Notes · BiologyUK · A-Levels

Organisms respond to changes in their internal and external environments

Survival depends on detecting stimuli and responding appropriately, and on keeping the internal environment stable. This A-level chapter covers simple responses and the reflex arc, receptors and the nervous impulse, synaptic transmission, skeletal muscle contraction, and the homeostatic control of blood glucose and of water balance by the kidney.

6 sections~19 min reading time3 competenciesLevel Standard 1 · Advanced 5

T·0666 / 8

Exam profile

AO1 · Describe nervous and hormonal coordination, muscle contraction and homeostatic controlAO2 · Apply the action-potential and negative-feedback models and interpret glucose and kidney dataAO3 · Analyse data on synaptic transmission and control systems and evaluate treatments for diabetes

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basic level

This whole topic is A-level (A2) only; it is not part of the AS qualification.

higher level

The full A-Level expects the mechanism of the nerve impulse and muscle contraction in detail and the quantitative interpretation of homeostatic data.

Depth

Text

Contents · 6 sections

Organisms respond to changes in their internal and external environments

Survival, responses and the reflex arc#

StandardAQA 7402 3.6.1.1DfE GCE Biology - survival and response

The reflex arc

Fig. 1A fixed pathway that gives a fast, automatic, protective response.

Responding to the environment increases an organism's chance of survival, so the ability to respond is selected for. Simple mobile organisms show taxes and kineses. A taxis is a directional response - the organism moves towards or away from a directional stimulus (for example, woodlice moving away from light, a negative phototaxis). A kinesis is a non-directional response in which the rate of movement or turning changes with the intensity of a non-directional stimulus (for example, woodlice moving faster and turning less in dry air), which tends to bring the organism back to favourable conditions.

Plants respond to directional stimuli by growth responses called tropisms, controlled by the plant growth factor indoleacetic acid (IAA), an auxin. In phototropism, IAA is produced at the shoot tip and diffuses down, but it moves to the shaded side; because IAA causes cell elongation in shoots, the shaded side elongates more and the shoot bends towards the light (positive phototropism). In roots, high IAA concentrations inhibit elongation, so the same redistribution makes roots bend the opposite way - the same substance, opposite effect in different organs.

In animals, a rapid, automatic, protective response is a reflex, carried out by a fixed pathway called the reflex arc. The pathway runs: stimulus, receptor, sensory neurone, a relay (intermediate) neurone in the central nervous system, motor neurone, effector, response. Because the response does not require processing by the conscious brain, it is fast, and because it is automatic it does not have to be learned - both of which increase its protective, survival value.

The survival value of the reflex arc lies precisely in its speed and automatic nature: a spinal reflex such as withdrawing a hand from a hot object protects the body from damage before the brain is even aware, and involuntary reflexes (for example, the pupil reflex) protect delicate structures. The relay neurone also allows the reflex to be modified or overridden by the brain when necessary, but the basic arc can act alone.

Worked example

Explaining positive phototropism

A shoot is illuminated from the left. Explain, using IAA, why it bends to grow towards the light.

IAA production and movement
IAA is produced at the shoot tip and moves to the shaded (right) side.
Effect on cells
In shoots, IAA promotes cell elongation, so cells on the shaded side elongate more than those on the light side.
Result
Unequal elongation makes the shoot bend towards the light - a positive phototropism that maximises light capture for photosynthesis.

Result: IAA accumulates on the shaded side and promotes elongation there, bending the shoot towards the light.

Typical mistakes

Confusing taxis and kinesis, or describing a kinesis as directional.
Leaving the relay neurone out of the reflex arc, or routing the reflex through the conscious brain.

Active revision

Explain how the redistribution of IAA in a shoot tip causes the shoot to grow towards a light source coming from one side.

Active recall

Recall the key points — then reveal.

Sources: GCE AS and A level subject content for the sciences (Department for Education) · AQA A-level Biology 7402 specification (AQA)

Receptors and the nervous impulse#

AdvancedAQA 7402 3.6.1.2DfE GCE Biology - receptors and nerve impulses

An action potential

Fig. 2Depolarisation (sodium in), repolarisation (potassium out), then hyperpolarisation before recovery.

A receptor detects a specific stimulus and is a transducer - it converts the energy of the stimulus into a nerve impulse (a generator potential). The Pacinian corpuscle, a pressure receptor in the skin, illustrates this: pressure deforms its layered (lamellae) structure, stretching the membrane of the sensory neurone; this opens stretch-mediated sodium ion channels, sodium enters, and if enough enters the membrane reaches threshold and an action potential is generated. Each receptor is specific to one type of stimulus because only that stimulus can open its channels.

A neurone at rest maintains a resting potential of about

-70\ \text{mV}

across its membrane, with the inside negative relative to the outside. This is set up by the sodium-potassium pump (which pumps 3 sodium ions out for every 2 potassium ions in, using ATP) together with the membrane being more permeable to potassium than to sodium. The membrane is described as polarised, and this stored electrochemical gradient is the basis of the impulse.

An action potential is a rapid, brief reversal of this potential. When a stimulus depolarises the membrane to a threshold (about

-55\ \text{mV}

), voltage-gated sodium channels open and sodium floods in, depolarising the membrane to about

+40\ \text{mV}

; the sodium channels then close and potassium channels open, so potassium leaves and the membrane repolarises, often overshooting into a brief hyperpolarisation before the resting potential is restored. The action potential is all-or-nothing: any stimulus above threshold produces the same size of impulse, and stimulus intensity is coded by the frequency of impulses, not their size.

After each action potential there is a refractory period during which the sodium channels are recovering and no new action potential can be fired. This ensures action potentials are discrete and travel in one direction only, and it limits their frequency. Speed of conduction is increased by myelination: in myelinated neurones the impulse jumps between the gaps in the myelin sheath (the nodes of Ranvier) in a process called saltatory conduction, which is much faster than continuous conduction along an unmyelinated axon; a wider axon and higher temperature also increase the speed.

\text{resting potential} \approx -70\ \text{mV}; \quad \text{threshold} \approx -55\ \text{mV}

Key potentials

The membrane must depolarise to threshold for the all-or-nothing action potential to fire.

Rods and cones compared

Fig. 3Rods give high sensitivity but low acuity; cones give colour vision and high acuity.

Worked example

Coding stimulus intensity

A neurone fires action potentials of identical size whether the stimulus is moderate or strong. Explain how the nervous system can nevertheless distinguish a strong stimulus from a weak one.

All-or-nothing
Every action potential above threshold is the same size, so amplitude cannot carry intensity information.
Frequency coding
A stronger stimulus generates action potentials at a higher frequency (more per second).
Recruitment
A stronger stimulus may also excite a greater number of neurones; the brain interprets higher frequency and more neurones as a stronger stimulus.

Result: Intensity is coded by the frequency of impulses (and the number of neurones), not their size.

Typical mistakes

Saying a bigger stimulus gives a bigger action potential - it is all-or-nothing; intensity is coded by frequency.
Muddling depolarisation (sodium in) with repolarisation (potassium out).

Active revision

Explain why a myelinated neurone conducts an impulse faster than an unmyelinated neurone of the same diameter.

Active recall

Recall the key points — then reveal.

Sources: GCE AS and A level subject content for the sciences (Department for Education) · AQA A-level Biology 7402 specification (AQA)

Synapses and the neuromuscular junction#

AdvancedAQA 7402 3.6.1.3DfE GCE Biology - synaptic transmission

A cholinergic synapse

Fig. 4Calcium entry triggers acetylcholine release; it binds postsynaptic receptors, then is broken down.

A synapse is the junction between two neurones (or between a neurone and an effector), across which the impulse is transmitted chemically by a neurotransmitter. At a cholinergic synapse the transmitter is acetylcholine. When an action potential arrives at the presynaptic knob, it causes voltage-gated calcium ion channels to open; calcium ions enter and cause vesicles of acetylcholine to fuse with the presynaptic membrane and release the transmitter into the synaptic cleft by exocytosis.

The acetylcholine diffuses across the cleft and binds to specific receptors on the postsynaptic membrane, opening sodium ion channels; sodium enters, depolarising the postsynaptic membrane, and if threshold is reached a new action potential is generated in the next neurone. The transmitter is then broken down (acetylcholine by the enzyme acetylcholinesterase) and the products are reabsorbed into the presynaptic knob to be recycled - which stops continuous stimulation and frees the receptors.

Synapses ensure that impulses travel in one direction only, because the neurotransmitter is made and released only on the presynaptic side and the receptors are only on the postsynaptic side. They also allow integration through summation. In spatial summation, several presynaptic neurones release transmitter together so that enough accumulates to reach threshold; in temporal summation, one presynaptic neurone fires rapidly in succession so that transmitter builds up. Summation lets a postsynaptic neurone act as a decision point, firing only when input is sufficient.

The neuromuscular junction is a specialised synapse between a motor neurone and a skeletal muscle fibre; it too uses acetylcholine. It differs in that it is always excitatory (it always leads to muscle contraction if enough transmitter is released, rather than being a decision point), and the postsynaptic membrane is the muscle fibre membrane, which has many folds and receptors. Understanding synapses also explains how many drugs and toxins act - by mimicking or blocking transmitters, or by inhibiting the enzyme that breaks them down.

Worked example

Effect of an acetylcholinesterase inhibitor

Explain why a chemical that inhibits acetylcholinesterase causes continued stimulation of the postsynaptic neurone.

Normal role of the enzyme
Acetylcholinesterase normally breaks down acetylcholine in the cleft, so receptors are freed and stimulation stops.
Effect of inhibition
If the enzyme is inhibited, acetylcholine is not broken down, so it remains bound to the postsynaptic receptors.
Consequence
Sodium channels stay open and the postsynaptic membrane is repeatedly or continuously depolarised, firing repeated action potentials.

Result: Acetylcholine persists, so the postsynaptic neurone is continuously stimulated.

Typical mistakes

Forgetting the role of calcium ions in triggering vesicle fusion, or the role of the enzyme in breaking down the transmitter.
Confusing spatial summation (several neurones) with temporal summation (one neurone firing rapidly).

Active revision

A drug inhibits acetylcholinesterase. Explain the effect this would have on transmission across a cholinergic synapse.

Active recall

Recall the key points — then reveal.

Sources: GCE AS and A level subject content for the sciences (Department for Education) · AQA A-level Biology 7402 specification (AQA)

Skeletal muscle and the sliding-filament mechanism#

AdvancedAQA 7402 3.6.1.4DfE GCE Biology - muscle contraction

A sarcomere

Fig. 5On contraction the I-band and H-zone shorten while the A-band stays the same.

Skeletal (striated) muscle is made of muscle fibres containing many myofibrils, whose striped appearance comes from the overlap of two protein filaments: thick filaments of myosin and thin filaments of actin. The repeating functional unit is the sarcomere, running from one Z-line to the next; within it are the A-band (the full length of the myosin, appearing dark), the lighter I-band (actin only, no myosin overlap) and the H-zone (myosin only, no actin overlap) in the middle.

Muscle contracts by the sliding-filament mechanism: the actin and myosin filaments slide past one another, shortening the sarcomere, without the filaments themselves changing length. As the sarcomere shortens, the Z-lines are pulled closer, and the I-band and the H-zone both get shorter, while the A-band (the length of the myosin) stays the same. Recognising these band changes is a favourite examined test of whether a student really understands the mechanism.

The mechanism is powered by myosin heads forming cross-bridges with actin. When a nerve impulse arrives, calcium ions are released from the sarcoplasmic reticulum; the calcium binds to tropomyosin, moving it to expose the myosin-binding sites on the actin. Myosin heads then bind, forming cross-bridges, and flex (the power stroke) to pull the actin along; ATP then binds to the myosin head, causing it to detach, and its hydrolysis re-cocks the head ready to bind again further along. This cycle repeats many times, ratcheting the filaments past each other, as long as calcium and ATP are present.

Two energy points are examined. ATP is essential both for the power stroke cycle and for pumping calcium back into the sarcoplasmic reticulum for relaxation. Because muscle stores only a little ATP, it is rapidly regenerated: creatine phosphate acts as an immediate reserve, donating a phosphate to ADP to make ATP anaerobically for a few seconds of intense activity. Slow-twitch fibres, adapted for endurance, have many mitochondria and a good blood supply and respire aerobically; fast-twitch fibres, adapted for short bursts of power, rely more on anaerobic respiration and creatine phosphate.

Band changes on contraction

Fig. 6The A-band never changes because it equals the length of the myosin.

Worked example

The cross-bridge cycle

Describe, in order, the events from calcium release to the sliding of the filaments in a stimulated muscle.

Expose binding sites
Calcium ions released from the sarcoplasmic reticulum bind to tropomyosin, moving it to expose the binding sites on actin.
Cross-bridge and power stroke
Myosin heads bind to actin, forming cross-bridges, and flex (the power stroke), pulling the actin towards the centre of the sarcomere.
Detach and re-cock
ATP binds to each myosin head, causing it to detach; its hydrolysis re-cocks the head, which binds further along and repeats the cycle.

Result: Calcium exposes the sites; myosin heads cycle through binding, power stroke and detachment (using ATP), sliding the filaments.

Typical mistakes

Saying the filaments themselves shorten - they slide past one another; the sarcomere shortens.
Saying the A-band shortens - it stays constant because it is the length of the myosin filament.

Active revision

Explain the roles of calcium ions and ATP in the contraction and subsequent relaxation of a skeletal muscle.

Active recall

Recall the key points — then reveal.

Sources: GCE AS and A level subject content for the sciences (Department for Education) · AQA A-level Biology 7402 specification (AQA)

Homeostasis and the control of blood glucose#

AdvancedAQA 7402 3.6.4.1AQA 7402 3.6.4.2DfE GCE Biology - homeostasis and blood glucose

Negative feedback control of blood glucose

Fig. 7Two antagonistic hormones correct departures in either direction from the set point.

Homeostasis is the maintenance of a stable internal environment within narrow limits, despite changes outside. It matters because enzymes and cells work best under particular conditions: stable temperature keeps enzymes near their optimum, stable pH protects enzyme shape, and stable blood glucose provides a reliable respiratory substrate and the correct water potential of the blood. Homeostatic control is achieved by negative feedback.

Negative feedback works by detecting a deviation from a set point and triggering a response that reverses it, returning the factor towards normal. A receptor detects the change, a coordinator (often the endocrine system) processes it, and an effector brings about the corrective response; the correction then removes the original stimulus. Because separate mechanisms usually control departures in each direction, control is more sensitive - the body can both raise and lower a factor.

Blood glucose is controlled mainly by two antagonistic hormones from the pancreas. When blood glucose rises (for example after a meal), beta cells of the islets of Langerhans secrete insulin, which lowers it: insulin binds to receptors on liver and muscle cells, increasing their uptake of glucose and its conversion to glycogen (glycogenesis) and to fat. When blood glucose falls, alpha cells secrete glucagon, which raises it by stimulating the breakdown of glycogen (glycogenolysis) and the formation of glucose from other molecules (gluconeogenesis) in the liver; adrenaline has a similar raising effect in a fight-or-flight situation.

Insulin and glucagon act on liver cells through the second messenger model, especially glucagon and adrenaline: the hormone binds to a receptor on the cell surface, activating an enzyme that produces cyclic AMP inside the cell, and this second messenger activates further enzymes that break down glycogen. Failure of this control is diabetes: in type 1 the beta cells cannot produce insulin (treated with insulin injections), while in type 2 the cells become less responsive to insulin (managed by diet and exercise). Interpreting glucose-tolerance data and evaluating treatments are core AO2/AO3 tasks.

Worked example

Correcting a rise in blood glucose

Explain the sequence of events that lowers blood glucose after it rises above the normal level.

Detection
The rise is detected by the beta cells of the islets of Langerhans in the pancreas.
Hormone secretion
The beta cells secrete insulin, which binds to receptors on liver and muscle cells.
Effector response
Insulin increases glucose uptake and its conversion to glycogen (glycogenesis) and fat, lowering blood glucose back to normal - which then reduces insulin secretion (negative feedback).

Result: Beta cells release insulin, which promotes glucose uptake and glycogenesis, returning blood glucose to normal.

Typical mistakes

Saying insulin 'turns glucose into glycogen' without the fuller mechanism (increased uptake and glycogenesis in liver/muscle).
Confusing glycogenesis (making glycogen), glycogenolysis (breaking glycogen) and gluconeogenesis (making new glucose).

Active revision

Describe how the body restores a normal blood glucose concentration after a person has eaten a meal rich in carbohydrate.

Active recall

Recall the key points — then reveal.

Sources: GCE AS and A level subject content for the sciences (Department for Education) · AQA A-level Biology 7402 specification (AQA)

The kidney and osmoregulation#

AdvancedAQA 7402 3.6.4.3DfE GCE Biology - the kidney

A nephron

Fig. 8Ultrafiltration at the glomerulus; selective reabsorption and water regulation along the tubule.

The kidney excretes nitrogenous waste (urea) and regulates the water potential of the blood (osmoregulation). Its functional unit is the nephron. Blood enters a knot of capillaries, the glomerulus, in the Bowman's capsule, where ultrafiltration occurs: the blood is under high hydrostatic pressure (the efferent arteriole is narrower than the afferent), forcing water, glucose, ions and urea out of the blood, through the basement membrane which acts as a molecular filter, into the capsule. Blood cells and large proteins are too big to pass and remain in the blood.

The filtrate then flows along the nephron and its composition is adjusted. In the proximal convoluted tubule, selective reabsorption returns all the glucose and much of the salt and water to the blood; glucose is reabsorbed by active transport and co-transport with sodium (the mechanism met in the exchange chapter), and the cells here have microvilli and many mitochondria to support this. By the time the filtrate leaves the proximal tubule, all the useful glucose has been reclaimed.

Water balance is fine-tuned by the loop of Henle and the collecting duct. The loop of Henle acts as a counter-current multiplier: the ascending limb pumps sodium and chloride ions out into the medulla, making the medulla tissue fluid increasingly concentrated (low water potential); as fluid then flows down the descending limb and, crucially, as the filtrate passes down the collecting duct through this concentrated medulla, water leaves it by osmosis and is reabsorbed. A longer loop makes a more concentrated medulla, so desert mammals with long loops can produce very concentrated urine.

The final adjustment is under hormonal control by antidiuretic hormone (ADH), an example of negative feedback. When the blood water potential falls (dehydration), osmoreceptors in the hypothalamus detect it and the posterior pituitary releases more ADH; ADH makes the walls of the collecting duct more permeable to water (by inserting aquaporin channels), so more water is reabsorbed and a small volume of concentrated urine is produced. When the blood is too dilute, less ADH is released, the duct is less permeable, and a large volume of dilute urine is produced - restoring the water potential in each case.

Worked example

The ADH response to dehydration

Describe how ADH restores the blood water potential of a dehydrated person.

Detection
Dehydration lowers the blood water potential; osmoreceptors in the hypothalamus detect this.
Hormone release
The posterior pituitary releases more ADH into the blood.
Effector response
ADH makes the collecting duct walls more permeable to water (more aquaporins), so more water is reabsorbed into the blood; a small volume of concentrated urine is produced and the water potential rises back to normal.

Result: More ADH increases collecting-duct permeability, so more water is reabsorbed and concentrated urine is produced.

Typical mistakes

Saying proteins are reabsorbed - they are too large to be filtered in the first place.
Getting the ADH response backwards (more ADH when dehydrated, giving less, more concentrated urine).

Active revision

Explain how the body responds to restore the water potential of the blood after a person has sweated heavily and become dehydrated.

Active recall

Recall the key points — then reveal.

Sources: GCE AS and A level subject content for the sciences (Department for Education) · AQA A-level Biology 7402 specification (AQA)

References & sources

Sources

Department for Education

GCE AS and A level subject content for the sciences

AQA

AQA A-level Biology 7402 specification

Organisms respond to changes in their internal and external environments

6 sections~19 min reading time3 competenciesLevel Standard 1 · Advanced 5

Organisms respond to changes in their internal and external environments

Key points

Explaining positive phototropism

Key points

Coding stimulus intensity

Key points

Effect of an acetylcholinesterase inhibitor

Key points

The cross-bridge cycle

Key points

Correcting a rise in blood glucose

Key points

The ADH response to dehydration

Sources

Organisms respond to changes in their internal and external environments

Key points

Explaining positive phototropism

Key points

Coding stimulus intensity

Key points

Effect of an acetylcholinesterase inhibitor

Key points

The cross-bridge cycle

Key points

Correcting a rise in blood glucose

Key points

The ADH response to dehydration

Sources