CIE AS/A Level Biology -15.1 Control and coordination in mammals- Study Notes- New Syllabus
CIE AS/A Level Biology -15.1 Control and coordination in mammals- Study Notes- New Syllabus
Ace A level Biology Exam with CIE AS/A Level Biology -15.1 Control and coordination in mammals- Study Notes- New Syllabus
Key Concepts:
- describe the features of the endocrine system with reference to the hormones ADH, glucagon and insulin (see 14.1.8, 14.1.9 and 14.1.10)
- compare the features of the nervous system and the endocrine system
- describe the structure and function of a sensory neurone and a motor neurone and state that intermediate neurones connect sensory neurones and motor neurones
- outline the role of sensory receptor cells in detecting stimuli and stimulating the transmission of impulses in sensory neurones
- describe the sequence of events that results in an action potential in a sensory neurone, using a chemoreceptor cell in a human taste bud as an example
- describe and explain changes to the membrane potential of neurones, including:
• how the resting potential is maintained
• the events that occur during an action potential
• how the resting potential is restored during the refractory period - describe and explain the rapid transmission of an impulse in a myelinated neurone with reference to saltatory conduction
- explain the importance of the refractory period in determining the frequency of impulses
- describe the structure of a cholinergic synapse and explain how it functions, including the role of calcium ions
- describe the roles of neuromuscular junctions, the T-tubule system and sarcoplasmic reticulum in stimulating contraction in striated muscle
- describe the ultrastructure of striated muscle with reference to sarcomere structure using electron micrographs and diagrams
- explain the sliding filament model of muscular contraction including the roles of troponin, tropomyosin, calcium ions and ATP
Endocrine System & Hormone Examples
🌟 General Features of the Endocrine System
- The endocrine system is made up of glands and cells that secrete hormones directly into the bloodstream.
- Hormones are chemical messengers that travel in blood to target cells with specific receptors.
- Key features:
- Hormones act at low concentrations but produce large effects (signal amplification).
- They produce slower, longer-lasting responses compared to the nervous system.
- Hormone secretion is usually regulated by negative feedback to maintain homeostasis.
📌 Hormone Examples
1. Antidiuretic Hormone (ADH)
- Secreted by: Posterior pituitary gland (produced by hypothalamus).
- Target: Collecting ducts of kidneys.
- Action: Increases water reabsorption by inserting aquaporins into collecting duct membranes.
- Feature shown: Endocrine control of osmoregulation.
2. Insulin
- Secreted by: β-cells of the islets of Langerhans (pancreas).
- Target: Liver, muscle, fat cells.
- Action: Increases glucose uptake, stimulates glycogenesis (glucose → glycogen), lowers blood glucose.
- Feature shown: Negative feedback to control blood glucose homeostasis.
3. Glucagon
- Secreted by: α-cells of the islets of Langerhans (pancreas).
- Target: Liver cells.
- Action: Stimulates glycogenolysis and gluconeogenesis, raising blood glucose levels.
- Feature shown: Negative feedback during low blood glucose conditions.
📊 Summary Table
| Hormone | Source | Target | Effect | Role in Homeostasis |
|---|---|---|---|---|
| ADH | Posterior pituitary | Kidney collecting ducts | ↑ Water reabsorption | Maintains water balance (osmoregulation) |
| Insulin | Pancreatic β-cells | Liver, muscle, fat | ↓ Blood glucose (↑ uptake, ↑ glycogenesis) | Maintains glucose levels (high → normal) |
| Glucagon | Pancreatic α-cells | Liver | ↑ Blood glucose (↑ glycogenolysis, ↑ gluconeogenesis) | Maintains glucose levels (low → normal) |
✅ In short:
The endocrine system maintains homeostasis using hormones like:
• ADH → water balance
• Insulin → lowers blood glucose
• Glucagon → raises blood glucose
Each hormone acts on specific target cells via the bloodstream and is controlled by negative feedback.
Nervous System vs. Endocrine System
🌟 Similarities
- Both are involved in coordination and control of body functions.
- Both rely on communication between cells.
- Both help maintain homeostasis.
📊 Comparison Table
| Feature | Nervous System | Endocrine System |
|---|---|---|
| Mode of transmission | Electrical impulses (neurones) + neurotransmitters at synapses | Hormones transported in blood |
| Speed of response | Very fast (milliseconds) | Slower (seconds to hours, sometimes days) |
| Duration of effect | Short-lived | Long-lasting |
| Specificity | Impulses travel to specific target cells via neurones | Hormones reach all cells, but act only on target cells with receptors |
| Type of response | Immediate, rapid, short-term (e.g. reflexes, muscle contraction) | Gradual, long-term (e.g. growth, metabolism, osmoregulation) |
| Examples | Reflex arc, movement, pain response | Insulin regulating glucose, ADH regulating water balance |
| Energy use | High (neuronal firing requires ATP) | Relatively low (hormones secreted in small amounts) |
📌 Summary:
• Nervous system → fast, precise, short-term control.
• Endocrine system → slower, widespread, long-term regulation.
• Both systems work together to maintain homeostasis.
Structure & Function of Neurones
Sensory Neurone
Structure
- Cell body: Located off to the side of the axon.
- Dendrites: Receive impulses from receptors (e.g. in skin, eyes, ears).
- Long dendron: Carries impulse towards cell body.
- Axon: Carries impulse away from cell body to the CNS.
- Myelin sheath: Insulates axon → speeds up transmission.
Function
- Transmits electrical impulses from sensory receptors to the CNS (spinal cord/brain).
Motor Neurone
Structure
- Cell body: Located at one end of the neurone, inside the CNS.
- Many dendrites: Receive impulses from other neurones.
- Long axon: Extends out of CNS to effectors.
- Myelin sheath: Insulates axon → faster conduction.
- Axon terminals: Synapse with muscles or glands (effectors).
Function
- Transmits impulses from CNS to effectors (muscles → contraction, glands → secretion).
Intermediate / Relay Neurone
- Found within CNS.
- Connects sensory neurones to motor neurones.
- Usually short, unmyelinated axons.
- Allows integration & coordination of responses.
📊 Comparison Table
| Feature | Sensory Neurone | Motor Neurone |
| Direction of impulse | Receptor → CNS | CNS → Effector |
| Cell body position | Side branch of axon (outside CNS, in dorsal root ganglion) | Inside CNS, at one end |
| Function | Detects and transmits sensory info | Sends commands to muscles/glands |
| Connection | Connects with relay neurones | Connects with effectors |
✅ Key Point:
Sensory neurones bring information into the CNS.
Motor neurones carry commands out of the CNS.
Relay neurones link them inside the CNS.
Role of Sensory Receptor Cells
👁️ What are Sensory Receptors?
- Specialised cells or nerve endings that detect changes in the environment (stimuli).
- Located in sense organs (eyes, ears, skin, nose, tongue).
- Each receptor is specific to one type of stimulus (e.g., light, pressure, chemicals, temperature).
⚡ How They Work
Detection of Stimulus
- Receptor proteins detect a specific form of energy (e.g., light, vibration, pressure).
Transduction
- Stimulus energy is converted into an electrical signal (generator potential / receptor potential).
Threshold & Action Potential
- If generator potential reaches threshold, an action potential is triggered in the sensory neurone.
- This is an all-or-nothing response → stronger stimuli = higher frequency of impulses, not larger ones.
Transmission
- Action potential is carried along the sensory neurone to the CNS for processing.
🔬 Examples of Receptors
| Receptor Type | Stimulus Detected | Location | Example |
| Photoreceptors | Light | Retina (eye) | Rods & cones |
| Mechanoreceptors | Pressure, vibration, sound | Skin, inner ear | Pacinian corpuscle |
| Chemoreceptors | Chemicals (taste, smell) | Nose, tongue | Olfactory cells, taste buds |
| Thermoreceptors | Temperature | Skin, hypothalamus | Hot & cold receptors |
📌 Summary
Sensory receptors detect stimuli.
Convert energy into electrical signals.
Generate action potentials in sensory neurones.
Send signals to CNS for interpretation → leading to a response.
Sequence of Events Leading to an Action Potential (Chemoreceptor in Taste Buds)
1. Stimulus Detection
- A chemical stimulus (e.g., sugar or salt molecules) dissolves in saliva.
- These chemicals bind to chemoreceptor proteins in the taste bud receptor cell membrane.
2. Generator Potential
- Binding of the chemical opens ion channels in the receptor cell membrane.
- Sodium (Na⁺) or hydrogen ions (H⁺) enter the receptor cell.
- This causes depolarisation (inside becomes less negative).
- If depolarisation is large enough → a generator potential is produced.
3. Threshold Reached
- If the generator potential reaches the threshold value:
- Voltage-gated sodium channels in the sensory neurone open.
- A full action potential is triggered.
4. Action Potential Propagation
- Sodium ions flood into the neurone → rapid depolarisation.
- The action potential is conducted along the sensory neurone axon towards the CNS.
- The strength of the stimulus is coded by the frequency of action potentials, not their size.
📌 Summary
Chemical stimulus binds → ion channels open.
Ion influx depolarises receptor → generator potential.
Threshold reached → action potential triggered.
Action potential travels to CNS → interpreted as taste.
Changes in Membrane Potential of Neurones
1. Resting Potential (–70 mV)
- The neurone membrane is polarised.
- Maintained by the sodium–potassium pump and membrane permeability:
- Pumps 3 Na⁺ ions out and 2 K⁺ ions in (active transport using ATP).
- Membrane is more permeable to K⁺ than Na⁺ → more positive ions leave than enter.
- Inside of the axon becomes negatively charged relative to outside (–70 mV).
- This creates the resting potential, ready for excitation.
2. Events of an Action Potential
- a) Depolarisation (Stimulus):
- Stimulus causes Na⁺ channels to open.
- Na⁺ rushes into axon (down electrochemical gradient).
- Membrane potential becomes less negative.
- If threshold (≈ –55 mV) is reached → full action potential triggered.
- b) Rising Phase:
- More Na⁺ channels open (positive feedback).
- Rapid Na⁺ influx makes inside of axon positive (+30 mV).
- c) Repolarisation:
- At +30 mV, Na⁺ channels close.
- K⁺ channels open, K⁺ diffuses out of axon.
- This restores negative charge inside.
- d) Hyperpolarisation:
- Too many K⁺ ions leave → membrane becomes more negative than resting (below –70 mV).
3. Refractory Period (Restoration of Resting Potential)
- Na⁺ channels cannot open immediately → ensures one-way transmission of impulses.
- Sodium–potassium pump restores original ion balance:
- Pumps Na⁺ back out and K⁺ back in.
- Membrane potential returns to resting –70 mV.
📌 Summary Flow
- Resting potential: maintained by Na⁺/K⁺ pump.
- Depolarisation: Na⁺ influx.
- Repolarisation: K⁺ efflux.
- Hyperpolarisation: overshoot.
- Refractory period: restores resting potential.
Rapid Transmission of an Impulse in a Myelinated Neurone (Saltatory Conduction)
Structure of a Myelinated Neurone
- Myelin sheath: layers of lipid membrane formed by Schwann cells.
- Nodes of Ranvier: small gaps (2–3 µm) between adjacent Schwann cells where the axon membrane is exposed.
- Ion channels concentrated only at the nodes, not along myelinated sections.
Saltatory Conduction (Jumping Conduction)
- In myelinated neurones, depolarisation occurs only at the nodes of Ranvier.
- Action potential jumps from node to node rather than moving continuously along the axon.
- Between nodes, the myelin prevents ion movement → speeding transmission.
🔍 Why It Is Faster
- Fewer depolarisation events → less time required.
- Local currents travel further under myelin before needing to regenerate an action potential.
- Uses less ATP as fewer Na⁺/K⁺ pump operations are needed.
📊 Comparison: Myelinated vs. Non-myelinated Neurone
| Feature | Myelinated Neurone | Non-myelinated Neurone |
|---|---|---|
| Speed of transmission | Fast (up to 120 m/s) due to saltatory conduction | Slow (≈ 2 m/s), impulse moves continuously |
| Energy use | Lower (fewer ion pumps active) | Higher (more continuous pumping) |
| Impulse conduction | Jumps node to node | Continuous along entire axon |
| Found in | Vertebrates, longer axons | Many invertebrates, short axons |
📌 Summary: Saltatory conduction allows impulses in myelinated neurones to travel faster and more efficiently, ensuring rapid communication in the nervous system.
Importance of the Refractory Period in Determining the Frequency of Impulses
🧩 What is the Refractory Period?
- The short time (≈ 2–10 ms) after an action potential when a neurone cannot immediately fire another action potential.
- Two phases:
- Absolute refractory period: no new impulse can be generated (Na⁺ channels inactivated).
- Relative refractory period: a stronger-than-normal stimulus is required (K⁺ channels still open, membrane hyperpolarised).
⚡ Importance in Controlling Impulse Frequency
- Limits maximum frequency: ensures impulses cannot follow each other too closely → sets an upper limit to how fast neurones can fire.
- Prevents overlap of action potentials: each impulse remains a separate, discrete event.
- Prevents bidirectional impulses: ensures impulses travel in one direction only along the axon.
- Stimulus strength coding:
- Stronger stimuli = more frequent impulses (up to maximum, limited by refractory period).
- Weaker stimuli = lower frequency of impulses.
📊 Summary Table
| Function of Refractory Period | Explanation |
|---|---|
| Impulse separation | Ensures each action potential is distinct. |
| One-way transmission | Stops impulses from travelling backwards. |
| Frequency coding | Limits max impulse frequency → stimulus strength encoded by frequency, not size, of impulses. |
| Restoration | Allows ion gradients (Na⁺/K⁺) to reset before next action potential. |
📌 Summary: The refractory period ensures impulses are discrete, one-way, and frequency-limited, making it vital for reliable neural communication.
Cholinergic Synapse – Structure and Function
🧩 Structure of a Cholinergic Synapse
- A cholinergic synapse transmits impulses between neurones using the neurotransmitter acetylcholine (ACh).
- Presynaptic neurone
- Synaptic knob: swollen end of axon containing many mitochondria (ATP for neurotransmitter synthesis).
- Vesicles: contain acetylcholine.
- Voltage-gated Ca²⁺ channels: open in response to depolarisation.
Synaptic cleft- Tiny gap (~20–40 nm) between presynaptic and postsynaptic membranes.
- Postsynaptic neurone
- Receptors: protein receptors specific to acetylcholine, located on sodium ion channels.
- Enzyme acetylcholinesterase (AChE): located in cleft, breaks down acetylcholine.
🔄 Function of a Cholinergic Synapse
- Arrival of Impulse: Action potential reaches presynaptic knob → membrane depolarises.
- Role of Calcium Ions (Ca²⁺): Depolarisation opens voltage-gated Ca²⁺ channels → Ca²⁺ diffuses in → vesicles fuse with presynaptic membrane.
- Release of Neurotransmitter: Vesicles release acetylcholine (ACh) into synaptic cleft by exocytosis.
- Binding to Receptors: ACh diffuses across cleft → binds to receptors on postsynaptic membrane → Na⁺ channels open → depolarisation (EPSP). If threshold reached → new action potential.
- Termination of Signal: AChE breaks down ACh into choline + acetate → reabsorbed and recycled into new ACh using ATP → synapse reset, signal short-lived.
📊 Summary Table
| Step | Role of Ca²⁺ | Outcome |
|---|---|---|
| Impulse arrives | Depolarisation opens Ca²⁺ channels | Ca²⁺ enters presynaptic knob |
| Vesicle fusion | Ca²⁺ binds to proteins in vesicle membrane | Vesicles fuse with presynaptic membrane |
| Neurotransmitter release | Triggered by Ca²⁺ influx | ACh released by exocytosis |
📌 Summary: A cholinergic synapse transmits impulses using acetylcholine. Calcium ions trigger vesicle fusion, ACh binds to receptors to depolarise the postsynaptic neurone, and AChE rapidly breaks down ACh to reset the synapse.
Neuromuscular Junctions, T-tubules & Sarcoplasmic Reticulum in Muscle Contraction
⚡ Neuromuscular Junction (NMJ)
- Specialised synapse between a motor neurone and a muscle fibre.
- Uses acetylcholine (ACh) as neurotransmitter.
Steps:
- Action potential arrives at motor neurone terminal → Ca²⁺ enters.
- Vesicles release ACh into synaptic cleft.
- ACh binds to receptors on sarcolemma (muscle cell membrane).
- Opens Na⁺ channels → depolarisation of sarcolemma.
- If threshold reached → action potential generated in muscle fibre.
Role: Converts nerve impulse into muscle fibre action potential.
📡 T-tubule (Transverse Tubule) System
- Invaginations of sarcolemma that penetrate deep into muscle fibre.
- Carry the action potential from sarcolemma into the interior of muscle fibre.
Role: Ensures depolarisation spreads rapidly & simultaneously to all myofibrils for coordinated contraction.
🧪 Sarcoplasmic Reticulum (SR)
- Specialised smooth endoplasmic reticulum in muscle fibres.
- Stores calcium ions (Ca²⁺).
Steps:
- Action potential from T-tubules stimulates SR to open Ca²⁺ channels.
- Ca²⁺ released into sarcoplasm (cytoplasm of muscle cell).
- Ca²⁺ binds to troponin on actin filaments.
- This moves tropomyosin, exposing binding sites for myosin heads.
- Cross-bridge formation → muscle contraction.
Role: Provides the Ca²⁺ required to initiate actin–myosin interaction.
📊 Summary Table
| Structure | Function in Contraction |
|---|---|
| Neuromuscular junction | Transmits nerve impulse to muscle fibre via acetylcholine, initiating depolarisation |
| T-tubule system | Rapidly conducts action potential deep into muscle fibre for synchronous activation |
| Sarcoplasmic reticulum | Releases Ca²⁺ into sarcoplasm, triggering actin–myosin cross-bridge formation |
✨ Key Idea: Nerve impulse → NMJ → Sarcolemma depolarisation → T-tubules → SR releases Ca²⁺ → Actin-myosin interaction → Contraction.
Ultrastructure of Striated Muscle & Sarcomere
🔬 Overview of Striated (Skeletal) Muscle
- Made up of long, multinucleate fibres containing myofibrils.
- Myofibrils are repeating units of sarcomeres (the contractile units).
- Striated appearance due to alternating light and dark bands.
📏 Sarcomere Structure (from Z-line to Z-line)
- A sarcomere = functional unit of contraction.
- Z-line (Z-disc): boundary of a sarcomere; anchors actin (thin filaments).
- M-line: centre of sarcomere; anchors myosin (thick filaments).
- A-band (dark band): entire length of thick (myosin) filaments; includes overlap with actin.
- I-band (light band): only thin (actin) filaments; spans between thick filaments.
- H-zone: central part of A-band where only myosin is present (no overlap with actin).
⚙️ Filament Arrangement
- Thin filaments (actin): Composed of actin, tropomyosin, and troponin; anchored at the Z-line.
- Thick filaments (myosin): Made of myosin molecules with projecting myosin heads; anchored at the M-line.
- Overlap of actin & myosin → cross-bridge formation during contraction.
📊 Summary Table
| Band/Line | Description | Visible in EM |
|---|---|---|
| Z-line | Boundary of sarcomere, actin anchored | Dark thin line |
| M-line | Centre of sarcomere, myosin anchored | Thin line in H-zone |
| A-band | Myosin length (with overlap of actin) | Dark band |
| I-band | Actin only | Light band |
| H-zone | Myosin only (no overlap) | Lighter region in middle of A-band |
✨ Key Idea: The sarcomere shortens during contraction → Z-lines move closer, I-band and H-zone shrink, A-band remains constant (myosin filament length unchanged).
Sliding Filament Model of Muscle Contraction
🔬 Overview
- Explains how sarcomeres shorten → muscle contraction.
- Relies on interaction between actin (thin filaments) and myosin (thick filaments).
- Controlled by calcium ions (Ca²⁺), troponin, tropomyosin, and ATP.
⚙️ Steps in the Sliding Filament Model
- At Rest: Tropomyosin covers actin’s binding sites → prevents cross-bridge formation. Troponin attached to tropomyosin. Myosin heads cocked (primed by ATP hydrolysis).
- Calcium Ion Release: Action potential → T-tubules → SR releases Ca²⁺. Ca²⁺ binds troponin → tropomyosin moves → actin binding sites exposed.
- Cross-Bridge Formation: Myosin head (ADP + Pi) binds to actin → cross-bridge forms.
- Power Stroke: Myosin head tilts, pulling actin towards M-line. ADP + Pi released → energy from ATP hydrolysis moves actin. Sarcomere shortens.
- Cross-Bridge Detachment: New ATP binds myosin head → detaches from actin.
- Re-cocking of Myosin Head: ATP hydrolysed → ADP + Pi. Myosin head resets, ready for next cycle.
🔁 Cycle Repeats: As long as Ca²⁺ is present and ATP available, cross-bridge cycling continues. I-band and H-zone shorten; A-band constant.
📊 Key Roles of Molecules
| Molecule | Role |
|---|---|
| Calcium ions (Ca²⁺) | Released from SR; bind troponin → expose actin binding sites |
| Troponin | Ca²⁺ binding causes shift → moves tropomyosin |
| Tropomyosin | Blocks actin’s myosin-binding sites at rest; moves when troponin changes shape |
| ATP | Energy for detachment & resetting of myosin heads; hydrolysis primes power stroke |
✨ Key Idea: Muscle contraction = sarcomere shortening caused by sliding of actin over myosin, not shortening of filaments themselves.