposing flow maintains a steep gradient so that the collecting duct can reabsorb water and make concentrated urine.

Finally, ADH controls blood water potential by negative feedback. When osmoreceptors in the hypothalamus detect a fall in water potential, the posterior pituitary releases more ADH, which inserts more aquaporins into the collecting duct, increasing water reabsorption and producing a small volume of concentrated urine. When water potential is too high, less ADH is released, less water is reabsorbed, and dilute urine is produced.

How section 3.6 is examined

A typical AQA profile for this topic:

• Multiple choice and short answer. Labelling action potential graphs, identifying ion movements, naming nephron regions, distinguishing taxis from kinesis, reading the sarcomere bands.
• Structured (4 to 6 marks). Describe the cholinergic synapse, the sliding filament cycle, the resting potential, ultrafiltration, or the ADH feedback loop in order.
• Application and data (5 to 6 marks). Predict a drug's effect at a synapse, interpret nerve conduction or kidney data, or explain a diabetes scenario. These reward precise, named, mechanism-led reasoning.

Check your knowledge

A mix of definitional, mechanism, and exam-style multi-part questions across section 3.6. Attempt them under timed conditions, then check against the solutions.

1. Distinguish between a taxis and a kinesis, and explain how a kinesis keeps woodlice in a humid environment. (4 marks)
2. (a, 4) Explain how the resting potential of about -70 mV is established. (b, 4) Using the values -70 mV, -55 mV and +40 mV, describe the changes in membrane potential and ion movements during an action potential. (c, 2) Explain the importance of the refractory period. (10 marks)
3. Describe the sequence of events by which an action potential arriving at a cholinergic synapse generates an action potential in the postsynaptic neurone. (6 marks)
4. (a, 3) Explain why rod cells allow vision in dim light. (b, 3) Explain why cone cells give greater visual acuity than rod cells. (6 marks)
5. (a, 5) Describe the sliding filament theory of muscle contraction, including the roles of calcium ions and ATP. (b, 2) Explain why muscles stiffen during rigor mortis. (7 marks)
6. (a, 4) Describe how insulin and glucagon control blood glucose concentration. (b, 4) Describe the second messenger model by which glucagon raises blood glucose. (c, 3) Compare the causes of type 1 and type 2 diabetes. (11 marks)
7. (a, 3) Explain how ultrafiltration occurs in the Bowman's capsule. (b, 4) Explain how the loop of Henle enables the production of concentrated urine. (c, 4) Describe how the body responds to a fall in blood water potential. (11 marks)