Co-ordination and control in animals

Biology 1010 · CCEA A Level · 14 min read · Updated: 31 Aug 2026

Welcome to Co-ordination and Control in Animals

Hello and welcome to one of the most exciting topics in A2 Biology! In this chapter, we will explore how complex multicellular organisms detect changes in their internal and external environments, process that information, and produce coordinated responses. From the lightning-fast reflexes that pull your hand away from a hot stove to the microscopic sliding of protein filaments that allow your muscles to contract, you are about to discover how your body communicates with itself.

Don't worry if this chapter feels detailed at first! We will break down every process step-by-step, provide memorable analogies, highlight common exam pitfalls, and give you simple tricks to master the content for your CCEA A2 exams.

1. Communication Systems: Nervous vs Hormonal Control

To survive, animals need effective communication systems to respond to stimuli. Mammals rely on two interconnected systems: the nervous system and the endocrine (hormonal) system.

Comparing the Two Systems

• Nature of transmission: The nervous system uses electrical impulses carried along neurones and chemical messengers (neurotransmitters) at synapses. The endocrine system uses chemical messengers (hormones) transported in the bloodstream.
• Speed of transmission: Nervous responses are extremely rapid (milliseconds), whereas hormonal responses are typically much slower (seconds to days).
• Duration of response: Nervous responses are short-lived and temporary, while hormonal responses are usually long-lasting.
• Target area: Nervous impulses are delivered to highly specific, localized effectors (individual muscles or glands). Hormones travel throughout the body, targeting specific organs or tissues bearing complementary receptors.
• Pathways: Nervous signals travel along dedicated pathways (neurones), whereas hormones travel widely through the circulatory system.

Key Takeaway

Quick Summary: Think of the nervous system as a direct phone call (fast, direct, specific) and the endocrine system as a radio broadcast (widespread, slower, picked up only by tuned-in receivers).

2. Structure of Neurones

Neurones are specialized cells adapted for the transmission of electrical nerve impulses. There are three main types you must be able to recognize:

1. Sensory Neurones: Transmit impulses from sensory receptors to the Central Nervous System (CNS - brain and spinal cord). They feature a long dendron, a cell body positioned off to the side in the dorsal root ganglion, and a short axon.
2. Relay (Interneurones): Located entirely within the CNS. They have short dendrites, a central cell body, and a short axon, connecting sensory and motor neurones.
3. Motor Neurones: Transmit impulses from the CNS to effectors (muscles or glands). They have large cell bodies located inside the CNS, numerous branching dendrites, and a single long axon.

Structure of a Myelinated Motor Neurone

• Cell Body (Soma): Contains the nucleus, mitochondria, and large amounts of rough endoplasmic reticulum (Nissl granules) for protein synthesis.
• Dendrites: Highly branched extensions that receive incoming signals from other neurones and carry impulses toward the cell body.
• Axon: A single, elongated fibre that conducts nerve impulses away from the cell body toward an effector.
• Schwann Cells: Specialized glial cells that wrap tightly around the axon in layers, forming the myelin sheath.
• Myelin Sheath: A lipid-rich insulating layer that prevents ion movement across the axonal membrane.
• Nodes of Ranvier: Uninsulated gaps in the myelin sheath occurring at regular intervals (\(\approx 1\text{ mm}\)), where voltage-gated ion channels are concentrated.
• Axon Terminals: Swollen endings (synaptic knobs) that release neurotransmitters to stimulate adjacent cells.

3. The Nerve Impulse: Electrical Signalling

A nerve impulse is not an electric current flowing like electricity in a wire; it is a temporary, self-propagating wave of electrical reversal across the axonal membrane, known as an action potential.

Step 1: The Resting Potential (\(-70\text{ mV}\))

When a neurone is not conducting an impulse, the inside of the axon is negatively charged relative to the outside. This polarized state is typically \(-70\text{ mV}\).

How is resting potential established and maintained?
1. Active Transport: The sodium-potassium pump (\(Na^+/K^+\) ATPase) in the membrane actively transports \(3\text{ }Na^+\) ions OUT of the axon for every \(2\text{ }K^+\) ions pumped IN, using energy from \(ATP\) hydrolysis.
2. Differential Membrane Permeability: The resting membrane has many permanently open \(K^+\) leak channels, but very few open \(Na^+\) leak channels. Thus, \(K^+\) ions diffuse rapidly back out down their concentration gradient, while \(Na^+\) ions cannot readily diffuse back in.
3. Organic Anions: Large, negatively charged proteins and organic ions are trapped inside the cytoplasm (axoplasm).
The net result is an accumulation of positive charge outside the membrane relative to the inside.

Memory Trick: Remember the phone company 321 NOKIA \(\rightarrow\) 3 \(Na^+\) Out, 2 \(K^+\) In, using 1 \(ATP\)!

Step 2: Generation of the Action Potential

When a stimulus arrives at an axon, it changes the permeability of the membrane to ions by opening voltage-gated channels:

1. Depolarisation:
• An incoming stimulus causes some voltage-gated \(Na^+\) channels to open, allowing \(Na^+\) ions to diffuse rapidly into the axon down their electrochemical gradient.
• If the influx of \(Na^+\) causes the membrane potential to reach the threshold potential (around \(-55\text{ mV}\)), a positive feedback loop is triggered: all remaining voltage-gated \(Na^+\) channels burst open.
• Rapid \(Na^+\) influx reverses the charge across the membrane until the inside reaches approximately \(+40\text{ mV}\).

2. Repolarisation:
• At \(\approx +40\text{ mV}\), voltage-gated \(Na^+\) channels close (inactivate), stopping further \(Na^+\) entry.
• Voltage-gated \(K^+\) channels open. \(K^+\) ions diffuse rapidly out of the axon down their electrochemical gradient, removing positive charge from the inside and restoring the negative potential.

3. Hyperpolarisation (The Undershoot):
• Voltage-gated \(K^+\) channels are slow to close, allowing an excess of \(K^+\) ions to diffuse out.
• The membrane potential temporarily drops lower than the resting level, reaching approximately \(-80\text{ mV}\).
• The \(Na^+/K^+\) pump and baseline leak channels gradually restore the resting potential of \(-70\text{ mV}\).

The "All-or-Nothing" Principle

An action potential either occurs completely or does not occur at all. If a stimulus fails to reach the threshold level (\(\approx -55\text{ mV}\)), no action potential is generated. Any stimulus that reaches or exceeds the threshold produces an action potential of the exact same magnitude (\(\approx +40\text{ mV}\)).

Did you know? The brain determines stimulus intensity not by the size of the action potential, but by the frequency of impulses and the number of different neurones firing!

The Refractory Period

Immediately following an action potential, a region of axon enters a recovery period during which it cannot generate another impulse:

• Absolute Refractory Period: Voltage-gated \(Na^+\) channels are completely inactive; no stimulus, however strong, can trigger another impulse.
• Relative Refractory Period: Voltage-gated \(Na^+\) channels are resetting, but voltage-gated \(K^+\) channels remain open. A new action potential can be triggered, but only by a stimulus significantly stronger than normal threshold.

Importance of the Refractory Period:
1. Unidirectional Propagation: Ensures impulses travel in one direction only, because the region behind the active zone is temporarily unresponsive.
2. Discrete Impulses: Keeps individual action potentials separated as distinct pulses.
3. Limits Maximum Frequency: Sets an upper limit on the number of impulses an axon can transmit per second.

Factors Affecting the Speed of Conduction

1. Myelination and Saltatory Conduction: In unmyelinated axons, depolarisation must occur continuously along every point of the membrane (\(\approx 1\text{ m/s}\)). In myelinated axons, the myelin sheath acts as an electrical insulator, preventing ion flow. Depolarisation can only occur at the Nodes of Ranvier. The electrical current jumps from one node to the next. This process is called saltatory conduction and increases conduction speed dramatically (up to \(120\text{ m/s}\)).
2. Axon Diameter: Axons with larger diameters have a smaller surface-area-to-volume ratio and encounter less internal resistance to local ion flow, resulting in faster conduction.
3. Temperature: Higher temperatures increase the kinetic energy of ions, speeding up diffusion through channel proteins, and accelerate the rate of respiration to supply \(ATP\) for active transport.

Key Takeaway

Quick Summary: Resting potential is maintained by the \(Na^+/K^+\) pump and \(K^+\) leakage (\(-70\text{ mV}\)). Depolarisation is caused by \(Na^+\) influx (\(+40\text{ mV}\)), repolarisation by \(K^+\) efflux, and saltatory conduction makes this process lightning-fast across myelinated fibres.

4. Synaptic Transmission

A synapse is a specialized junction between two neurones, or between a neurone and an effector. The tiny gap between the cells is called the synaptic cleft (around \(20\text{ nm}\) wide).

Structure of a Cholinergic Synapse

• Presynaptic Knob: The swollen end of the upstream neurone. It is packed with mitochondria (to provide \(ATP\) for neurotransmitter synthesis and vesicle transport) and numerous synaptic vesicles filled with the neurotransmitter acetylcholine (ACh).
• Presynaptic Membrane: Contains voltage-gated calcium ion (\(Ca^{2+}\)) channels.
• Synaptic Cleft: The fluid-filled extracellular space separating the two cells.
• Postsynaptic Membrane: Contains specific receptor proteins coupled to chemically-gated (ligand-gated) \(Na^+\) channels.

Step-by-Step Mechanism of Synaptic Transmission

1. Arrival of Action Potential: An action potential reaches the presynaptic knob, causing the presynaptic membrane to depolarise.
2. Calcium Influx: Depolarisation causes voltage-gated \(Ca^{2+}\) channels to open. \(Ca^{2+}\) ions diffuse into the presynaptic knob down their concentration gradient.
3. Exocytosis: Influx of \(Ca^{2+}\) stimulates synaptic vesicles to move toward and fuse with the presynaptic membrane, releasing acetylcholine into the synaptic cleft by exocytosis.
4. Diffusion: Acetylcholine molecules diffuse rapidly across the narrow synaptic cleft.
5. Receptor Binding: Acetylcholine binds to complementary receptor sites on the ligand-gated \(Na^+\) channels of the postsynaptic membrane.
6. Postsynaptic Depolarisation: Binding causes the \(Na^+\) channels to open, allowing \(Na^+\) ions to diffuse into the postsynaptic neurone. This generates an Excitatory Postsynaptic Potential (EPSP).
7. Action Potential Generation: If sufficient \(Na^+\) enters and the postsynaptic membrane potential reaches the threshold value, voltage-gated \(Na^+\) channels open, initiating a new action potential.
8. Breakdown of Acetylcholine: The enzyme acetylcholinesterase (AChE), located on the postsynaptic membrane, rapidly hydrolyses acetylcholine into choline and ethanoic acid (acetate).
9. Recycling: The breakdown products diffuse back across the cleft and are reabsorbed by the presynaptic knob. Mitochondria supply \(ATP\) to recombine choline and ethanoic acid back into acetylcholine, which is stored in vesicles for future use.

Why must acetylcholine be broken down?
If acetylcholine remained bound to the receptors, ligand-gated \(Na^+\) channels would stay permanently open, causing continuous firing of action potentials and muscle spasms or receptor desensitisation.

Functions of Synapses

• Unidirectionality: Impulses travel in one direction only because neurotransmitter vesicles are found exclusively in the presynaptic knob, and complementary receptors are found exclusively on the postsynaptic membrane.
• Summation: Low-frequency action potentials may not release enough neurotransmitter to reach threshold. Summation allows sub-threshold signals to combine:
• Spatial Summation: Multiple different presynaptic neurones release neurotransmitters simultaneously onto a single postsynaptic neurone.
• Temporal Summation: A single presynaptic neurone releases neurotransmitter multiple times in rapid succession.
• Filtering Low-Level Stimuli: Background, non-threatening stimuli produce low-frequency impulses that are filtered out because they fail to reach threshold.
• Inhibition: Inhibitory synapses release neurotransmitters (such as GABA) that open chloride (\(Cl^-\)) or potassium (\(K^+\)) channels, making the inside of the postsynaptic neurone even more negative (hyperpolarisation), thus preventing action potential generation.

5. Muscle Contraction: The Sliding Filament Model

Skeletal muscle (striated/voluntary muscle) is attached to the skeleton and responsible for body movement. It is controlled via neuromuscular junctions.

Structure of Skeletal Muscle

• Muscle Fibres: Skeletal muscle is made up of bundles of long, multinucleated cells called muscle fibres.
• Sarcolemma: The specialized plasma membrane surrounding a muscle fibre. It folds inward to form T-tubules (transverse tubules) that run deep into the fibre.
• Sarcoplasm: The cytoplasm of the muscle fibre, containing high concentrations of glycogen granules, myoglobin (oxygen-storing pigment), and mitochondria.
• Sarcoplasmic Reticulum (SR): A specialized endoplasmic reticulum network that stores and releases high concentrations of calcium ions (\(Ca^{2+}\)).
• Myofibrils: Cylindrical organelles packed with two types of protein myofilaments: thick filaments (myosin) and thin filaments (actin).

Structure of the Sarcomere

A sarcomere is the repeating functional unit of a myofibril, bounded between two Z-lines:

• Z-line: The boundary at each end of the sarcomere to which actin filaments are anchored.
• I-band (Isotropic): The light band containing only thin actin filaments.
• A-band (Anisotropic): The dark band spanning the entire length of the thick myosin filaments, including regions where actin and myosin overlap.
• H-zone: The lighter central region of the A-band containing only thick myosin filaments.
• M-line: The central protein line supporting the middle of myosin filaments.

What happens to sarcomere bands during contraction?
• The sarcomere shortens (Z-lines move closer together).
• The I-band shortens (narrows).
• The H-zone shortens (and may disappear entirely).
• The A-band remains the same length (as myosin filaments do not shorten; actin simply slides over them).

Proteins Involved in the Thin and Thick Filaments

• Myosin (Thick): Composed of fibrous tail proteins and globular heads that project outward. Each head has an actin-binding site and an \(ATP\)-binding site with \(ATPase\) enzyme activity.
• Actin (Thin): Two chains of globular actin molecules twisted into a helix, containing specific myosin-binding sites.
• Tropomyosin: A fibrous protein strand wrapped around actin that physically blocks the myosin-binding sites when muscle is at rest.
• Troponin: A globular protein complex attached to tropomyosin with binding sites for \(Ca^{2+}\) ions.

Mechanism of Muscle Contraction (The Cross-Bridge Cycle)

1. Neuromuscular Stimulation: An action potential arrives at the neuromuscular junction, causing acetylcholine release. Acetylcholine binds to sarcolemma receptors, generating a wave of depolarisation that spreads down the T-tubules.
2. Release of \(Ca^{2+}\): Depolarisation of T-tubules stimulates voltage-sensitive channels in the sarcoplasmic reticulum to open, releasing stored \(Ca^{2+}\) into the sarcoplasm.
3. Uncovering Binding Sites: \(Ca^{2+}\) binds to troponin, causing a conformational (shape) change. This pulls tropomyosin away, exposing the myosin-binding sites on the actin filaments.
4. Cross-Bridge Formation: The energized myosin head (carrying bound \(ADP\) and inorganic phosphate, \(P_i\)) attaches to the exposed binding site on actin, forming an actomyosin cross-bridge.
5. The Power Stroke: The myosin head tilts and pivots (approximately \(45^\circ\)), releasing \(ADP\) and \(P_i\). This pulls the actin filament toward the centre of the sarcomere (M-line).
6. Cross-Bridge Detachment: A new molecule of \(ATP\) binds to the myosin head, causing it to detach from the actin filament.
7. Resetting the Head: The enzyme \(ATPase\) on the myosin head hydrolyses \(ATP\) into \(ADP\) and \(P_i\). The energy released returns the myosin head to its original "cocked" upright position.
8. Cycle Repetition: If \(Ca^{2+}\) is still present, the myosin head binds to the next binding site further along the actin filament, repeating the cycle and ratchet-sliding the actin filament inward.

Relaxation: When nervous stimulation stops, \(Ca^{2+}\) is actively pumped back into the sarcoplasmic reticulum using \(ATP\). Troponin returns to its original shape, tropomyosin once again blocks the myosin-binding sites, and the muscle relaxes passively.

6. Types of Muscle Fibres

Human skeletal muscles contain a mixture of two distinct fibre types adapted for different types of work:

Fast-Twitch Muscle Fibres

• Contraction Speed: Contract very rapidly with high force output.
• Respiration Type: Adapted for anaerobic respiration.
• Fatigue Resistance: Fatigue very rapidly due to lactate accumulation.
• Structural Features:
    • Fewer mitochondria.
    • Low concentration of myoglobin (appear white/pale).
    • Fewer capillary networks.
    • High stores of glycogen and phosphocreatine.
    • Higher concentrations of \(ATPase\) and glycolytic enzymes.
• Function: Short bursts of explosive power (e.g. sprinting, weightlifting, eye movements).

Slow-Twitch Muscle Fibres

• Contraction Speed: Contract more slowly with less instantaneous force.
• Respiration Type: Adapted for aerobic respiration.
• Fatigue Resistance: Highly resistant to fatigue; can sustain prolonged activity.
• Structural Features:
    • Abundant, large mitochondria.
    • High concentration of myoglobin (appear deep red).
    • Dense capillary network to ensure rich \(O_2\) supply.
    • Lower glycogen stores.
• Function: Sustained aerobic endurance activities and maintaining posture (e.g. calf and spine postural muscles, marathon running).

Common Pitfalls to Avoid in the Exam

• Confusion over ion directions: Remember that in resting potential, \(Na^+\) is pumped OUT and \(K^+\) is pumped IN. During depolarisation, \(Na^+\) moves IN; during repolarisation, \(K^+\) moves OUT.
• Forgetting \(ATP\)'s role in cross-bridge detachment: \(ATP\) is required to break the actomyosin cross-bridge, not to form it! (This is why in death, when \(ATP\) is depleted, muscles become permanently rigid—a condition known as rigor mortis).
• A-band length: The A-band length does not change during contraction. Only the I-band and H-zone shorten.
• Confusing electrical and chemical stages: Remember that an electrical action potential does NOT jump across the synaptic cleft; it is converted into a chemical signal (neurotransmitter), which then initiates a new electrical signal on the other side.

Chapter Review & Summary Checklist

Use this quick checklist to test your mastery before your CCEA A2 exam:
• Can you explain the roles of the \(Na^+/K^+\) pump, leak channels, and organic anions in maintaining \(-70\text{ mV}\)?
• Can you describe the sequence of events in an action potential (\(-70\text{ mV} \rightarrow -55\text{ mV} \rightarrow +40\text{ mV} \rightarrow -80\text{ mV} \rightarrow -70\text{ mV}\))?
• Can you explain why saltatory conduction is faster than continuous conduction?
• Can you outline all 9 steps of synaptic transmission across a cholinergic synapse?
• Can you detail the roles of \(Ca^{2+}\), troponin, tropomyosin, myosin heads, and \(ATP\) in the sliding filament theory?
• Can you compare slow-twitch and fast-twitch muscle fibres across structural and metabolic adaptations?

Quick check

Can you answer these now?

Open each question to check the key ideas from this chapter.

What are the key differences between nervous and hormonal communication systems in mammals?

The nervous system uses electrical impulses and neurotransmitters for rapid, short-lived, localized responses along neurones, while the endocrine system uses hormones in the blood for slower, long-lasting, widespread responses.

What are the three main types of neurones and their primary functions?

Sensory neurones transmit impulses from receptors to the CNS, relay neurones connect neurones within the CNS, and motor neurones transmit impulses from the CNS to effectors.

What are the main structural components of a myelinated motor neurone?

It consists of a cell body (soma), branching dendrites, an elongated axon wrapped by Schwann cells forming the myelin sheath, gaps called Nodes of Ranvier, and terminal synaptic knobs.

How is the resting membrane potential of \(-70\text{ mV}\) established and maintained in a neurone?

It is maintained by the active transport of \(3\text{ }Na^+\) out for every \(2\text{ }K^+\) in via the \(Na^+/K^+\) pump, high membrane permeability to \(K^+\) leak channels, and trapped cytoplasmic organic anions.

What sequence of ion movements occurs during an action potential?

Depolarisation occurs due to \(Na^+\) influx through voltage-gated channels, repolarisation occurs due to \(K^+\) efflux through voltage-gated channels, and hyperpolarisation results from delayed \(K^+\) channel closure.

What is the 'all-or-nothing' principle in nerve impulse generation?

If a stimulus reaches the threshold potential, an action potential of full and constant magnitude is produced; if the threshold is not reached, no action potential is generated at all.

What is the refractory period and why is it biologically important?

It is the recovery period following an impulse where no new impulse can be initiated, ensuring unidirectional conduction, discrete impulses, and a limit on maximum transmission frequency.

How do myelination, axon diameter, and temperature affect the speed of nerve impulse conduction?

Conduction is accelerated by myelination (via saltatory conduction jumping between Nodes of Ranvier), larger axon diameter (reduced internal resistance), and higher temperature (faster ion diffusion and ATP production).

What are the key steps involved in synaptic transmission across a cholinergic synapse?

Depolarisation opens presynaptic \(Ca^{2+}\) channels; \(Ca^{2+}\) triggers ACh exocytosis; ACh diffuses across the cleft, binds postsynaptic receptors, opens ligand-gated \(Na^+\) channels, and is degraded by AChE.

What is synaptic summation and what are its two types?

Summation is the accumulation of neurotransmitter from sub-threshold stimuli to trigger an action potential, occurring either spatially (multiple presynaptic neurones) or temporally (one neurone firing repeatedly in rapid succession).

How does the structure of a sarcomere change during muscle contraction according to the sliding filament model?

During contraction, the sarcomere shortens, the I-band narrows, and the H-zone narrows/disappears, while the A-band remains constant in length.

What are the roles of \(Ca^{2+}\), troponin, and tropomyosin in initiating muscle contraction?

\(Ca^{2+}\) released from the sarcoplasmic reticulum binds to troponin, altering its shape and pulling tropomyosin away to expose myosin-binding sites on actin.

What role does \(ATP\) play in the cross-bridge cycle of muscle contraction?

\(ATP\) binding is required to detach the myosin head from actin, and its hydrolysis by ATPase re-cocks the myosin head to the high-energy position for the next power stroke.

How do fast-twitch and slow-twitch muscle fibres differ in structure and function?

Fast-twitch fibres are adapted for rapid, powerful anaerobic contractions with high glycogen and low myoglobin/mitochondria, while slow-twitch fibres are adapted for fatigue-resistant aerobic endurance with abundant myoglobin, mitochondria, and capillaries.

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