Neural Signaling & Homeostasis

Complete Study Guide

Topics Covered

1. Neural Signaling (C2.2)
2. Homeostasis (D3.3)
3. Chemical Signaling (C2.1)
4. Integration of Body Systems (C3.1) HL
5. Mixed Practice — Exam Style

Aligned to IB Biology HL 2025 syllabus — C2.2, D3.3, C2.1, C3.1

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Watch: Neural Signaling & Homeostasis

Stephanie Castle · 8 min · Action potentials, resting potential, impulse propagation along myelinated axons

Stephanie Castle · 7 min · Negative feedback loops, blood glucose regulation, thermoregulation

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Section 1: Neural Signaling (C2.2)

The nervous system enables rapid communication between different parts of the body. Signals travel as electrical impulses along neurons and are transmitted between neurons via chemical messengers (neurotransmitters) at synapses. Understanding the structure of neurons, the ionic basis of nerve impulses, and synaptic transmission is essential for IB Biology HL.

1.1 Neuron Structure

Neurons are specialised cells that transmit electrical signals. Although neurons vary in shape, most share a common set of structural features.

There are three main types of neuron: sensory neurons (carry impulses from receptors to the CNS), motor neurons (carry impulses from the CNS to effectors), and relay neurons (interneurons; connect sensory and motor neurons within the CNS).

1.2 Resting Potential

When a neuron is not transmitting a signal, it maintains a resting potential of approximately $-70 \text{ mV}$ across its membrane. The inside of the axon is negatively charged relative to the outside. This charge difference is called the membrane potential.

The resting potential is established and maintained by:

1. The $\text{Na}^+$/$\text{K}^+$ ATPase pump — actively transports 3 $\text{Na}^+$ out and 2 $\text{K}^+$ in per cycle, using one molecule of ATP. This creates a net outward movement of positive charge.
2. Potassium leak channels — the membrane is more permeable to $\text{K}^+$ than to $\text{Na}^+$ at rest. $\text{K}^+$ diffuses out through leak channels, making the inside more negative.
3. Large intracellular anions — negatively charged proteins and organic molecules inside the cell cannot cross the membrane.

1.3 Action Potential

An action potential is a rapid, temporary reversal of the membrane potential that travels along the axon as a nerve impulse. It follows an all-or-nothing principle: if the stimulus reaches the threshold (approximately $-55 \text{ mV}$), a full action potential is generated; if not, nothing happens.

Phases of the action potential:

1. Resting state — membrane at $-70 \text{ mV}$; voltage-gated $\text{Na}^+$ and $\text{K}^+$ channels are closed.
2. Depolarization — a stimulus causes voltage-gated $\text{Na}^+$ channels to open; $\text{Na}^+$ rushes in (down its electrochemical gradient); the membrane potential rises rapidly toward $+40 \text{ mV}$.
3. Repolarization — $\text{Na}^+$ channels inactivate (close); voltage-gated $\text{K}^+$ channels open; $\text{K}^+$ rushes out; the membrane potential returns toward resting level.
4. Hyperpolarization — $\text{K}^+$ channels are slow to close, so $\text{K}^+$ continues to leave the cell, briefly driving the potential below $-70 \text{ mV}$ (to about $-90 \text{ mV}$).
5. Return to resting potential — $\text{K}^+$ channels close; the $\text{Na}^+$/$\text{K}^+$ ATPase pump restores the original ion distribution.

1.4 Myelination and Saltatory Conduction (HL)

HL

In myelinated neurons, the myelin sheath acts as an electrical insulator, preventing ion exchange across the membrane where it is present. Ion channels are concentrated at the nodes of Ranvier — the small gaps between adjacent Schwann cells.

The action potential “jumps” from node to node. This is called saltatory conduction (from the Latin saltare, to jump). Saltatory conduction dramatically increases the speed of impulse transmission:

• Unmyelinated axon: ~1—2 m/s (continuous conduction)
• Myelinated axon: ~100—120 m/s (saltatory conduction)

1.5 Synaptic Transmission

Neurons communicate at junctions called synapses. Most synapses are chemical synapses, where the signal is carried across the synaptic cleft by neurotransmitters.

Steps of synaptic transmission:

1. An action potential arrives at the presynaptic axon terminal.
2. Voltage-gated $\text{Ca}^{2+}$ channels open; $\text{Ca}^{2+}$ enters the terminal.
3. $\text{Ca}^{2+}$ triggers synaptic vesicles to fuse with the presynaptic membrane (exocytosis).
4. Neurotransmitter is released into the synaptic cleft (~20 nm wide).
5. Neurotransmitter binds to specific receptors on the postsynaptic membrane.
6. This binding opens (or closes) ligand-gated ion channels, generating a postsynaptic potential.
7. The signal is terminated by: (a) enzymatic breakdown of the neurotransmitter, (b) reuptake into the presynaptic neuron, or (c) diffusion away from the cleft.

1.6 Neurotransmitters: Excitatory vs Inhibitory

Neurotransmitters can be classified by their effect on the postsynaptic neuron:

• An excitatory postsynaptic potential (EPSP) depolarizes the membrane, making it more likely to reach threshold and fire an action potential.
• An inhibitory postsynaptic potential (IPSP) hyperpolarizes the membrane, making it less likely to fire.
• Summation — a postsynaptic neuron integrates multiple EPSPs and IPSPs. If the sum exceeds the threshold, an action potential is triggered. Summation can be temporal (rapid signals from one synapse) or spatial (simultaneous signals from multiple synapses).

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Section 2: Homeostasis (D3.3)

Homeostasis is the maintenance of a relatively constant internal environment despite changes in external conditions. It is essential for enzyme function, cell integrity, and survival.

2.1 Negative Feedback Loops

Most homeostatic mechanisms use negative feedback: the response opposes the change, returning the variable to its set point. This produces oscillations around the set point rather than a perfectly stable value.

The negative feedback model:

Stimulus (deviation from set point) $\rightarrow$ Receptor (detects change) $\rightarrow$ Coordinator (processes signal) $\rightarrow$ Effector (produces response) $\rightarrow$ Variable returns toward set point $\rightarrow$ Receptor detects return $\rightarrow$ Response diminishes

2.2 Thermoregulation

Humans are endotherms — we maintain a core body temperature of approximately 37 degrees C regardless of the external temperature. The hypothalamus acts as the thermostat, receiving input from thermoreceptors in the skin and blood.

Response to overheating (above 37 degrees C):

Mechanism	How it works
Vasodilation	Arterioles near the skin surface dilate; more blood flows near the surface; more heat is lost by radiation
Sweating	Sweat glands secrete sweat; evaporation of water from the skin removes heat (latent heat of vaporization)
Behavioural responses	Seeking shade, removing clothing, reducing activity
Reduced metabolic heat production	Less cellular respiration generates less heat

Response to cooling (below 37 degrees C):

Mechanism	How it works
Vasoconstriction	Arterioles near the skin surface constrict; less blood flows near the surface; less heat is lost
Shivering	Involuntary rapid muscle contractions generate heat from increased cellular respiration
Piloerection	Erector pili muscles contract, raising body hairs; traps an insulating layer of air (minimal effect in humans)
Behavioural responses	Adding clothing, curling up, seeking warmth
Increased metabolic rate	Thyroxine and adrenaline increase basal metabolic rate over time

2.3 Blood Glucose Regulation

Blood glucose concentration is maintained at approximately 4—6 mmol/L (fasting) by the hormones insulin and glucagon, both produced by the islets of Langerhans in the pancreas.

Key terms:

• Glycogenesis — synthesis of glycogen from glucose (stimulated by insulin)
• Glycogenolysis — breakdown of glycogen to glucose (stimulated by glucagon)
• Gluconeogenesis — synthesis of new glucose from non-carbohydrate sources such as amino acids, glycerol, and lactate (stimulated by glucagon)

2.4 Osmoregulation

Osmoregulation is the control of water potential (osmolarity) of the blood. The kidney is the primary organ responsible for this, under the control of antidiuretic hormone (ADH).

Kidney structure — the nephron:

The functional unit of the kidney is the nephron. Each kidney contains approximately 1 million nephrons. Key structures:

The Loop of Henle — Countercurrent Multiplier:

The loop of Henle creates a concentration gradient in the kidney medulla that allows the collecting duct to produce concentrated urine. This is the countercurrent multiplier mechanism:

1. Descending limb — permeable to water, impermeable to ions. Water leaves by osmosis as the filtrate passes into the increasingly concentrated medulla. The filtrate becomes more concentrated as it descends.
2. Ascending limb — impermeable to water, actively pumps $\text{Na}^+$ and $\text{Cl}^-$ out into the medulla. The filtrate becomes more dilute as it ascends, while the medullary interstitial fluid becomes more concentrated.
3. The countercurrent flow (descending and ascending limbs running in opposite directions) multiplies the osmotic gradient, creating a very high solute concentration deep in the medulla.

ADH and Water Reabsorption:

Antidiuretic hormone (ADH), also called vasopressin, is produced by the hypothalamus and released from the posterior pituitary gland.

• When blood is too concentrated (high osmolarity, e.g. after sweating or low water intake):

  • Osmoreceptors in the hypothalamus detect the change
  • More ADH is released
  • ADH makes the collecting duct walls more permeable to water (by inserting aquaporin channels)
  • More water is reabsorbed from the collecting duct back into the blood
  • Small volume of concentrated urine is produced

• When blood is too dilute (low osmolarity, e.g. after drinking a large volume of water):

  • Less ADH is released
  • Collecting duct walls become less permeable to water
  • Less water is reabsorbed
  • Large volume of dilute urine is produced

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Section 3: Chemical Signaling (C2.1)

3.1 Hormones and Glands

Hormones are chemical messengers secreted by endocrine glands directly into the blood. They travel to target cells with specific receptors and produce a response.

3.2 Signal Transduction: First and Second Messengers

Many hormones are hydrophilic (e.g. peptide hormones like insulin, glucagon, ADH) and cannot cross the cell membrane. They bind to receptors on the cell surface and trigger an intracellular signaling cascade.

First messenger: The hormone itself (e.g. adrenaline binding to a receptor on a liver cell).

Second messenger: An intracellular molecule produced in response to the first messenger that amplifies the signal inside the cell. The most common second messenger is cyclic AMP (cAMP).

Signal transduction pathway (cAMP example):

1. Hormone (first messenger) binds to a G-protein-coupled receptor on the cell surface.
2. The receptor activates a G-protein on the inner surface of the membrane.
3. The activated G-protein activates the enzyme adenylyl cyclase.
4. Adenylyl cyclase converts ATP $\rightarrow$ cAMP (the second messenger).
5. cAMP activates protein kinases (enzymes that phosphorylate other proteins).
6. A cascade of protein phosphorylation amplifies the signal and produces the cellular response.

Steroid hormones (e.g. estrogen, testosterone, cortisol) are hydrophobic and can cross the cell membrane directly. They bind to intracellular receptors (often in the nucleus) and act as transcription factors, directly activating or repressing gene expression. No second messenger is needed.

3.3 Neural vs Hormonal Signaling

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Section 4: Integration of Body Systems (C3.1) HL

The nervous system and endocrine system do not operate in isolation. In a living organism, coordinated responses require integration — multiple organ systems communicating through both neural and hormonal pathways. C3.1 focuses on how the body achieves this integration, with the hypothalamus as the central link between the two systems.

4.1 The Hypothalamus-Pituitary Axis

The hypothalamus is the key integration point between the nervous and endocrine systems. It is a brain structure (part of the CNS) that also functions as an endocrine organ, controlling the pituitary gland — often called the “master gland” because its hormones regulate many other endocrine glands.

4.2 The Fight-or-Flight Response: Neuroendocrine Integration

The fight-or-flight response is a classic example of how the nervous and endocrine systems work together to produce a rapid, coordinated, whole-body response to a perceived threat.

Sequence of events:

1. A threat is perceived by the cerebral cortex and relayed to the hypothalamus.
2. The hypothalamus activates two parallel pathways:

Pathway 1 — Neural (fast, seconds):

• The hypothalamus stimulates the sympathetic nervous system.
• Sympathetic neurons directly innervate target organs: heart (increases rate and force), bronchioles (dilate), pupils (dilate), gut (decreases activity), blood vessels to skeletal muscle (dilate).
• Sympathetic neurons also stimulate the adrenal medulla.

Pathway 2 — Hormonal (sustained, minutes to hours):

• The adrenal medulla releases adrenaline (epinephrine) and noradrenaline (norepinephrine) into the blood.
• These hormones reinforce and prolong the neural effects: increased heart rate, increased blood glucose (via glycogenolysis in the liver), redirection of blood flow to muscles, bronchodilation.
• The hypothalamus also triggers the HPA axis (hypothalamus $\rightarrow$ CRH $\rightarrow$ anterior pituitary $\rightarrow$ ACTH $\rightarrow$ adrenal cortex $\rightarrow$ cortisol). Cortisol sustains the stress response over hours by maintaining blood glucose and suppressing non-essential functions (immune response, digestion).

4.3 Osmoregulation: Integration of Nervous, Endocrine, and Renal Systems

Osmoregulation is an excellent example of three organ systems working together through negative feedback. The kidney’s ability to concentrate or dilute urine depends on signals from the nervous and endocrine systems.

Integrated pathway — response to dehydration:

1. Detection (nervous): Osmoreceptors in the hypothalamus detect increased blood osmolarity (more concentrated blood).
2. Neural signaling: The hypothalamus sends nerve impulses that trigger two responses:
   • Stimulates the thirst centre in the cerebral cortex (behavioural response — drink water)
   • Stimulates neurosecretory cells in the hypothalamus to increase ADH synthesis
3. Hormonal signaling (endocrine): More ADH is released from the posterior pituitary into the blood.
4. Target organ response (renal): ADH travels via the blood to the kidneys. ADH binds to receptors on collecting duct cells, triggering insertion of aquaporin water channels into the apical membrane.
5. Effect: More water is reabsorbed from the collecting duct into the medullary interstitial fluid and then into the blood. A small volume of concentrated urine is produced.
6. Negative feedback: As blood osmolarity returns to normal, osmoreceptors detect the change, ADH release decreases, and fewer aquaporins are present — restoring the balance.

4.4 The Medulla Oblongata: Autonomic Integration Centre

The medulla oblongata (in the brainstem) is the primary integration centre for autonomic (involuntary) functions. It continuously monitors and adjusts vital processes without conscious input.

4.5 Negative Feedback Across Multiple Organ Systems

C3.1 requires you to understand how negative feedback loops connect the nervous, endocrine, and other organ systems in an integrated network. Here are the key multi-system feedback loops you need to know:

1. Thyroid regulation (HPT axis):

Hypothalamus $\rightarrow$ TRH $\rightarrow$ Anterior pituitary $\rightarrow$ TSH $\rightarrow$ Thyroid gland $\rightarrow$ Thyroxine ($\text{T}_4$)

Thyroxine increases metabolic rate. When thyroxine levels are sufficient, it inhibits both the hypothalamus (less TRH) and the anterior pituitary (less TSH) — negative feedback at two levels.

2. Stress response (HPA axis):

Hypothalamus $\rightarrow$ CRH $\rightarrow$ Anterior pituitary $\rightarrow$ ACTH $\rightarrow$ Adrenal cortex $\rightarrow$ Cortisol

Cortisol inhibits both CRH release from the hypothalamus and ACTH release from the anterior pituitary. This prevents the stress response from escalating indefinitely.

3. Blood calcium regulation:

• Low blood $\text{Ca}^{2+}$ $\rightarrow$ parathyroid glands release PTH $\rightarrow$ increased $\text{Ca}^{2+}$ reabsorption in kidneys, increased $\text{Ca}^{2+}$ release from bone, increased vitamin D activation (which increases $\text{Ca}^{2+}$ absorption from gut)
• High blood $\text{Ca}^{2+}$ $\rightarrow$ thyroid C-cells release calcitonin $\rightarrow$ decreased bone resorption, increased $\text{Ca}^{2+}$ excretion

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Mixed Practice — Exam Style

1. [Resting Potential] The resting potential of a neuron is approximately $-70 \text{ mV}$. Which of the following contributes most directly to maintaining this resting potential?

   A. Voltage-gated $\text{Na}^+$ channels being open at rest

   B. Equal concentrations of $\text{Na}^+$ and $\text{K}^+$ on both sides of the membrane

   C. $\text{K}^+$ diffusing out of the cell through leak channels, making the inside more negative relative to the outside

   D. Active transport of $\text{Ca}^{2+}$ out of the axon

2. [Synaptic Transmission] A drug blocks the reuptake of serotonin from the synaptic cleft. The most likely effect is:

   A. Serotonin is broken down faster in the synapse

   B. Serotonin remains in the synaptic cleft longer, prolonging its effect on the postsynaptic neuron

   C. The presynaptic neuron stops releasing serotonin

   D. The postsynaptic neuron becomes permanently depolarized

3. [Thermoregulation] On a hot day, the hypothalamus detects a rise in core body temperature. Which response would help cool the body?

   A. Vasoconstriction of arterioles near the skin surface

   B. Increased shivering thermogenesis

   C. Vasodilation of arterioles near the skin surface and increased sweating

   D. Piloerection to trap a layer of warm air

4. [Blood Glucose] After a 24-hour fast, blood glucose is maintained primarily by:

   A. Continued absorption of glucose from the small intestine

   B. Insulin stimulating glucose uptake by muscle cells

   C. Glucagon stimulating glycogenolysis and gluconeogenesis in the liver

   D. ADH increasing water reabsorption to concentrate glucose in the blood

5. [Action Potential] During the absolute refractory period of an action potential, the neuron cannot fire again because:

   A. All $\text{K}^+$ channels are closed and cannot open

   B. The $\text{Na}^+$/$\text{K}^+$ pump is temporarily inactive

   C. Voltage-gated $\text{Na}^+$ channels are inactivated and cannot reopen until the membrane repolarizes

   D. The threshold has permanently increased to $+40 \text{ mV}$

6. [Osmoregulation] A person drinks 2 litres of water in a short period. Which sequence correctly describes the homeostatic response?

   A. Blood osmolarity rises $\rightarrow$ more ADH released $\rightarrow$ more water reabsorbed $\rightarrow$ concentrated urine

   B. Blood osmolarity falls $\rightarrow$ less ADH released $\rightarrow$ collecting duct less permeable to water $\rightarrow$ large volume of dilute urine

   C. Blood osmolarity falls $\rightarrow$ more ADH released $\rightarrow$ more water reabsorbed $\rightarrow$ concentrated urine

   D. Blood osmolarity rises $\rightarrow$ less ADH released $\rightarrow$ dilute urine produced

7. [Myelination — HL] Saltatory conduction in myelinated neurons is faster than continuous conduction because:

   A. Myelin increases the diameter of the axon, allowing more ions to flow

   B. The action potential jumps between nodes of Ranvier, skipping the insulated myelinated regions

   C. Myelination increases the number of ion channels along the entire axon

   D. Schwann cells actively pump $\text{Na}^+$ along the axon

8. [Signal Transduction] Adrenaline binds to a receptor on a liver cell, activating adenylyl cyclase. What is the role of cAMP in this pathway?

   A. cAMP is the first messenger that travels through the blood to the liver

   B. cAMP acts as a second messenger inside the cell, amplifying the signal by activating protein kinases

   C. cAMP directly breaks down glycogen into glucose

   D. cAMP binds to DNA to activate gene transcription

9. [Neurotransmitters] GABA is the main inhibitory neurotransmitter in the brain. When GABA binds to receptors on the postsynaptic membrane, the most likely effect is:

   A. $\text{Na}^+$ channels open, causing depolarization

   B. $\text{Cl}^-$ channels open, causing hyperpolarization (IPSP), making the postsynaptic neuron less likely to fire

   C. $\text{Ca}^{2+}$ channels open, triggering neurotransmitter release

   D. $\text{K}^+$ leak channels close, causing depolarization

10. [Negative Feedback — Integration] A student claims that “negative feedback always returns a variable to exactly its set point.” Evaluate this claim:

    A. Correct — negative feedback mechanisms are perfectly precise and always restore the exact set point

    B. Incorrect — negative feedback produces oscillations around the set point; the variable is maintained within a narrow range but is never held at a single exact value

    C. Correct — the hypothalamus acts as a perfect thermostat with zero error

    D. Incorrect — negative feedback amplifies deviations, so the variable moves further from the set point over time

Show Answers

1. C — The resting potential is primarily maintained by $\text{K}^+$ diffusing out through leak channels (the membrane is ~40x more permeable to $\text{K}^+$ than $\text{Na}^+$ at rest). This outward movement of positive charge makes the inside of the cell negative. A is incorrect — voltage-gated $\text{Na}^+$ channels are closed at rest. B is incorrect — ion concentrations are very different on each side. D is not directly relevant to the resting potential.

2. B — Blocking reuptake means serotonin stays in the synaptic cleft longer and continues to bind to postsynaptic receptors, prolonging and enhancing its effect. This is the mechanism of SSRI antidepressants (selective serotonin reuptake inhibitors). A is the opposite effect. C and D are not direct consequences of blocking reuptake.

3. C — Vasodilation increases blood flow near the skin surface, increasing heat loss by radiation. Sweating enables evaporative cooling. A and B would increase body temperature (vasoconstriction conserves heat; shivering generates heat). D traps heat, the opposite of what is needed.

4. C — During prolonged fasting, glucagon from alpha cells stimulates glycogenolysis (breakdown of stored glycogen) and gluconeogenesis (synthesis of glucose from amino acids, glycerol, and lactate) in the liver to maintain blood glucose. A is incorrect after 24 hours. B would lower, not maintain, blood glucose. D does not affect blood glucose concentration.

5. C — During the absolute refractory period, voltage-gated $\text{Na}^+$ channels are in an inactivated state (distinct from being simply closed). They cannot reopen until the membrane has repolarized sufficiently. This ensures the action potential propagates in one direction. A is incorrect — $\text{K}^+$ channels are open during repolarization. B is incorrect — the pump works continuously.

6. B — Drinking a large volume of water dilutes the blood (lowers osmolarity). The hypothalamus detects this and reduces ADH secretion. Less ADH means fewer aquaporins are inserted in the collecting duct wall, so less water is reabsorbed and a large volume of dilute urine is produced, restoring blood osmolarity to normal.

7. B — In saltatory conduction, the action potential effectively jumps from one node of Ranvier to the next. Between nodes, the myelin sheath prevents ion exchange, so the electrical signal travels rapidly as a local current through the myelinated region. This is much faster than continuous depolarization along every segment of an unmyelinated axon. A is incorrect — myelin does not change axon diameter. C is incorrect — ion channels are concentrated at nodes, not distributed along the whole axon.

8. B — cAMP is the second messenger. When adrenaline (first messenger) activates adenylyl cyclase via a G-protein, adenylyl cyclase converts ATP to cAMP. cAMP then activates protein kinases inside the cell, creating a cascade that amplifies the original signal. A confuses first and second messenger. C is incorrect — cAMP activates enzymes that break down glycogen, not cAMP directly. D describes steroid hormone action.

9. B — GABA opens $\text{Cl}^-$ channels on the postsynaptic membrane. $\text{Cl}^-$ enters the cell, making the inside more negative (hyperpolarization). This inhibitory postsynaptic potential (IPSP) makes it harder for the neuron to reach threshold and fire. A describes an excitatory effect. C describes presynaptic $\text{Ca}^{2+}$ influx, not a postsynaptic GABA effect.

10. B — Negative feedback does not achieve perfect precision. The response takes time to act, and the effector may overshoot or undershoot the set point, producing oscillations. Body temperature, for example, fluctuates slightly around 37 degrees C throughout the day. A and C are incorrect because no biological system operates with zero error. D describes positive feedback, not negative feedback.

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May 2026 Prediction Questions

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Question 1 — Synaptic Transmission and Pharmacology [8 marks]

(a) Outline the sequence of events that occurs at a cholinergic synapse when an action potential arrives at the presynaptic terminal. [4 marks]

(b) Organophosphate nerve agents inhibit acetylcholinesterase, the enzyme that breaks down acetylcholine in the synaptic cleft. Predict and explain the effects on the postsynaptic neuron and on the organism. [3 marks]

(c) State one other way in which a drug could modify synaptic transmission, giving an example. [1 mark]

Model Answer:

(a) Action potential arrives at presynaptic terminal (1); calcium ion channels open and $\text{Ca}^{2+}$ enters the terminal (1); vesicles containing acetylcholine fuse with the presynaptic membrane by exocytosis (1); acetylcholine diffuses across the synaptic cleft and binds to receptors on the postsynaptic membrane, triggering an EPSP (1).

(b) Acetylcholine accumulates in the cleft (1); the postsynaptic neuron is continuously stimulated — the EPSP is prolonged and repeated (1); at the organism level, this causes uncontrolled muscle contraction (convulsions), paralysis of respiratory muscles, and potentially death due to respiratory failure (1).

(c) A drug could block postsynaptic receptors (antagonist), e.g. curare blocks nicotinic acetylcholine receptors at the neuromuscular junction, causing muscle paralysis. Accept any valid example: SSRIs blocking serotonin reuptake; beta-blockers blocking adrenaline receptors. (1)

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Question 2 — Blood Glucose Regulation and Diabetes [7 marks]

(a) Explain how blood glucose is regulated after a high-carbohydrate meal, naming the hormones and target organs involved. [4 marks]

(b) Compare Type 1 and Type 2 diabetes mellitus in terms of cause, insulin levels, and treatment. [3 marks]

Model Answer:

(a) Blood glucose rises after a meal (1); beta cells in the islets of Langerhans detect the rise and secrete insulin (1); insulin stimulates glucose uptake by liver and muscle cells (via GLUT4 transporters) and promotes glycogenesis (glycogen synthesis) in the liver (1); blood glucose returns to the set point (approximately 5 mmol/L), completing the negative feedback loop (1).

(b)

	Type 1	Type 2
Cause	Autoimmune destruction of beta cells	Insulin resistance (cells don’t respond to insulin) / reduced insulin secretion
Insulin level	Very low / absent	Normal or elevated initially, may fall over time
Treatment	Daily insulin injections (cannot be managed by diet alone)	Diet, exercise, oral hypoglycaemics (e.g. metformin); insulin in later stages

Award 1 mark per correctly compared row, maximum 3.

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Question 3 — Osmoregulation and ADH [6 marks]

(a) Explain the role of antidiuretic hormone (ADH) in regulating blood osmolarity when a person is dehydrated. [3 marks]

(b) A patient with diabetes insipidus cannot produce ADH. Predict the effect on urine volume and osmolarity, and explain the consequences for blood osmolarity. [3 marks]

Model Answer:

(a) Dehydration causes blood osmolarity to rise above the set point (1); osmoreceptors in the hypothalamus detect this and trigger the posterior pituitary to release more ADH into the blood (1); ADH increases the permeability of the collecting duct of the kidney tubule (by inserting aquaporins), so more water is reabsorbed by osmosis back into the blood, reducing osmolarity and producing small volumes of concentrated urine (1).

(b) Without ADH, the collecting duct remains relatively impermeable to water (1); very large volumes of dilute urine are produced (polyuria) because water is not reabsorbed (1); blood osmolarity rises above normal (hyperosmolarity/hypernatraemia), which — if untreated — can cause dehydration, cellular damage, and neurological symptoms (1).

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IB Biology HL — Neural Signaling & Homeostasis — Complete Study Guide — 2025 Syllabus — Good luck!