Lesson 16: Nervous Coordination

You withdraw your hand from a flame before you feel the pain — nervous coordination operating in milliseconds. The nervous system is the body's rapid, precise, short-lived control network, built from neurones that generate electrical impulses and synapses that process them. This lesson covers neurone structure and the myelin sheath, the resting potential and how the action potential is generated and propagated (including saltatory conduction), the factors affecting conduction speed, synaptic transmission with summation, and the reflex arc — plus how drugs and disease interfere.

Neurones — structure and types

Three neurone types form the pathway: sensory neurones (receptor → CNS; long dendron, short axon, cell body at one end), relay neurones (within the CNS; short, many dendrites) and motor neurones (CNS → effector; long axon, cell body with many dendrites at one end). All share: dendrites/dendrons collecting signals, a cell body (soma) with the nucleus, an axon transmitting the impulse, and synaptic terminals releasing neurotransmitter. The myelin sheath (Schwann cells wrapping the axon, with nodes of Ranvier between them) insulates the axon.

Myelin is made by glial cells — Schwann cells in the peripheral nervous system, oligodendrocytes in the CNS. Myelinated axons conduct far faster (saltatory conduction, below) and save energy (fewer ion-pumping events). Demyelinating diseases (multiple sclerosis — immune attack on CNS myelin) cause slowed, disrupted signalling: muscle weakness, vision problems, fatigue (Worked example 3). Structure–function: "explain" answers link the sheath's insulation to speed and the nodes to impulse regeneration.

The nervous system's organisation: CNS (brain, spinal cord — coordination) and peripheral nerves (sensory in, motor out); the autonomic system subdivides into sympathetic (fight-or-flight: increased heart rate, adrenaline synergies) and parasympathetic (rest-and-digest). Voluntary responses involve the brain; reflexes bypass conscious processing (below). Draw and label a motor neurone — the standard diagram question.

The resting potential

The resting potential (~−70 mV, inside negative relative to outside) is maintained by: the sodium–potassium pump (active transport: 3 Na⁺ out, 2 K⁺ in per ATP — creating concentration gradients), potassium ion channels (many open at rest — K⁺ diffuses out down its gradient, carrying positive charge out) and sodium ion channels (mostly closed at rest — Na⁺ cannot flood back in). Large negatively charged proteins inside the axon, unable to leave, also contribute. The result: the axoplasm is negative relative to the tissue fluid.

This is an electrochemical gradient — both concentration and charge differences — maintained at constant ATP cost. It is the loaded spring of nervous signalling: the action potential releases this stored potential. Exam questions ask you to "explain how the resting potential is maintained": name the pump (with its 3:2 stoichiometry), the differential channel permeability (K⁺ leaks out, Na⁺ largely blocked) and the trapped anions. Each mechanism earns a mark.

The pump's ATP dependence links nervous signalling to respiration (Lesson 12) — the brain consumes ~20% of the body's resting energy, largely on ion pumping. Metabolic poisons that halt ATP production abolish nerve function rapidly — another causal chain for "explain" questions.

The action potential and propagation

A stimulus that depolarises the membrane past threshold (~−55 mV) opens voltage-gated Na⁺ channels: Na⁺ floods in down its electrochemical gradient → depolarisation (inside becomes positive, ~+40 mV). Then Na⁺ channels close (and inactivate) and voltage-gated K⁺ channels open: K⁺ flows out → repolarisation, overshooting to hyperpolarisation (~−80 mV) before the resting potential is restored. During the refractory period (Na⁺ channels inactivated) the neurone cannot fire again — this limits impulse frequency and ensures one-way propagation (the impulse cannot reverse into the still-refractory region behind it).

The action potential is all-or-nothing: stimuli above threshold produce identical impulses; stronger stimuli increase impulse frequency, not size. Propagation: each depolarised region generates local currents that depolarise the next (continuous conduction); in myelinated axons, saltatory conduction "jumps" between nodes of Ranvier (the only places with voltage-gated channels) — far faster (~100 m s⁻¹ vs ~1 m s⁻¹ unmyelinated) and more energy-efficient.

Factors affecting speed: myelination (saltatory = faster), axon diameter (wider = less internal resistance = faster — squid giant axons) and temperature (higher = faster ion movement and channel kinetics, within limits). Exam graphs show membrane potential vs time — learn to label depolarisation, repolarisation, hyperpolarisation and the refractory period, and to explain each phase by channel states. This graph is among the most examined in the subject.

Synapses — transmission and summation

Synapses are junctions between neurones (or neurone and effector). Transmission at a cholinergic synapse: the action potential arrives → voltage-gated Ca²⁺ channels open → Ca²⁺ influx triggers synaptic vesicles to fuse with the presynaptic membrane → acetylcholine (ACh) diffuses across the cleft → binds receptors on the postsynaptic membrane → Na⁺ channels open → depolarisation (an excitatory postsynaptic potential, EPSP); if threshold is reached, a new action potential fires. Acetylcholinesterase in the cleft hydrolyses ACh, ending the signal — essential for discrete impulses (organophosphate insecticides block this enzyme, causing fatal overstimulation).

Summation: one EPSP rarely reaches threshold — spatial summation (multiple presynaptic neurones firing together) and temporal summation (one neurone firing rapidly) add up to trigger the postsynaptic cell. Inhibitory synapses (e.g. using GABA) hyperpolarise the postsynaptic membrane (an IPSP), raising the effective threshold. The decision to fire integrates all inputs — synapses are the nervous system's microprocessors, enabling complex processing, learning and memory.

Synapses ensure one-way transmission (vesicles exist only on the presynaptic side — pairing with the refractory period's role in the axon) and allow filtering (isolated weak signals fade) and convergence/divergence of pathways. Drugs act at synapses: nicotine mimics ACh (an agonist), atropine blocks ACh receptors (an antagonist), cocaine blocks neurotransmitter reuptake, benzodiazepines enhance GABA (sedative). "Explain drug action" questions trace: drug → synaptic target → effect on transmission → physiological consequence.

Reflexes — the reflex arc

The reflex arc: stimulus → receptor → sensory neurone → relay neurone (spinal cord) → motor neurone → effector → response — bypassing conscious brain processing for speed. Examples: the withdrawal reflex (hand from heat), the knee-jerk (a stretch reflex maintaining posture) and the blinking reflex (protecting the eye), plus autonomic reflexes (pupil dilation, heart-rate adjustment). The brain is informed afterwards (you feel the pain after withdrawing) — the response does not wait for it.

Survival value: speed minimises damage (milliseconds vs the brain's longer processing), and the response is automatic and stereotyped — no learning needed. Investigations measure reaction time (ruler drop, computer tests): identify variables (age, caffeine, practice, distraction), take repeats, calculate means, and evaluate (the ruler-drop measures the whole pathway including muscle response, not just nerve conduction; anticipation skews results — Worked example 4).

Compare nervous and hormonal coordination (previewing Lesson 17): nervous is fast, short-lived, localised and electrochemical; hormonal is slow, long-lasting, widespread and chemical. This comparison table is a guaranteed question — learn it as a table. Reflexes show the nervous system at its simplest; the brain shows it at its most complex, with the same neurone-and-synapse building blocks.

Worked examples — summation, drugs and disease

Worked example 1: summation arithmetic. A postsynaptic neurone rests at −70 mV with a threshold of −55 mV (needs +15 mV of depolarisation). Each EPSP from one synapse contributes +5 mV. A single impulse (+5) fails; three impulses arriving together (spatial summation: 3 × 5 = +15) just reach threshold; or one synapse firing three times in rapid succession (temporal summation) does the same before the depolarisation decays. Meanwhile an IPSP of −8 mV from an inhibitory synapse raises the requirement: excitation must now cover 15 + 8 = +23 mV, so five EPSPs of +5 are required (4 × 5 = +20 falls short). This arithmetic is how neural circuits compute — excitation and inhibition integrated into a firing decision.

Worked example 2: drug actions at the synapse. Nicotine binds ACh receptors (an agonist — it mimics acetylcholine, stimulating the postsynaptic cell; hence its stimulant and addictive effects). Atropine (from deadly nightshade) blocks muscarinic ACh receptors (an antagonist — used medically to dilate pupils and treat abnormally slow heart rate). Organophosphate insecticides inhibit acetylcholinesterase — ACh accumulates, causing continuous stimulation, paralysis and death (the same mechanism as the nerve agent sarin). For each drug: name the synaptic target, state agonist/antagonist/enzyme-blocker, and trace to the physiological effect.

Worked example 3: multiple sclerosis. The immune system attacks oligodendrocyte myelin in the CNS, slowing or blocking saltatory conduction — impulses arrive late, weakened or not at all. Symptoms (muscle weakness, numbness, vision problems, fatigue) reflect disrupted signalling, and they fluctuate as inflammation waxes and wanes (relapsing-remitting MS). Treatments suppress immunity (reducing attacks) but do not repair myelin — linking Lessons 9 and 16. "Explain" answers trace: demyelination → loss of saltatory conduction → slow/failed impulses → functional deficits.

Worked example 4: a reaction-time investigation. Research question: does caffeine reduce reaction time? Design: double-blind, participants receive caffeine or placebo drinks, then complete computerised reaction tests; control age, sleep and practice (randomise order, allow a washout period). Measure: mean of 10 trials per participant. Statistics: a paired t-test comparing each participant's caffeine vs placebo means. Evaluate: the ruler-drop test is cheaper but cruder (it measures the whole arc including muscle movement); computer tests isolate decision time better. Expect small effects — and note that high caffeine doses cause jitteriness, worsening performance (a dose–response nuance worth evaluating).

Common mistakes

• "Impulses travel faster in bigger stimuli." No — action potentials are all-or-nothing and always the same size and speed in a given axon; stimulus intensity is coded by frequency. Speed depends on myelination, diameter and temperature only.
• Swapping the channels. Depolarisation = Na⁺ in; repolarisation = K⁺ out. Drawing the graph without naming which channels are open in each phase forfeits the mechanism marks.
• "The impulse jumps along the axon" for unmyelinated fibres. Saltatory (jumping) conduction occurs only between nodes of Ranvier in myelinated axons; elsewhere conduction is continuous, via local currents.
• Resting potential attributed to the pump alone. The pump sets up the gradients, but the −70 mV itself depends on the membrane being far more permeable to K⁺ than Na⁺ at rest. Answers need both halves.
• Synapse direction errors. Vesicles and ACh release are presynaptic; receptors are postsynaptic; acetylcholinesterase sits in the cleft. One-way transmission follows from this anatomy — state it.

Exam Experience

Q1 (data). A membrane-potential trace shows rest at −70 mV, a peak of +40 mV and a trough of −80 mV. Explain the ion movements producing the rising phase and the trough, and the role of the refractory period that follows. [6 marks] Q2. Describe transmission at a cholinergic synapse, in sequence. [5 marks]

Mark scheme — Q1: Rising phase: threshold reached → voltage-gated Na⁺ channels open → Na⁺ influx down its electrochemical gradient → depolarisation to +40 mV [2]. Repolarisation: Na⁺ channels close/inactivate, voltage-gated K⁺ channels open [1]; K⁺ efflux overshoots because K⁺ channels close slowly → hyperpolarisation to −80 mV (the trough) [1]. Refractory period: inactivated Na⁺ channels prevent a new action potential — ensuring one-way propagation and limiting firing frequency [2].

Mark scheme — Q2: Action potential arrives at the presynaptic terminal [1] → voltage-gated Ca²⁺ channels open, Ca²⁺ enters [1] → vesicles fuse with the presynaptic membrane, releasing acetylcholine into the cleft [1] → ACh binds receptors on the postsynaptic membrane, opening Na⁺ channels → EPSP [1] → if threshold is reached, a postsynaptic action potential fires; acetylcholinesterase hydrolyses ACh to end the signal [1]. Sequence must be in order; naming the enzyme earns the final mark only with its function.