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15.1 Control and Coordination in Mammals

Syllabus
9700–2028–2029
Topic
15.1
Level
A2

Learning objectives

15.1.1Endocrine system features• Endocrine system features: ADH, glucagon, insulin15.1.2Nervous and endocrine systems• Compare nervous system and endocrine system15.1.3Sensory, motor and intermediate neurones• Sensory neurone and motor neurone structure and function; intermediate neurones15.1.4Sensory receptor cells• Sensory receptor cells: detect stimuli, stimulate impulse transmission15.1.5Action potential sequence• Action potential sequence in sensory neurone using taste bud chemoreceptor example15.1.6Membrane potential changes• Membrane potential changes:- Resting potential maintenance- Action potential events- Resting potential restoration during refractory period15.1.7Rapid transmission in myelinated neurone• Rapid transmission in myelinated neurone: saltatory conduction15.1.8Refractory period• Refractory period importance in determining impulse frequency15.1.9Cholinergic synapse structure and function• Cholinergic synapse structure and function: calcium ion role15.1.10Muscle contraction stimulation• Neuromuscular junctions, T-tubule system, sarcoplasmic reticulum in stimulating contraction15.1.11Striated muscle ultrastructure• Striated muscle ultrastructure: sarcomere structure15.1.12Sliding filament model of contraction• Sliding filament model of contraction: roles of troponin, tropomyosin, calcium ions, ATP

Endocrine hormones travel in blood to specific target cells

Endocrine glands release hormones directly into the blood. Blood carries each chemical signal around the body, but only target cells with a complementary receptor respond, so a widely distributed hormone can produce a selective response.

Hormone Release and target example Coordinated response
ADH released from the posterior pituitary; acts on collecting-duct cells increases aquaporins and water reabsorption when blood water potential is low
Insulin released by pancreatic beta cells; acts on muscle and liver cells lowers raised blood glucose through uptake/use and glycogen formation
Glucagon released by pancreatic alpha cells; acts on liver cells raises low blood glucose through glycogen breakdown and glucose formation

Hormones are blood-borne chemical signals, not electrical impulses. Exposure alone is insufficient: a cell must have the appropriate receptor to respond.

Nervous and endocrine systems coordinate by different routes

Feature Nervous system Endocrine system
Signal electrical impulses along neurones; neurotransmitter at synapses chemical hormones
Route directed neurone pathways carried throughout the body in blood
Targeting connected effector at the end of a pathway cells with complementary receptors
Typical speed rapid slower because transport is through blood and cellular responses develop
Typical duration short-lived once impulses stop often longer-lasting while hormone remains active
Best suited to rapid, precise responses such as muscle action coordinated, sustained regulation such as water potential or blood glucose

Both systems carry information and depend on cells able to receive the signal. Their signal and route explain the contrast: a wired neurone pathway is rapid and localised, whereas blood distributes hormones and receptor distribution selects responding cells.

These are typical contrasts, not claims that one system is always superior. Nervous and endocrine control can cooperate in the same homeostatic response.

Sensory and motor neurones have structures fitted to their pathway roles

Neurone Structure and cell-body position Direction and role
Sensory long dendron from receptor to a cell body positioned off the fibre, followed by a shorter axon into the CNS; may be myelinated carries impulses from receptor towards CNS
Intermediate (relay) shorter neurone contained within the CNS, with branching connections connects sensory neurones to motor neurones
Motor cell body at one end in the CNS with many dendrites; one long axon, often myelinated, reaches an effector carries impulses from CNS to a muscle or gland

All neurones have a cell-surface membrane and cytoplasm, and their long processes provide a route for electrical impulses. Where present, Schwann-cell myelin insulates the fibre and nodes of Ranvier interrupt the sheath.

Do not identify neurone type from the presence of an axon alone. Use cell-body position, arrangement of processes and direction in the receptor → CNS → effector pathway.

Sensory receptors transduce specific stimuli into receptor potentials and nerve signals

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 threshold stimulus triggers an action potential through ordered Na⁺ and K⁺ movements

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.

Ion gradients create resting, action and refractory membrane potentials

At resting potential, the neurone membrane is polarised: its inside is negative relative to outside. Sodium–potassium pumps use ATP to move 3 Na+ out for every 2 K+ moved in, maintaining unequal ion concentrations. More K+ leak than Na+ leak, together with trapped negative ions inside, sustains the negative interior.

After threshold is reached:

  1. voltage-gated Na+ channels open; Na+ enters and rapidly depolarises the membrane
  2. near the peak, Na+ channels close/inactivate and voltage-gated K+ channels open
  3. K+ leaves, repolarising the membrane
  4. K+ channels close slowly, causing brief hyperpolarisation

During the refractory period, voltage-gated channels reset and the membrane returns to resting potential. The sodium–potassium pump and existing membrane transport maintain or restore the ion gradients needed for later impulses.

The pump maintains Na+ and K+ gradients over time; rapid depolarisation and repolarisation are caused mainly by voltage-gated channel opening and ion diffusion down electrochemical gradients.

Saltatory conduction rapidly regenerates impulses at nodes

In a myelinated neurone, Schwann-cell myelin electrically insulates most of the axon. Gaps called nodes of Ranvier contain the membrane channels needed to generate action potentials.

  1. An action potential at one node causes local currents inside and outside the axon.
  2. Because the internode membrane is insulated, current spreads rapidly to the next node with little ion exchange across the covered region.
  3. The next node reaches threshold and regenerates a full action potential.
  4. The refractory node behind prevents immediate re-excitation, preserving direction.

Only the nodes, rather than every adjacent patch of axon membrane, need to depolarise. This saltatory conduction makes transmission along a myelinated neurone rapid while each regenerated action potential remains all-or-nothing.

The impulse does not disappear and physically jump through empty space. Local current travels through the insulated region and a new action potential is generated at the next node.

The refractory period separates impulses and enforces one-way transmission

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 converts an impulse into a one-way signal in the next cell

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.

Motor-neurone signalling releases Ca²⁺ to expose actin binding sites

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.

Sarcomeres organise actin and myosin filaments into repeating striated muscle units

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.

Calcium exposes actin sites and ATP powers the cross-bridge cycle

Ca2+ binds to troponin, changing its shape and moving tropomyosin away from myosin-binding sites on actin. Energised myosin heads can then form cross-bridges with exposed sites.

  1. A myosin head carrying ADP and inorganic phosphate binds to actin.
  2. Release of phosphate triggers the power stroke: the head pivots and pulls actin towards the M line; ADP is released.
  3. A new ATP molecule binds to myosin, causing the head to detach from actin.
  4. ATP is hydrolysed to ADP and phosphate, releasing energy that returns the head to its energised position.
  5. With Ca2+ present, the cycle repeats at a new actin site.

Actin slides between myosin filaments; neither filament shortens. Z lines move closer, so the sarcomere shortens. The A band stays the same width, while I and H bands narrow as overlap increases. ATP also supports active transport of Ca2+ back into the sarcoplasmic reticulum, allowing tropomyosin to cover the sites during relaxation.

Keep the ATP steps distinct: ATP binding detaches myosin from actin; ATP hydrolysis re-energises and repositions the myosin head for another cycle.