15. Control and Coordination

The endocrine system is a set of glands whose secretions are hormones. An endocrine gland releases a hormone into the blood, allowing it to travel to distant cells and coordinate a response.

• A hormone acts as a chemical signal carried in the bloodstream.
• Only target cells with a complementary receptor respond directly. Receptor location depends on the hormone and target cell.
• This receptor match makes signalling selective even though the hormone circulates widely.

Blood-borne endocrine signalling is suited to coordination that does not require an instant response and can persist beyond the initial release. The same system can influence distant target tissues, while receptor distribution determines which cells respond.

Endocrine signalling is not the same route as a nerve impulse: the message is a hormone carried in blood rather than an electrical impulse travelling along a neurone. The detailed nervous pathway, synapse, and muscle-response mechanisms are covered separately.

• Nervous system: CNS (brain and spinal cord) coordinates with the PNS (nerves); information is carried as electrical impulses along neurones to effectors such as muscles or glands.
• Endocrine system: endocrine glands release chemical hormones into the bloodstream; hormones travel to target cells with complementary receptors.

The nervous route is suited to rapid, localised control and usually ends when impulses stop. The endocrine route can reach distant target tissues through the blood and usually produces a slower response that lasts while the hormone remains active.

Both systems coordinate body functions by carrying information to cells that can respond. The route and signal type explain the main contrast: neurones provide a directed electrical pathway, whereas blood distributes a chemical signal and receptor distribution selects the target cells.

The nervous and endocrine systems are complementary, not interchangeable labels for every response. This card stops at the system-level comparison; detailed neurone structure, synapses, and muscle contraction are covered in later cards.

A neurone has a cell body, dendrites that receive input, and an axon that carries an impulse away from the cell body. Myelin made by Schwann cells insulates the axon, leaving nodes of Ranvier between myelinated sections.

• Sensory neurone: carries impulses from a sensory receptor towards the central nervous system (CNS).
• Intermediate/relay neurone: lies within the CNS and connects sensory and motor neurones.
• Motor neurone: carries impulses from the CNS to an effector such as a muscle or gland.

Dendrites provide receiving extensions, the axon provides a long conducting fibre, and myelin helps impulses travel efficiently between nodes. The different neurone types therefore assemble a receptor → CNS → effector route; synaptic transmission and action-potential stages are covered separately.

Axons carry impulses away from their cell body, but the three neurone types are distinguished by their position and connection in the pathway, not simply by whether they have an axon. This card does not explain neurotransmitters or the detailed phases of an action potential.

A sensory receptor is a specialised cell, or a sensory neurone ending, that detects a particular type of stimulus. As a transducer it converts stimulus energy into a change in electrical state, beginning a sensory signal.

• A suitable stimulus changes the receptor cell or receptor ending and causes depolarisation, producing a receptor potential.
• A weak stimulus may not depolarise the receptor enough to activate the sensory neurone.
• If the change reaches the required threshold, the sensory neurone is activated and carries impulses towards the CNS.

Receptor specificity links the type of stimulus to the appropriate sense system: for example, light receptors detect light and taste-bud chemoreceptors detect chemical stimuli. The receptor potential is the graded transduction step; detailed action-potential stages and synaptic transmission are covered separately.

A receptor does not respond equally to every form of energy, and a weak stimulus does not automatically produce a nerve impulse. This card explains detection and threshold activation, not the full membrane-potential sequence or neurotransmitter release.

A receptor stimulus first produces a graded receptor potential. If depolarisation reaches threshold, voltage-gated channels produce an all-or-nothing action potential in the sensory neurone; a weaker stimulus does not trigger the impulse.

1. Depolarisation: voltage-gated Na⁺ channels open and Na⁺ enters the axon, making the inside less negative. Positive feedback opens more Na⁺ channels.
2. Action-potential peak: once threshold is crossed, depolarisation continues and the membrane briefly becomes positive.
3. Repolarisation: Na⁺ channels close and voltage-gated K⁺ channels open; K⁺ leaves the axon, returning the membrane towards its resting state.
4. Recovery: K⁺ channels close and the membrane passes through a brief hyperpolarised phase before resting conditions are restored.

In the salt-taste example, sodium ions enter a chemoreceptor and depolarise it. A sufficiently large receptor potential opens voltage-gated Ca²⁺ channels, causing neurotransmitter release that stimulates an action potential in the sensory neurone. Stimulus strength is represented by impulse frequency rather than a larger action-potential amplitude.

Threshold is a boundary: below it there is no action potential, while crossing it produces a stereotyped impulse. This card explains generation and recovery at one membrane region; detailed synaptic transmission and long-distance conduction are covered separately.

An action potential at one axon region changes the local electrical charge across the membrane. Local Na⁺ movement depolarises the adjacent membrane, bringing its voltage-gated Na⁺ channels towards opening and regenerating the impulse there.

• The action potential therefore passes from one membrane section to the next rather than travelling as one unchanged object along the whole axon.
• Immediately behind the active region, the refractory membrane is temporarily unresponsive, so a new action potential is generated ahead of the original event.
• This local regeneration plus the refractory boundary gives the impulse one-way propagation.

Myelin electrically insulates much of the axon, while uninsulated nodes of Ranvier remain available for membrane exchange. The impulse is therefore regenerated at exposed membrane regions; the detailed speed advantage of saltatory conduction is treated separately.

Local current is not a flow of electrons like an ordinary wire, and the refractory region does not create a second impulse behind the original one. This card explains propagation along adjacent axon regions, not synaptic transmission, muscle activation, or quantitative conduction speed.

Two structural factors strongly affect how quickly an impulse travels along a neurone: whether the axon is insulated by myelin and the axon diameter.

• Myelin prevents ion diffusion and depolarisation across the insulated sections.
• Voltage-gated action potentials are regenerated at the exposed nodes of Ranvier.
• Local circuits between nodes depolarise the next node, so the impulse appears to jump from node to node: saltatory conduction.
• This gives a myelinated axon faster conduction than an otherwise comparable unmyelinated axon.

A thicker axon provides a larger membrane surface over which ions can diffuse. Faster ion movement supports faster changes in membrane potential and therefore faster regeneration of action potentials.

Myelin and diameter affect conduction speed; they do not change the basic all-or-nothing nature of an action potential. This card explains structural speed factors, while the basic adjacent-membrane mechanism and the refractory period are treated separately.

After an action potential, the same axon region enters a refractory recovery period. Na⁺ voltage-gated channels close, K⁺ channels open and K⁺ leaves, repolarising the membrane; once the resting state is nearly restored, the channels become responsive again.

• During recovery, the membrane cannot immediately generate another normal action potential, so impulses remain separate rather than merging.
• A new action potential is generated in the membrane ahead of the original event, not behind it, because the region behind is refractory.
• The minimum interval between impulses limits the maximum impulse frequency.

The essential boundary is temporary unresponsiveness followed by restored responsiveness. The refractory period therefore links Na⁺/K⁺ channel recovery to discrete impulses, one-way propagation and a ceiling on firing frequency, without requiring a larger action-potential amplitude.

The refractory period is not a synapse and does not make an impulse travel faster. It is the recovery state of an axon membrane after an action potential; detailed synaptic transmission and muscle responses are covered separately.

A cholinergic synapse has a presynaptic membrane, a synaptic cleft and a postsynaptic membrane. The cleft separates the cells, so an electrical impulse cannot cross it directly.

1. An action potential reaches the presynaptic membrane and opens voltage-gated Ca²⁺ channels.
2. Ca²⁺ enters the presynaptic neurone and causes vesicles to fuse with the membrane, releasing acetylcholine (ACh).
3. ACh diffuses across the cleft and temporarily binds to receptors on the postsynaptic membrane.
4. The receptors open Na⁺ channels; Na⁺ entry depolarises the postsynaptic membrane and can initiate a new impulse.
5. Acetylcholinesterase breaks down ACh, preventing continued stimulation; choline can be recycled to make more ACh.

Transmission is directional because release occurs at the presynaptic membrane and receptors are on the postsynaptic membrane. The chemical step also introduces a short delay compared with direct electrical continuity.

ACh is a temporary messenger, not a permanent bridge between neurones. This card ends when the next cell is depolarised; the neuromuscular junction and muscle contraction are covered separately.

At the neuromuscular junction, a motor-neurone action potential causes Ca²⁺ entry at the presynaptic membrane. Acetylcholine (ACh) is released and binds receptors on the muscle-fibre sarcolemma.

1. ACh opens ion channels in the sarcolemma; Na⁺ entry depolarises the muscle membrane.
2. The action potential travels along the sarcolemma and down the transverse (T-) tubules.
3. This opens Ca²⁺ channels in the sarcoplasmic-reticulum membrane, so Ca²⁺ enters the sarcoplasm around the myofibrils.
4. Ca²⁺ binds to troponin, shifting troponin and tropomyosin and exposing myosin-binding sites on actin.
5. The sliding-filament contraction process can then begin.

The T-tubule and sarcoplasmic-reticulum arrangement carries the surface electrical event into the muscle fibre and converts it into a Ca²⁺ signal. This card ends when actin sites are exposed; sarcomere structure and the full cross-bridge/sliding-filament cycle are covered separately.

The neuromuscular junction is between a neurone and a muscle fibre, not between two neurones. ACh starts the muscle electrical response, while Ca²⁺ and troponin/tropomyosin provide the link to contractile-filament interaction.

A striated muscle fibre contains sarcoplasm, mitochondria and myofibrils. Each myofibril is a bundle of thin actin and thick myosin protein filaments arranged in repeating units called sarcomeres.

• A sarcomere extends from one Z line to the next; Z lines anchor thin actin filaments.
• The M line anchors thick myosin filaments at the centre.
• The A band contains the full length of the myosin region, including overlap with actin.
• The I band contains actin without myosin, while the H band contains myosin without actin.

The sarcolemma surrounds the muscle fibre, and the sarcoplasm contains the contractile myofibrils and mitochondria that provide ATP for contraction. T-tubules and the sarcoplasmic reticulum are structural components associated with excitation and calcium handling; their activation sequence is covered in the preceding card.

The bands and lines describe the arrangement of filaments; actin and myosin are the filaments, not separate bands. This card identifies static ultrastructure and stops before explaining how cross-bridges make the filaments slide.

Ca²⁺ released during excitation binds to troponin, moving troponin and tropomyosin so myosin-binding sites on actin are exposed. This is the starting condition for the sliding-filament cycle, not a repeat of the upstream excitation pathway.

1. Myosin heads bind exposed sites on actin, forming cross-bridges.
2. The heads move and pull actin towards the centre of the sarcomere: the power stroke.
3. ATP hydrolysis supplies energy for the heads to detach and return to a position where they can bind a new site.
4. Repeated attachment, pulling, ATP-dependent detachment and reset draw actin further towards the centre.
5. Z lines move closer together, so each sarcomere shortens and the muscle contracts.

The filaments slide past one another; actin and myosin do not themselves become shorter. Because the A band represents the myosin-containing length, it remains approximately unchanged, while the I band and H band become narrower as overlap increases. When Ca²⁺ is removed, troponin/tropomyosin again block binding sites and the cycle stops, allowing relaxation.

ATP is needed for myosin-head detachment/reset as well as for repeating the cycle; it is not a single one-off pull. This card begins after the Ca²⁺ release chain in 4700 and does not add unsupported mechanical detail.

The Venus flytrap converts touch to a rapid electrical response that closes its leaf trap. Sensory hairs detect movement, and the resulting signal causes hinge cells to swell so the two leaf lobes fold together.

1. An insect touches the sensory hairs on the leaf.
2. Calcium ion channels open in hinge cells at the base of a sensory hair, so calcium ions enter and generate a receptor potential.
3. Repeated stimulation is required: two hairs stimulated together, or one hair stimulated twice within a short interval, can reach the condition for an action potential. The action potential is propagated across the trap cells; without the required repeat stimulation, the trap resets.
4. Water moves into the hinge cells, making them swell. This change in cell shape causes the two lobes to fold together and close the trap.

Continued movement by prey can maintain the closed state. Further stimulation can cause calcium ions to enter gland cells and stimulate release of digestive enzymes, but this is a downstream response after the electrical closure pathway.

This is plant electrical coordination, not an animal nervous pathway: the card does not require neurones, synapses, or neurotransmitters. The electrical signal is the trigger, while water-driven hinge-cell swelling provides the immediate mechanical change that closes the trap.

Auxin is a plant growth regulator that promotes elongation growth. Its effect is local and cell-specific: auxin binds to a receptor on the cell-surface membrane and activates changes that allow the cell to extend.

1. Auxin binds to a receptor protein on the cell-surface membrane.
2. Proton pumps move H+ into the cell wall, lowering its pH. This activates expansins, which loosen bonds between cellulose microfibrils.
3. Auxin also opens potassium ion channels. More K+ in the cytoplasm lowers its water potential, so water enters by osmosis through aquaporins.
4. Water entry increases internal pressure; with the loosened wall able to stretch, the cell elongates.

The result is auxin-controlled elongation growth in roots or shoots, contributing to plant growth and form. The reliable mechanism here is receptor activation → wall loosening plus water uptake → turgor-driven cell elongation; this card does not assert a particular shaded-side or phototropic redistribution unless separately supported by the matched objective source.

Auxin does not lengthen a cell by supplying water directly, and water entry alone is insufficient if the cellulose wall cannot stretch. The card stays with the general elongation mechanism and does not replace it with gibberellin signalling or an unsupported phototropism-specific explanation.

In a dormant barley seed, water uptake starts germination and enables the embryo to produce gibberellin. Gibberellin coordinates the mobilisation of stored starch so the embryo receives soluble sugars for growth.

1. The dry, dormant seed absorbs water. The embryo then produces and releases gibberellin.
2. Gibberellin diffuses to the protein-rich aleurone layer surrounding the starch-containing endosperm.
3. In aleurone cells, gibberellin regulates gene expression, increasing transcription of mRNA coding for the hydrolytic enzyme amylase.
4. Amylase is released into the endosperm and hydrolyses stored starch to soluble maltose. Maltose is converted to glucose, which is transported to the embryo.

The embryo respires the glucose to obtain energy for growth, linking hormone signalling to seedling development. The causal chain is water uptake → embryo gibberellin → aleurone gene expression → amylase → starch hydrolysis → soluble sugar → embryo respiration and growth.

Gibberellin is a signal, not the digestive enzyme: amylase performs the starch hydrolysis. The aleurone layer makes the enzyme, while the endosperm stores the starch and the embryo uses the resulting sugars. This card does not describe auxin elongation or Venus flytrap electrical signalling.