Control and coordination in mammals

1. Overview

Mammals respond to changes in their internal and external environment using two coordinating systems. The nervous system sends rapid, short-lived electrical impulses along neurones to bring about fast responses, while the endocrine system releases hormones into the blood for slower, longer-lasting effects. This topic explains how a stimulus is detected by a receptor cell, how a neurone generates and conducts an action potential, how impulses cross a synapse using a neurotransmitter, and how a nerve impulse finally triggers contraction in striated muscle through the sliding filament model.

Key Definitions

• Endocrine system: a system of ductless glands that secrete hormones directly into the blood to act on distant target cells.
• Hormone: a chemical messenger secreted by an endocrine gland into the blood that alters the activity of specific target cells.
• Sensory neurone: a neurone that carries impulses from a receptor to the central nervous system.
• Motor neurone: a neurone that carries impulses from the central nervous system to an effector such as a muscle or gland.
• Resting potential: the potential difference across the membrane of a neurone that is not transmitting an impulse, typically about -70 mV inside relative to outside.
• Action potential: a brief reversal of the membrane potential, from about -70 mV to about +30 mV, that travels along a neurone as a nerve impulse.
• Refractory period: the short time after an action potential during which a region of membrane cannot be depolarised again.
• Saltatory conduction: the rapid jumping of an action potential from one node of Ranvier to the next along a myelinated neurone.
• Synapse: the junction between two neurones, or between a neurone and an effector, across which an impulse is passed using a neurotransmitter.
• Sarcomere: the functional contractile unit of a myofibril, lying between two Z-discs.

Content

The endocrine system

The endocrine system is made of ductless glands that secrete hormones straight into the blood, which carries them all over the body. Only target cells with the correct complementary receptors respond, so a hormone can act selectively on distant tissues. Three hormones illustrate this:

• ADH (antidiuretic hormone), from the pituitary gland, increases the permeability of the collecting ducts of the kidney to water, so more water is reabsorbed and a smaller volume of more concentrated urine is produced.
• Glucagon, from the alpha cells of the islets of Langerhans in the pancreas, raises blood glucose concentration by stimulating the breakdown of glycogen to glucose (glycogenolysis) in the liver.
• Insulin, from the beta cells of the islets of Langerhans, lowers blood glucose concentration by increasing glucose uptake by cells and stimulating its conversion to glycogen.

Comparing the nervous and endocrine systems

Both systems coordinate responses, but they differ in their speed, transmission and duration.

Feature	Nervous system	Endocrine system
Transmission	electrical impulses along neurones	hormones carried in the blood
Speed	very fast	slower
Pathway	neurones (a defined pathway)	the bloodstream (reaches the whole body)
Target	specific cells/effectors	only cells with complementary receptors
Duration of effect	short-lived	usually longer-lasting
Response	localised	can be widespread

Structure and function of neurones

A neurone is a specialised cell that conducts electrical impulses. All neurones have a cell body containing the nucleus, fine dendrites that receive signals, and a long axon that carries the impulse.

• A sensory neurone carries impulses from a receptor to the central nervous system (CNS). It has a cell body on a side branch, with a long dendron carrying the impulse towards the cell body and a shorter axon carrying it onward.
• A motor neurone carries impulses from the CNS to an effector (a muscle or gland). Its cell body lies in the CNS and it has many dendrites and a single long axon.
• Intermediate neurones (relay neurones) lie within the CNS and connect sensory neurones to motor neurones.

Many neurones are myelinated: Schwann cells wrap around the axon forming an insulating myelin sheath, broken at intervals by gaps called nodes of Ranvier.

Receptor cells and the generator potential

A sensory receptor cell acts as a transducer: it converts the energy of a stimulus into an electrical signal. When a suitable stimulus is detected, ion channels in the receptor cell membrane open, ions move across the membrane and the membrane potential changes, producing a generator potential. If this generator potential is large enough to reach the threshold, it triggers an action potential in the sensory neurone, which then transmits impulses to the CNS. A stronger stimulus produces a larger generator potential, which leads to action potentials being fired more frequently.

Producing an action potential: the taste bud example

A chemoreceptor cell in a human taste bud shows how a stimulus leads to an action potential:

1. Dissolved chemicals from food bind to receptor proteins on the chemoreceptor cell membrane.
2. This causes ion channels to open, ions move across the membrane and a generator potential is produced.
3. If the generator potential reaches threshold, it stimulates the release of neurotransmitter onto the sensory neurone.
4. Neurotransmitter binding opens channels in the sensory neurone membrane, depolarising it and triggering an action potential.
5. The action potential is conducted along the sensory neurone to the brain, where the taste is perceived.

Maintaining the resting potential

In a resting neurone the inside of the membrane is about -70 mV relative to the outside. This is set up and maintained by two main features:

• The sodium-potassium pump uses ATP to actively transport 3 Na⁺ out of the cell for every 2 K⁺ in, so more positive ions are pumped out than in.
• The membrane is far more permeable to K⁺ than to Na⁺, because some potassium channels stay open, so K⁺ tends to leak back out down its concentration gradient.
• Together these leave the inside of the membrane negative relative to the outside.

The action potential and the refractory period

The shape of an action potential is illustrated in the graph shown below for this topic: the membrane sits at the resting potential, rises sharply through the threshold to a positive peak, falls back during repolarisation, and dips briefly below the resting value before recovering. When the membrane is stimulated to threshold, the following events occur across that region of membrane (note that it is the membrane, not the whole neurone, that depolarises):

1. Depolarisation: voltage-gated sodium channels open, so Na⁺ diffuses rapidly into the cell, making the inside more positive. As more channels open the potential rises to about +30 mV.
2. Repolarisation: the sodium channels close and voltage-gated potassium channels open, so K⁺ diffuses out of the cell, restoring the inside to negative.
3. Hyperpolarisation: the potassium channels are slow to close, so a little too much K⁺ leaves and the potential briefly overshoots to below -70 mV.
4. The sodium-potassium pump and closure of the potassium channels then restore the resting potential.

The refractory period is the short recovery time after an action potential. During it the sodium channels are inactivated and cannot reopen, so that region of membrane cannot be depolarised again straight away.

Worked example

Exam-style question: The membrane potential of a sensory neurone changes during a single action potential, with the values quoted in the parts below. Point X lies on the steep upstroke and point Y lies on the falling phase. (a) State the value of the resting potential and the value at the peak. (b) State whether voltage-gated sodium channels or potassium channels are mainly open at point X and at point Y. (c) A stronger stimulus is applied. Explain why this increases the frequency of action potentials rather than their height. [5]

Model answer:

• (a) The resting potential is about -70 mV and the peak of the action potential is about +30 mV.
• (b) At point X (the upstroke) the voltage-gated sodium channels are open, so Na⁺ diffuses into the cell and depolarises the membrane.
• (b) At point Y (the falling phase) the voltage-gated potassium channels are open, so K⁺ diffuses out of the cell and repolarises the membrane.
• (c) Action potentials are all-or-nothing, so once threshold is reached every action potential reaches the same peak height regardless of stimulus strength.
• (c) A stronger stimulus therefore cannot make a larger action potential; instead it triggers action potentials more often, and the brain interprets this higher frequency as a more intense stimulus. The refractory period sets the maximum frequency possible.

Saltatory conduction in myelinated neurones

In a myelinated neurone the myelin sheath is an electrical insulator, so ions can only cross the membrane at the nodes of Ranvier. Local currents flow from one node to the next, so the action potential effectively jumps from node to node rather than moving smoothly along the whole length. This is saltatory conduction, and it makes impulse transmission far faster than in an unmyelinated neurone of the same diameter.

The refractory period and impulse frequency

The refractory period limits how rapidly action potentials can follow one another, so it sets the maximum frequency of impulses. Crucially, action potentials are all-or-nothing and always reach the same peak, so a stronger stimulus does not produce a larger action potential. Instead, a stronger stimulus produces action potentials at a higher frequency, and the brain interprets this higher frequency as a more intense stimulus. The refractory period also ensures impulses travel in one direction only.

Cholinergic synapses

A synapse is the junction between two neurones. At a cholinergic synapse the neurotransmitter is acetylcholine (ACh). The arriving neurone ends in a swelling called the presynaptic knob, separated from the next neurone by a tiny gap, the synaptic cleft. Transmission occurs as follows:

1. An action potential arrives at the presynaptic knob and opens voltage-gated calcium ion channels.
2. Ca²⁺ diffuses into the knob. This causes vesicles of acetylcholine to move to the presynaptic membrane and fuse with it, releasing ACh into the synaptic cleft by exocytosis.
3. ACh diffuses across the cleft and binds to receptors on the postsynaptic membrane, opening sodium channels.
4. Na⁺ diffuses into the postsynaptic neurone and depolarises its membrane. If threshold is reached, a new action potential is generated.
5. The enzyme acetylcholinesterase breaks ACh down into choline and ethanoic acid. These are reabsorbed into the presynaptic knob and recombined using ATP. This stops continuous stimulation, so the synapse can respond to new impulses.

A single impulse may release too little ACh to depolarise the postsynaptic membrane to threshold. Several impulses arriving in quick succession at one knob (temporal summation), or impulses from several presynaptic neurones at once (spatial summation), can add together to reach threshold and trigger an action potential.

Synapses ensure one-way transmission, because the vesicles are only on the presynaptic side, and they allow signals to be integrated. Some chemicals modify synaptic transmission - for example endorphins bind to specific receptors on the presynaptic membrane and inhibit the release of neurotransmitter, reducing the sensation of pain.

The neuromuscular junction and muscle stimulation

A neuromuscular junction is a specialised cholinergic synapse between a motor neurone and a striated muscle fibre. An action potential arriving here releases acetylcholine, which depolarises the muscle fibre membrane (the sarcolemma). This wave of depolarisation then spreads deep into the fibre. It travels along infoldings of the sarcolemma called T-tubules (transverse tubules).

The T-tubules carry the impulse to the sarcoplasmic reticulum, a specialised endoplasmic reticulum that stores calcium ions. Depolarisation causes the sarcoplasmic reticulum to release Ca²⁺ into the sarcoplasm. There, these ions trigger contraction by the sliding filament mechanism described below. During contraction ATP is regenerated rapidly by transfer of a phosphate group from creatine phosphate (phosphocreatine) to ADP, maintaining the ATP supply needed by the myosin heads.

Ultrastructure of striated muscle

A muscle fibre contains many parallel myofibrils. Each myofibril is divided into repeating units called sarcomeres, which give striated muscle its banded appearance. Within a sarcomere:

• The Z-discs (Z-lines) mark the two ends of each sarcomere.
• The I-band (light band) contains only thin actin filaments. Each I-band is bisected by a Z-disc, so it is shared between two adjacent sarcomeres.
• The A-band (dark band) is the full length of the thick myosin filaments, including where they overlap with actin.
• The H-zone is the central region of the A-band where only myosin filaments are present (no overlap with actin).
• The M-line runs through the middle of the H-zone and holds the myosin filaments in place.

The sliding filament model of muscular contraction

Contraction occurs because the actin and myosin filaments slide over one another, shortening each sarcomere. The filaments themselves do not change in length. The process is controlled by troponin, tropomyosin, calcium ions and ATP:

1. At rest, the protein tropomyosin lies along the actin filament and blocks the myosin-binding sites, so the myosin heads cannot attach.
2. When an impulse arrives, Ca²⁺ released from the sarcoplasmic reticulum binds to troponin. This makes troponin change shape, pulling tropomyosin away from the binding sites and exposing them on the actin.
3. A myosin head (carrying a molecule of ADP and inorganic phosphate) binds to the exposed site on actin, forming a cross-bridge.
4. The myosin head then tilts, performing the power stroke: it pulls the actin filament towards the centre of the sarcomere, and ADP and phosphate are released. This is what makes the filaments slide past each other.
5. A new molecule of ATP binds to the myosin head, which causes the head to detach from the actin.
6. The myosin head hydrolyses the ATP (using the enzyme activity of myosin, which acts as an ATPase) to ADP and phosphate. The energy released re-cocks the head back to its upright position, ready to bind further along the actin filament.
7. This cross-bridge cycle repeats many times as long as Ca²⁺ and ATP are present, so the actin is pulled in repeated small steps and the sarcomere shortens.

When stimulation stops, Ca²⁺ is actively pumped back into the sarcoplasmic reticulum, troponin and tropomyosin return to their resting positions, the binding sites are covered again and the muscle relaxes. ATP is therefore needed both for the power stroke (energising the movement of the myosin head) and for the detachment of the myosin head from actin, as well as for pumping Ca²⁺ back into the sarcoplasmic reticulum.

Worked example

Exam-style question: A student examines an electron micrograph of a relaxed sarcomere and the same sarcomere after the muscle has contracted. Explain how the appearance of the I-band and the H-zone changes during contraction, and explain why the length of the A-band does not change. [3]

Model answer:

• During contraction the actin filaments slide past and over the myosin filaments, increasing the overlap between them, which pulls the Z-discs closer together and shortens the sarcomere.
• Because the overlap increases, the I-band gets shorter and the H-zone gets shorter (or disappears).
• The A-band stays the same length because the myosin filaments themselves do not shorten - only the degree of overlap changes, not the filament length.

Key Equations

This topic is largely qualitative. The standard numerical values to recall are the resting potential ($\approx -70\ \text{mV}$), the peak of the action potential ($\approx +30\ \text{mV}$), and the ratio of ions moved by the sodium-potassium pump (3 Na⁺ out for every 2 K⁺ in).

Common Mistakes to Avoid

• Using vague language for ion movement. Always write that ions move across or through the membrane, never "into" the membrane, and say that the membrane (not the whole neurone) becomes depolarised.
• Saying a stronger stimulus gives a bigger action potential. Action potentials are all-or-nothing and always reach the same peak; a stronger stimulus increases the frequency of impulses, not their size.
• Forgetting the role of ATP in muscle contraction. State that ATP is needed both to detach the myosin head from actin and to provide energy for the power stroke (and to pump Ca²⁺ back into the sarcoplasmic reticulum), not just "for energy" in general.
• Thinking the filaments shorten during contraction. The actin and myosin filaments stay the same length - they slide past each other, increasing overlap and shortening the sarcomere. This is why the A-band length is unchanged.
• Confusing troponin and tropomyosin. Calcium ions bind to troponin, which then moves tropomyosin off the myosin-binding sites on actin.
• Saying endorphins act on the postsynaptic acetylcholine receptors. Endorphins bind to receptors on the presynaptic membrane and inhibit neurotransmitter release.
• Mixing up the two coordinating systems. Nerve impulses are electrical, fast and short-lived; hormonal responses are chemical, slower and longer-lasting.

Exam Tips

• In synapse and action-potential questions, name the exact ion and direction each time (for example "Na⁺ diffuses into the cell", "K⁺ diffuses out of the cell") to gain the marking points.
• For "describe an action potential" questions, give the events in order - depolarisation, repolarisation, hyperpolarisation, restoration of resting potential - and quote the voltages (-70 mV and +30 mV).
• When explaining the sliding filament model, work through the cycle in sequence and link each named molecule (troponin, tropomyosin, calcium ions, ATP) to a specific step.
• For "compare" questions on the nervous and endocrine systems, write paired comparative sentences (for example "the nervous system is faster than the endocrine system") rather than two separate lists.
• Use precise terms: depolarisation, repolarisation, saltatory conduction, cross-bridge and power stroke - precise terminology earns the marks.