AQA A-level Biology · 3.6

Organisms respond to changes in their internal and external environments

50 revision questions with answers for 3.6 Organisms respond to changes in their internal and external environments in AQA A-level Biology (spec 7402). Practise with flashcards, a topic quiz, a random quiz across the course, 5 crosswords, or read every question and answer below.

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Question 1 · Spec 3.6.1.1 · Stimulus and reflex · Recall
How does a three-neurone reflex protect an organism?
Answer:
A receptor detects a stimulus and generates activity in a sensory neurone. A relay neurone transmits to a motor neurone, which activates an effector such as a muscle. The rapid, automatic response can reduce injury before conscious processing is complete.
Question 2 · Spec 3.6.1.1 · Taxes and kineses · Recall
Distinguish a taxis from a kinesis.
Answer:
A taxis is directional movement towards or away from a stimulus. A kinesis changes speed or turning rate according to stimulus intensity, without directing movement towards its source. Both can increase time spent in favourable conditions.
Question 3 · Spec 3.6.1.1, RP10 · Required practical 10 · Practical
How can a choice chamber test an animal's response to humidity?
Answer:
Provide humid and dry regions while controlling light, temperature and other variables. Place animals centrally, allow acclimatisation and record positions at fixed intervals. Repeat with sides reversed to test position bias. Keep conditions within the animals' tolerances and minimise handling.
Question 4 · Spec 3.6.1.1 · Phototropism · Application
How does IAA explain a shoot bending towards unilateral light?
Answer:
IAA is redistributed towards the shaded side of a shoot. At suitable concentrations, IAA stimulates cell elongation there. Greater elongation on the shaded side bends the shoot towards the light, improving light capture for photosynthesis.
Question 5 · Spec 3.6.1.1 · Gravitropism · Application
How can IAA cause shoots to grow upwards and roots downwards?
Answer:
Gravity leads to more IAA on the lower side. This stimulates elongation in shoots, bending them upwards. Roots are more sensitive, so the higher concentration inhibits elongation on the lower side. Faster upper-side growth bends the root downwards.
Question 6 · Spec 3.6.1.2 · Pacinian corpuscle · Recall
How does pressure produce a generator potential in a Pacinian corpuscle?
Answer:
Pressure deforms the layers of the corpuscle and the sensory-neurone membrane. Stretch-mediated sodium channels open, allowing sodium ions to enter down their electrochemical gradient. This depolarises the membrane, creating a generator potential.
Question 7 · Spec 3.6.1.2, 3.6.2.1 · Generator potentials · Recall
How do generator potentials differ from action potentials?
Answer:
Generator potentials are graded, so their size varies with stimulus strength. If depolarisation reaches threshold, action potentials are initiated. Action potentials are all-or-nothing events of similar amplitude; stronger stimuli can be represented by a higher impulse frequency.
Question 8 · Spec 3.6.1.2 · Rods and cones · Recall
How do rods and cones differ in sensitivity and colour detection?
Answer:
Rods respond at low light intensity but do not provide colour discrimination. Cones need higher light intensity and different cone types respond to different wavelength ranges, allowing colour vision. Differences in their visual pigments contribute to these properties.
Question 9 · Spec 3.6.1.2 · Visual acuity · Application
Why do rods provide high sensitivity while cones can provide high visual acuity?
Answer:
Many rods converge onto a shared pathway, allowing summation but reducing the ability to identify the precise source of light. Cone pathways, especially in the fovea, have less convergence, so stimulation of nearby cones can be distinguished more accurately.
Question 10 · Spec 3.6.1.3 · Myogenic heart · Recall
How do the SAN, AVN and Purkyne tissue coordinate a heartbeat?
Answer:
The SAN initiates electrical activity that spreads across the atria. Non-conducting tissue prevents direct spread to ventricles. The AVN delays transmission, then activity passes along the bundle of His and Purkyne tissue, producing ventricular contraction from the apex upwards.
Question 11 · Spec 3.6.1.3 · Heart-rate control · Recall
How do chemoreceptors, pressure receptors and autonomic pathways adjust heart rate?
Answer:
Chemoreceptors in the carotid and aortic bodies detect blood chemical changes, including reduced pH associated with increased carbon dioxide. Pressure receptors in carotid sinuses and the aortic arch detect stretch. Cardiovascular centres in the medulla alter sympathetic and parasympathetic output to the SAN, increasing or decreasing heart rate.
Question 12 · Spec 3.6.2.1 · Motor neurone · Application
How is a myelinated motor neurone adapted to transmit impulses?
Answer:
Dendrites receive inputs and the cell body maintains the cell. A long axon carries action potentials towards the effector. Myelin insulates sections of axon, leaving nodes of Ranvier where action potentials are regenerated. Terminal branches communicate with target cells.
Question 13 · Spec 3.6.2.1 · Resting potential · Recall
How is the resting potential maintained?
Answer:
The sodium-potassium pump uses ATP to move three sodium ions out for every two potassium ions moved in, maintaining concentration gradients. At rest, the membrane is more permeable to potassium than sodium. Potassium movement out leaves the inside relatively negative.
Question 14 · Spec 3.6.2.1 · Action potential · Recall
How is depolarisation generated once threshold is reached?
Answer:
Voltage-gated sodium channels open and sodium ions enter rapidly down their electrochemical gradient. Depolarisation opens more channels through positive feedback. The inside becomes briefly positive relative to the outside. Once threshold is reached, an action potential of standard amplitude follows.
Question 15 · Spec 3.6.2.1 · Repolarisation · Recall
How does the membrane repolarise and briefly become hyperpolarised?
Answer:
Sodium channels become inactivated and voltage-gated potassium channels open. Potassium leaves the axon, making the inside negative again. Delayed potassium-channel closure can cause hyperpolarisation. Pumps and leak pathways maintain the ionic gradients over time.
Question 16 · Spec 3.6.2.1 · Impulse propagation · Recall
How does an action potential move along an unmyelinated axon?
Answer:
Sodium entry creates local currents that depolarise adjacent membrane to threshold, opening its voltage-gated sodium channels. The action potential is regenerated along the axon. The region behind is refractory, helping prevent immediate backward propagation.
Question 17 · Spec 3.6.2.1 · Refractory period · Application
Why is the refractory period important?
Answer:
Sodium channels need time to recover from inactivation, and the membrane may be hyperpolarised. This separates action potentials, limits maximum impulse frequency and helps ensure forward propagation along an axon after the preceding region has fired.
Question 18 · Spec 3.6.2.1 · Conduction speed · Application
How do myelination, axon diameter and temperature affect impulse conduction speed?
Answer:
Myelin enables saltatory conduction between nodes, increasing speed. A larger axon diameter reduces internal resistance to local currents. Increasing temperature within a suitable range speeds channel processes, although excessive temperature can disrupt proteins and nerve function.
Question 19 · Spec 3.6.2.1, MS 0.2 · Impulse frequency calculation · Calculation
A neurone has a minimum refractory interval of 2.5 ms. Estimate its theoretical maximum impulse frequency.
Answer:
Convert 2.5 ms to 0.0025 s. Maximum frequency is approximately 1/0.0025 = 400 impulses s⁻¹, or 400 Hz. This is a theoretical limit based on the stated interval; actual firing rates depend on additional physiological conditions.
Question 20 · Spec 3.6.2.2 · Synaptic release · Recall
What causes acetylcholine release at a cholinergic synapse?
Answer:
An action potential depolarises the presynaptic membrane and opens voltage-gated calcium channels. Calcium ions enter and cause synaptic vesicles to fuse with the presynaptic membrane. Acetylcholine is released by exocytosis and diffuses across the synaptic cleft.
Question 21 · Spec 3.6.2.2 · Postsynaptic response · Recall
How does acetylcholine produce a postsynaptic response?
Answer:
Acetylcholine binds complementary receptors on the postsynaptic membrane. Receptor-associated ion channels open, allowing ion movement that depolarises the membrane. If the combined depolarisation reaches threshold, voltage-gated channels initiate an action potential in the postsynaptic neurone.
Question 22 · Spec 3.6.2.2 · Direction and removal · Recall
Why is chemical synaptic transmission unidirectional, and how is acetylcholine removed?
Answer:
Vesicles release transmitter from the presynaptic side, while receptors are on the postsynaptic side. Acetylcholinesterase hydrolyses acetylcholine, preventing continued stimulation. Choline is taken back into the presynaptic neurone for acetylcholine resynthesis, allowing repeated signalling.
Question 23 · Spec 3.6.2.2 · Summation · Recall
Distinguish temporal and spatial summation.
Answer:
Temporal summation occurs when closely spaced inputs from one presynaptic neurone produce overlapping postsynaptic potentials. Spatial summation combines inputs from several presynaptic neurones. Their net effect may reach threshold even if an individual input would be insufficient.
Question 24 · Spec 3.6.2.2 · Inhibition and drugs · Application
How can an inhibitory synapse reduce firing, and how could a receptor-blocking drug affect transmission?
Answer:
An inhibitory input can open chloride or potassium channels, producing an inhibitory postsynaptic effect and making threshold harder to reach. A drug blocking acetylcholine receptors reduces their activation. Predict effects from the stated target, binding and channel behaviour.
Question 25 · Spec 3.6.2.2 · Neuromuscular junction · Recall
Compare a neuromuscular junction with a cholinergic neurone-to-neurone synapse.
Answer:
Both use calcium-triggered acetylcholine release, diffusion, specific receptors and acetylcholinesterase. A neuromuscular junction has a motor neurone communicating with a muscle fibre and is excitatory. Its postsynaptic membrane is folded, and a normal motor impulse usually triggers a muscle action potential.
Question 26 · Spec 3.6.3 · Skeletal muscle organisation · Recall
How is skeletal muscle organised, and why do muscles act in antagonistic pairs?
Answer:
A muscle contains bundles of long muscle fibres. Each fibre contains many myofibrils made of repeating sarcomeres. Muscles generate pulling forces by contracting, so antagonistic muscles pull on opposite sides of a joint to produce movement in opposing directions.
Question 27 · Spec 3.6.3 · Sarcomeres · Recall
What changes in a sarcomere during contraction?
Answer:
Actin filaments slide further between myosin filaments. Z lines move closer together, and the I band and H zone become narrower. The A band's width stays constant because the myosin filaments do not shorten. Actin filament length also remains constant.
Question 28 · Spec 3.6.3 · Calcium and tropomyosin · Recall
How do calcium ions permit actin-myosin binding?
Answer:
A muscle action potential causes calcium release from the sarcoplasmic reticulum. Calcium causes tropomyosin to move away from myosin-binding sites on actin. Myosin heads can then attach, forming actinomyosin bridges. Calcium removal allows the binding sites to be covered again.
Question 29 · Spec 3.6.3 · Cross-bridge cycle · Recall
Describe the roles of myosin heads and ATP in the sliding-filament mechanism.
Answer:
A myosin head binds actin and pivots, pulling the actin filament. ATP binding causes detachment. ATP hydrolysis provides energy to reset the head so it can attach further along. Repeated cycles shorten the sarcomere while calcium remains available.
Question 30 · Spec 3.6.3 · Muscle energy · Application
What are the roles of ATP and phosphocreatine in muscle contraction?
Answer:
ATP supports myosin detachment and resetting and powers calcium pumping back into the sarcoplasmic reticulum. Phosphocreatine transfers phosphate to ADP, rapidly regenerating ATP during brief high demand. Its limited store must subsequently be replenished.
Question 31 · Spec 3.6.3 · Muscle fibres · Recall
Compare slow and fast skeletal muscle fibres.
Answer:
Slow fibres contract more slowly, resist fatigue and have many mitochondria, abundant myoglobin and a rich capillary supply for aerobic respiration. Fast fibres contract rapidly and strongly, usually have greater glycogen and phosphocreatine stores, and fatigue sooner. Fibre proportions vary among muscles.
Question 32 · Spec 3.6.4.1 · Homeostasis · Application
Why must core temperature, blood pH and blood glucose be maintained within limits?
Answer:
Temperature and pH affect enzyme activity and protein structure. Glucose supplies respiratory substrate, while excessive blood glucose lowers blood water potential. Keeping conditions within suitable limits supports cell function despite changes in the external environment or activity.
Question 33 · Spec 3.6.4.1 · Feedback · Recall
Distinguish negative from positive feedback.
Answer:
Negative feedback produces a response that opposes a departure from the normal range, helping restore conditions. Positive feedback reinforces the initial change until a particular endpoint. A receptor, coordinating centre and effector form a control pathway; identify them using the information supplied.
Question 34 · Spec 3.6.4.1, 3.6.4.2 · Antagonistic control · Application
Why can separate mechanisms for opposite departures improve homeostatic control?
Answer:
Different effectors can correct increases and decreases independently, providing more precise regulation over a wider range. Insulin reduces raised blood glucose, while glucagon raises low blood glucose. Each pathway reduces its own initiating stimulus through negative feedback.
Question 35 · Spec 3.6.4.2 · Liver metabolism · Recall
Define glycogenesis, glycogenolysis and gluconeogenesis.
Answer:
Glycogenesis converts glucose into glycogen for storage. Glycogenolysis breaks glycogen down to release glucose. Gluconeogenesis produces glucose from non-carbohydrate substrates such as glycerol and amino acids. The liver can adjust these pathways to regulate blood glucose.
Question 36 · Spec 3.6.4.2 · Insulin · Recall
How does insulin lower blood glucose?
Answer:
Pancreatic beta cells release insulin when blood glucose rises. Insulin binds to receptors on target cells, increasing glucose uptake in responsive tissues by increasing membrane glucose transport proteins. It also activates enzymes that promote glycogenesis, reducing blood glucose.
Question 37 · Spec 3.6.4.2 · Glucagon · Recall
How does glucagon increase blood glucose?
Answer:
When blood glucose falls, pancreatic alpha cells release glucagon. It binds to liver-cell receptors and activates pathways promoting glycogenolysis and gluconeogenesis. Glucose is released into blood. As the concentration rises, the stimulus for further glucagon secretion decreases.
Question 38 · Spec 3.6.4.2 · Second messengers · Recall
How do glucagon and adrenaline use the second-messenger model?
Answer:
Hormone binding to a cell-surface receptor activates adenylate cyclase, which converts ATP to cyclic AMP. cAMP activates protein kinase, initiating enzyme activation that promotes glycogen breakdown. The cascade amplifies the signal. Adrenaline helps increase glucose availability during heightened activity.
Question 39 · Spec 3.6.4.2 · Diabetes · Recall
Compare the causes and control of type I and type II diabetes.
Answer:
Type I involves loss of insulin-producing beta cells and requires insulin replacement with monitored glucose control. Type II involves reduced target-cell responsiveness to insulin and may also involve impaired secretion. Diet and activity changes, medication and sometimes insulin can help control it.
Question 40 · Spec 3.6.4.2, RP11, MS 2.3 · Required practical 11 · Calculation
How would you make 10 cm³ glucose standards of 0, 2, 4 and 6 mmol dm⁻³ from a 10 mmol dm⁻³ stock?
Answer:
Use 0, 2, 4 and 6 cm³ of stock respectively, adding water to 10 cm³ in each case. The dilution relation is C1V1 = C2V2. Mix thoroughly and label standards clearly before applying the same colorimetric procedure.
Question 41 · Spec 3.6.4.2, RP11 · Required practical 11 · Practical
How can colorimetry determine glucose in an unknown model urine sample?
Answer:
Treat standards and the unknown with the same glucose-detection reagents and timing. For a Benedict's method, heat consistently, remove precipitate if measuring residual blue solution, and use an appropriate filter and blank. Plot a calibration curve, interpolate the unknown and correct for any dilution.
Question 42 · Spec 3.6.4.3 · Glomerular filtration · Recall
How is glomerular filtrate formed?
Answer:
High hydrostatic pressure in glomerular capillaries drives water and small dissolved substances through the filtration barrier into Bowman's capsule. Blood cells and most plasma proteins are retained. The filtrate contains substances including glucose, ions, water and urea.
Question 43 · Spec 3.6.4.3 · Proximal convoluted tubule · Recall
How are glucose and water reabsorbed in the proximal convoluted tubule?
Answer:
Sodium gradients maintained by ATP-driven pumps support sodium-glucose co-transport from filtrate into epithelial cells. Glucose then moves into blood. Solute reabsorption lowers water potential outside the tubule, so water follows by osmosis. Microvilli and many mitochondria support these processes.
Question 44 · Spec 3.6.4.3 · Loop of Henle · Recall
How does the loop of Henle establish a medullary gradient?
Answer:
The ascending limb transfers sodium and chloride ions into the medulla and is relatively impermeable to water. The descending limb is permeable to water, which leaves by osmosis. Opposing flows help maintain a concentrated medulla, allowing water reabsorption from collecting ducts.
Question 45 · Spec 3.6.4.3 · Distal tubule and collecting duct · Recall
How do the distal convoluted tubule and collecting duct contribute to osmoregulation?
Answer:
They allow further regulated reabsorption of water from filtrate. Water moves by osmosis towards the lower water potential of surrounding tissue and blood. ADH increases water permeability, particularly in collecting ducts, allowing the body to conserve more water.
Question 46 · Spec 3.6.4.3 · ADH pathway · Recall
What happens when blood water potential becomes too low?
Answer:
Osmoreceptors in the hypothalamus detect the change. ADH made in the hypothalamus is released from the posterior pituitary. It increases insertion of aquaporins into collecting-duct cell membranes, increasing water reabsorption. A smaller volume of more concentrated urine is produced.
Question 47 · Spec 3.6.4.3 · Water-potential feedback · Application
How is ADH secretion reduced when blood water potential rises?
Answer:
Less stimulation of hypothalamic osmoreceptors reduces ADH release. Collecting ducts become less permeable to water as fewer aquaporins remain in their membranes. Less water is reabsorbed, producing a larger volume of more dilute urine and opposing the initial rise in water potential.
Question 48 · Spec 3.6.4.3, MS 0.3 · Osmoregulation data · Calculation
After dehydration, urine volume falls from 1.6 to 0.6 dm³ per day. Calculate the percentage decrease and explain it.
Answer:
Decrease = 1.0 dm³ per day. Percentage decrease = (1.0/1.6) x 100 = 62.5%. Dehydration lowers blood water potential, increasing ADH release and collecting-duct permeability, so more water is reabsorbed and less is lost in urine.
Question 49 · Spec 3.6.4.3 · Interpreting hormone data · Application
A drug blocks ADH receptors. Predict its effect on urine and explain why increased ADH might not correct the effect.
Answer:
Fewer receptors respond to ADH, so collecting ducts insert fewer aquaporins and reabsorb less water. Urine volume rises and becomes more dilute. Increased ADH may have limited effect because the pathway is blocked at the receptor; the result depends on the nature of the blockade.
Question 50 · Spec 3.6.2.1, 3.6.3, 3.6.4.3 · Synoptic link · Synoptic
Why is ATP important in nervous communication, muscle contraction and kidney function?
Answer:
ATP maintains neuronal ion gradients through sodium-potassium pumps. In muscle it supports cross-bridge cycling and calcium reuptake. In kidney tubules it maintains sodium gradients used in selective reabsorption. These processes connect respiration with coordinated responses and homeostasis.

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