amazon.co.ukA-Level Biology revision on homeostasis and the nervous system: negative feedback, blood glucose control, osmoregulation and the kidney, neurones and action potentials, synapses and thermoregulation, with multi-board exam practice.
Homeostasis maintains a stable internal environment (blood glucose, temperature, water potential, pH, ion concentrations) within set limits around a set point. Every control loop has four components: (1) receptors detecting the deviation (e.g. thermoreceptors in skin and hypothalamus, osmoreceptors in the hypothalamus, glucose-sensing β/α cells in the pancreas); (2) a coordination centre (usually the hypothalamus or endocrine gland) comparing the value with the set point; (3) hormonal or nervous signalling; (4) effectors (muscles, glands) producing the response. Negative feedback is the master principle: any deviation triggers responses that reverse the deviation, returning the value to the set point - e.g. high blood glucose triggers insulin release which lowers it; low glucose triggers glucagon which raises it. Because feedback loops need a deviation to act, homeostasis oscillates slightly around the set point rather than holding it perfectly - a subtlety the exam rewards. Positive feedback amplifies deviations: oxytocin release during childbirth intensifies uterine contractions (more stretch → more oxytocin → stronger contractions); blood clotting (platelet activation attracts more platelets); the sodium influx surge in an action potential. The exam tests whether you can distinguish the two: negative restores, positive amplifies - quote one example of each.
Homeostatic imbalance supplies the application scenarios: blood glucose outside set limits (hyperglycaemia damages vessels; hypoglycaemia starves the brain), core temperature outside limits (proteins denature above ~40 °C; enzymes slow and hypothermia sets in below 35 °C), and blood pH shifts altering enzyme and haemoglobin function. Set points differ between individuals and change with time of day (circadian rhythm) - body temperature peaks in the evening and falls overnight, so the hypothalamic set point is not fixed but cycles; exam questions reward recognising that homeostasis maintains conditions within narrow ranges, not exact values, and that oscillation around the set point is normal because feedback responds to deviations with a lag.
Blood glucose is controlled by the islets of Langerhans in the pancreas: β-cells (secrete insulin) and α-cells (secrete glucagon), both working by negative feedback around ~90 mg per 100 cm³. When glucose rises (after a meal): β-cells detect it and secrete insulin, which increases glucose uptake into cells via GLUT transporters (more transporters in muscle/fat membranes), promotes glycogenesis (glucose → glycogen) in liver and muscle, raises the rate of respiration of glucose, and converts excess glucose to fat. When glucose falls (fasting, exercise): α-cells secrete glucagon, which binds receptors on hepatocytes and activates adenylyl cyclase, producing cAMP (second messenger); cAMP activates phosphorylase for glycogenolysis (glycogen → glucose) and gluconeogenesis (glucose from glycerol/amino acids). Adrenaline also raises glucose via the same cAMP pathway in fight-or-flight. The second-messenger cascade is the A* detail: one glucagon molecule activates many adenylyl cyclase molecules, each producing many cAMP molecules, each activating many phosphorylase molecules - amplification explaining why tiny hormone concentrations have large effects.
Diabetes: type 1 - autoimmune destruction of β-cells, so no insulin is produced; onset in childhood; treated with insulin injections and blood-glucose monitoring; glucose cannot be taken up without insulin, so blood glucose rises (hyperglycaemia) and glucose appears in urine. type 2 - insulin resistance: receptors/transporters respond weakly, β-cells eventually decline; associated with obesity, age and inactivity; treated first with diet, exercise and metformin (increases insulin sensitivity), later insulin. Exam questions ask for the differences in cause, onset and treatment - learn the 3-row comparison. Response curves (glucose tolerance tests) and negative-feedback graphs are standard interpretation questions.
Osmoregulation controls blood water potential. The kidney contains ~1 million nephrons: Bowman's capsule (ultrafiltration), proximal convoluted tubule (PCT), loop of Henle, distal convoluted tubule (DCT) and collecting duct (CD). Ultrafiltration: high blood pressure (from the afferent arteriole being wider than the efferent) forces water, glucose, ions, urea and amino acids out of the glomerulus through the basement membrane into the capsule - proteins and cells are too large to pass (hence protein in urine indicates kidney damage). Selective reabsorption in the PCT: all glucose and amino acids (co-transport with Na⁺, as in the ileum), most ions and much water are reabsorbed (microvilli, many mitochondria). The loop of Henle is a counter-current multiplier (from the existing site content): the descending limb is permeable to water but not ions - water leaves by osmosis into the increasingly concentrated medulla; the ascending limb is impermeable to water - Na⁺ and Cl⁻ are actively transported out, concentrating the medulla and diluting the filtrate; because flow runs in opposite directions, the gradient is maintained and multiplied down the medulla (deepest at the tip); urine leaving the collecting duct equilibrates with the medullary gradient - long loops (desert mammals) produce more concentrated urine. ADH control: osmoreceptors in the hypothalamus detect low blood water potential; the hypothalamus signals the posterior pituitary to release ADH; ADH binds receptors on DCT/collecting-duct cells, activating cAMP and causing vesicles of aquaporins to fuse with the membrane, increasing water permeability; more water is reabsorbed, producing small volumes of concentrated urine; high water potential suppresses ADH, producing dilute urine - negative feedback. Kidney failure questions: dialysis (filtering blood against a dialysate with the right gradient) vs transplant (immune rejection, immunosuppressants).
Neurones: sensory (receptor → CNS; cell body in a dorsal root ganglion), relay/intermediate (within CNS), motor (CNS → effector); myelinated axons (Schwann cells) conduct faster by saltatory conduction (impulse jumps between nodes of Ranvier), up to ~120 m s⁻¹ vs ~2 m s⁻¹ unmyelinated. The resting potential of about -70 mV is maintained by the Na⁺/K⁺ pump (actively transports 3 Na⁺ out and 2 K⁺ in using ATP) and K⁺ leak channels (K⁺ diffuses out down its gradient, making the inside negative); the membrane is impermeable to Na⁺ at rest.
The action potential (from the existing site content): (1) a stimulus depolarises the membrane to threshold (~-55 mV); (2) voltage-gated Na⁺ channels open - Na⁺ floods in, depolarising to ~+40 mV (positive feedback: more Na⁺ in → more channels open); (3) voltage-gated Na⁺ channels close and K⁺ channels open - K⁺ leaves, repolarising the membrane; (4) brief hyperpolarisation (below -70 mV) before the refractory period resets the channels; (5) the Na⁺/K⁺ pump restores the resting potential. The impulse is all-or-nothing: sub-threshold stimuli produce no impulse; stronger stimuli increase frequency, not amplitude - the standard explanation for how intensity is coded. The refractory period ensures one-way transmission (the section behind cannot fire) and limits maximum frequency - a guaranteed explanation point. Myelination, axon diameter (larger = faster) and temperature (faster to a point) all increase conduction speed - know all three for the comparison questions.
Saltatory conduction earns its own marks: myelin (Schwann cell membranes wrapped around the axon) insulates the axon, so depolarisation can only occur at the nodes of Ranvier; the impulse jumps node to node, travelling much faster (~120 m s⁻¹) and using less ATP (fewer Na⁺/K⁺ pumps active over the length); demyelinating diseases (multiple sclerosis) slow or block conduction - the standard application question. All-or-nothing needs the precise statement: a stimulus below threshold produces no impulse at all; at or above threshold, a full-sized action potential fires; stimulus strength is therefore coded by frequency of impulses, not their amplitude - larger stimuli also recruit more neurones. Axon diameter increases conduction speed (less internal resistance) and temperature increases speed to a point (faster diffusion) before proteins denature.
Synaptic transmission at a cholinergic synapse (from the existing site content): (1) the action potential arrives at the presynaptic knob, opening voltage-gated Ca²⁺ channels; (2) Ca²⁺ enters, causing synaptic vesicles to fuse with the presynaptic membrane, releasing acetylcholine (ACh) by exocytosis; (3) ACh diffuses across the cleft and binds receptors on the postsynaptic membrane, opening Na⁺ channels; (4) depolarisation above threshold generates a new action potential; (5) acetylcholinesterase hydrolyses ACh into choline and ethanoic acid (choline is reabsorbed to reform ACh), preventing continuous stimulation. Synapses are unidirectional (vesicles only on one side, receptors only on the other) and show summation: temporal (rapid repeated releases from one neurone add up) or spatial (simultaneous releases from several neurones) can together reach threshold - the basis of integration. Synapses also allow inhibition (inhibitory neurotransmitters open Cl⁻/K⁺ channels, hyperpolarising) and amplification (few molecules release many ions). Neuromuscular junction: same mechanism but the postsynaptic membrane is the muscle sarcolemma (always excitatory, ACh). Drugs act on synapses: nicotine (mimics ACh), curare (blocks receptors), SSRIs (block serotonin reuptake) - a standard application question.
Thermoregulation (AQA 3.6.1.2; OCR 5.1.1): thermoreceptors in the skin (peripheral) and hypothalamus (central, monitoring blood temperature) feed the hypothalamic thermoregulatory centre, which compares core temperature with the set point (~37 °C). Cooling responses (temperature above set point): vasodilation of skin arterioles (more blood near the surface, more heat radiated), sweating (evaporation loses heat), less metabolic activity, hairs flatten (erector muscles relax). Warming responses (below set point): vasoconstriction, shivering (involuntary muscle contraction releases heat), raised metabolic rate via thyroxine/adrenaline, hairs erect (trapping insulating air). Both arms are negative feedback - identify receptors, coordination and effectors in any scenario. Hypothermia (core below 35 °C) and fever (set point reset by pyrogens) are the standard application scenarios: in fever the set point rises, so normal temperature feels cold and the body warms itself until the fever breaks. When answering, always name the receptor, the coordination centre and the effector with the specific response - three linked marks per mechanism.