Nervous Communication
The nervous system transmits information as electrical impulses — rapid, targeted, and short-lived. Three types of neurone link receptors to the central nervous system and from there to effectors. The resting neurone maintains a voltage across its membrane through continuous ion pumping; a stimulus above threshold triggers an action potential: a self-propagating wave of depolarisation that travels the length of the axon. At the synapse, the electrical signal is converted to a chemical one — neurotransmitter released by vesicle exocytosis, diffusing across the cleft, binding to receptors, and either exciting or inhibiting the next neurone.
Neurones & electrical potentials
Neurone types and structure
Three types of neurone link sensory receptors to the central nervous system and from there to effectors. All share the same fundamental structure — cell body, dendrites, and axon — but differ in the arrangement of these components and their functional role:
| Type | Function | Structural features | Where found |
|---|---|---|---|
| Sensory (afferent) | Carry impulses from receptor to CNS | Long peripheral process from receptor; cell body off to one side (unipolar); axon enters CNS via dorsal root | Peripheral nervous system; dorsal root ganglia |
| Relay (interneurone) | Connect sensory neurones to motor neurones within the CNS; integrate signals | Many short dendrites and axon branches; multiple synaptic connections | Brain and spinal cord (CNS only) |
| Motor (efferent) | Carry impulses from CNS to effectors (muscles or glands) | Long axon leaving CNS; cell body in spinal cord or brain | Peripheral nervous system; ventral root of spinal cord |
Myelinated vs unmyelinated neurones
The axon is wrapped in a myelin sheath formed by Schwann cells (in the peripheral nervous system) or oligodendrocytes (CNS). The sheath is interrupted at regular intervals by nodes of Ranvier — short gaps (~1 µm) where the axon is exposed. Voltage-gated Na⁺ and K⁺ channels are concentrated at the nodes.
Function: insulates the axon; action potentials only occur at nodes of Ranvier → saltatory conduction (faster and more energy-efficient).
The axon has no myelin sheath. Ion channels are distributed continuously along its entire length, and the action potential propagates as a continuous wave along the membrane.
Function: slower conduction; found in autonomic neurons and pain fibres. Less energy-demanding in terms of Schwann cell production, but the Na⁺/K⁺ pump must restore concentrations along the whole length after each impulse.
Resting membrane potential
At rest, a neurone maintains a resting membrane potential of approximately −70 mV (inside negative relative to outside). This is maintained by two mechanisms acting together:
Mechanism 1 — Na⁺/K⁺ ATPase pump (active transport):
- The pump actively transports 3 Na⁺ out of the cell for every 2 K⁺ in, per cycle
- This creates a higher Na⁺ concentration outside and a higher K⁺ concentration inside
- The unequal exchange (3 out vs 2 in) also contributes a small electrical charge difference
- This process requires ATP continuously
Mechanism 2 — selective permeability of resting membrane:
- At rest, the membrane has leak channels for K⁺ that allow K⁺ to diffuse slowly out down its concentration gradient
- K⁺ leaving takes positive charge out, making the inside more negative
- Na⁺ channels are mostly closed at rest — Na⁺ cannot enter to offset this
- Large negatively charged proteins remain inside the cell — they cannot cross the membrane, adding to the internal negative charge
The combined result: inside is ~−70 mV relative to outside. This is the resting membrane potential, maintained as long as the pump operates.
Action potential
A action potential is a transient, rapid reversal of membrane potential from −70 mV to approximately +30–40 mV, followed by return to resting potential. It is the electrical signal that travels along neurones. It is all-or-nothing: if the threshold potential (~−55 mV) is reached, an action potential fires; below threshold, nothing happens.
- Resting state (−70 mV): voltage-gated Na⁺ channels closed; K⁺ leak channels open; Na⁺/K⁺ pump maintaining ion gradients
- Depolarisation: a stimulus depolarises the membrane to threshold (~−55 mV); voltage-gated Na⁺ channels open; Na⁺ rushes IN down its electrochemical gradient; inside becomes less negative, then positive (reaches ~+30 to +40 mV)
- Repolarisation: Na⁺ channels inactivate (close); voltage-gated K⁺ channels open; K⁺ rushes OUT; inside becomes more negative again
- Hyperpolarisation (undershoot): K⁺ channels close slowly; K⁺ overshoots, taking the potential below −70 mV briefly (to ~−80 mV)
- Return to resting potential: K⁺ channels close; Na⁺/K⁺ pump restores ion concentrations; membrane returns to −70 mV
All-or-nothing principle and the refractory period
If stimulus is below threshold: no action potential. If stimulus reaches threshold: a full action potential fires, always to the same amplitude (~100 mV swing). Increasing stimulus intensity above threshold does NOT produce a larger action potential — instead, it increases the frequency of action potentials.
The interval after an action potential during which no new action potential can be generated (absolute refractory period) or requires a larger-than-normal stimulus (relative refractory period). Caused by Na⁺ channels being inactivated and K⁺ channels still open.
Roles of the refractory period:
- Ensures action potentials travel in one direction only (the membrane behind the impulse is refractory and cannot re-fire)
- Limits the maximum frequency of impulses (typically ~500 per second max)
- Preserves discrete action potentials — prevents summation into continuous depolarisation
Which change in ion movement is responsible for the depolarisation phase of an action potential?
- A. K⁺ flowing into the cell through voltage-gated channels
- B. Na⁺ flowing into the cell through voltage-gated channels
- C. Na⁺ being actively pumped into the cell
- D. K⁺ flowing out of the cell through voltage-gated channels
Conduction & synaptic transmission
Saltatory conduction vs continuous conduction
| Feature | Saltatory conduction (myelinated) | Continuous conduction (unmyelinated) |
|---|---|---|
| How AP propagates | Jumps from node of Ranvier to node of Ranvier; depolarisation occurs only at nodes; local currents flow through cytoplasm between nodes | Depolarises adjacent membrane continuously along entire axon length |
| Speed | Much faster: up to 120 m s⁻¹ in large myelinated fibres | Much slower: 0.5–2 m s⁻¹ in small unmyelinated fibres |
| Energy efficiency | More efficient: Na⁺/K⁺ pump only needs to restore gradients at nodes (small area) | Less efficient: pump must restore gradients along entire axon membrane |
| Ion channel distribution | Voltage-gated channels concentrated at nodes of Ranvier only | Voltage-gated channels distributed along the whole axon |
- An action potential occurs at node 1 — Na⁺ rushes in, making the inside of the axon locally positive
- The local positive charge flows through the axoplasm (cytoplasm) along the inside of the myelinated segment to node 2 — the myelin insulates the outside, so charge is not lost
- At node 2, this local current depolarises the membrane above threshold, triggering a new action potential
- Node 1 is now in the refractory period (cannot re-fire), so propagation continues only forward
- The action potential “jumps” from node to node (saltare = to jump in Latin) — far faster than continuous depolarisation
Synapse structure
A synapse is a junction between two neurones (or between a neurone and an effector cell) where a signal is transmitted from the presynaptic to the postsynaptic cell via chemical neurotransmitters. Because the conversion requires time and chemical diffusion, synapses introduce a slight delay in transmission.
| Structure | Description & function |
|---|---|
| Synaptic knob (bouton) | Swollen presynaptic terminal of the axon; contains vesicles and mitochondria |
| Synaptic vesicles | Small membrane-bound spheres in the presynaptic neurone, each containing hundreds of neurotransmitter molecules |
| Mitochondria (presynaptic) | Supply ATP for vesicle recycling, Ca²⁺ pumping, and active transport in the synapse |
| Synaptic cleft | ~20–30 nm gap between presynaptic and postsynaptic membranes; neurotransmitter diffuses across |
| Presynaptic membrane | Contains Ca²⁺ channels; vesicles fuse here by exocytosis |
| Postsynaptic membrane | Contains specific receptor proteins complementary to the neurotransmitter; contains chemically-gated ion channels |
Cholinergic synaptic transmission
A cholinergic synapse uses acetylcholine (ACh) as its neurotransmitter. This is the type of synapse required for the 9700 syllabus:
- An action potential arrives at the presynaptic axon terminal
- Depolarisation of the presynaptic membrane opens voltage-gated Ca²⁺ channels; Ca²⁺ flows into the presynaptic terminal from the synaptic cleft
- Ca²⁺ causes synaptic vesicles to move toward and fuse with the presynaptic membrane by exocytosis
- Acetylcholine (ACh) is released into the synaptic cleft
- ACh diffuses across the cleft (~20–30 nm) to the postsynaptic membrane
- ACh binds to specific receptor proteins (nicotinic ACh receptors) on the postsynaptic membrane, opening chemically-gated Na⁺ channels
- Na⁺ flows into the postsynaptic cell, depolarising the membrane — producing an excitatory postsynaptic potential (EPSP)
- If the EPSP reaches threshold, an action potential is generated in the postsynaptic neurone
- Acetylcholinesterase (AChE) in the synaptic cleft rapidly breaks down ACh into choline and ethanoate (acetate) — ending the signal
- Choline is actively reabsorbed by the presynaptic terminal and re-synthesised into ACh using ATP; ACh is repackaged into new vesicles
Ca²⁺ ions act as the coupling agent between the electrical signal (action potential) and the chemical event (vesicle exocytosis). Without Ca²⁺ influx, the action potential cannot trigger neurotransmitter release — this is why many nerve toxins and drugs target Ca²⁺ channels at synapses. The Ca²⁺ influx is proportional to depolarisation; a stronger/longer presynaptic signal releases more Ca²⁺ and more vesicles.
Excitatory and inhibitory synapses
Not all synapses excite the postsynaptic cell. Two types exist with opposite effects:
The neurotransmitter opens Na⁺ channels (or other cation channels); Na⁺ flows in; inside becomes less negative; membrane potential moves toward and possibly above threshold. This brings the postsynaptic cell closer to firing an action potential.
Example: acetylcholine at nicotinic receptors; glutamate (main excitatory neurotransmitter in brain).
The neurotransmitter opens K⁺ or Cl⁻ channels; K⁺ flows out or Cl⁻ flows in; inside becomes more negative than the resting potential; membrane potential moves away from threshold — making it harder to generate an action potential.
Example: GABA (gamma-aminobutyric acid — main inhibitory neurotransmitter in brain); glycine in spinal cord.
Describe the sequence of events at a cholinergic synapse, from an action potential arriving at the presynaptic terminal to the generation of an action potential in the postsynaptic neurone. [8]
- Action potential arrives at presynaptic terminal (axon knob) [1]
- Depolarisation opens voltage-gated Ca²⁺ channels in the presynaptic membrane [1]
- Ca²⁺ ions enter the presynaptic terminal from the synaptic cleft [1]
- Ca²⁺ causes synaptic vesicles to fuse with the presynaptic membrane by exocytosis [1]
- Acetylcholine (ACh) is released into the synaptic cleft [1]
- ACh diffuses across the synaptic cleft to the postsynaptic membrane [1]
- ACh binds to specific complementary receptor proteins on the postsynaptic membrane [1]
- Binding opens chemically-gated Na⁺ channels in the postsynaptic membrane [1]
- Na⁺ flows into the postsynaptic cell, depolarising the membrane (EPSP) [1]
- If EPSP reaches threshold, voltage-gated Na⁺ channels open and an action potential is generated [1]
- Acetylcholinesterase in the cleft breaks down ACh into choline and ethanoate, ending the signal [1]
- Choline is reabsorbed by the presynaptic terminal and ACh is resynthesised and repackaged into vesicles [1]
Summation, synapse roles & the reflex arc
Summation — spatial and temporal
Summation is the process by which postsynaptic potentials add together (or cancel) to determine whether an action potential is generated. A single EPSP is rarely strong enough alone — summation allows integration of multiple inputs:
Multiple different presynaptic neurones arrive at the same postsynaptic cell simultaneously. Each releases a small amount of neurotransmitter, producing a small EPSP. The EPSPs from different synaptic knobs across the postsynaptic cell add together. If their combined effect reaches threshold, an action potential fires.
One presynaptic neurone fires rapidly in succession. Each impulse produces a small EPSP; because the EPSPs arrive faster than they can decay, they overlap and add together. If the combined effect reaches threshold, an action potential fires.
An inhibitory postsynaptic potential (IPSP) from an inhibitory synapse can reduce or cancel the effect of EPSPs from excitatory synapses. The postsynaptic cell integrates all inputs — it fires only if the net effect (EPSPs − IPSPs) reaches threshold. This integration at the postsynaptic membrane is the cellular basis of many nervous system computations.
Roles of synapses
Neurotransmitter vesicles exist only in the presynaptic terminal; receptors exist only on the postsynaptic membrane. So the chemical signal can only travel from pre- to postsynaptic — the signal cannot go backwards. This directionality is essential for maintaining orderly information flow through neural circuits.
One presynaptic neurone can form synapses with many postsynaptic neurones (divergence): one signal can activate multiple pathways simultaneously. Many presynaptic neurones can converge on one postsynaptic neurone (convergence): a single cell integrates inputs from many sources.
Summation of EPSPs and IPSPs allows the postsynaptic cell to act as a decision-maker: only fire if the net input exceeds threshold. Weak or irrelevant signals are filtered out. This allows the nervous system to respond to stimuli selectively.
Repeated use of a synapse can strengthen it (long-term potentiation); new synaptic connections form as a result of experience. This synaptic plasticity is the cellular basis of memory and learning. Conversely, synapses that are rarely used may weaken.
The reflex arc
A reflex arc is the simplest neural pathway producing a reflex response — a rapid, involuntary, stereotyped response to a stimulus that does not require conscious processing. The CNS is involved but the response occurs before the brain is aware of the stimulus (the brain is informed afterwards via ascending pathways).
- Receptor: detects the stimulus (e.g. pain receptor in skin when touching a hot object); converts stimulus energy into a nerve impulse
- Sensory (afferent) neurone: carries impulse from receptor to the spinal cord via the dorsal root
- Relay (interneurone): in the spinal cord grey matter; connects sensory to motor neurone; may integrate input from other sources
- Motor (efferent) neurone: carries impulse from spinal cord via the ventral root to the effector
- Effector: muscle (contracts to withdraw limb) or gland (secretes)
The entire arc bypasses conscious brain processing — the spinal cord integrates and generates the response. The brain receives a copy of the signal and becomes aware of the pain after the withdrawal has already occurred.
Reflexes are much faster than voluntary responses because they use fewer synapses (often only 2–3 neurones in the arc) and do not involve the long pathway to and from the brain. This speed is adaptive — a fraction of a second can prevent or limit tissue damage from harmful stimuli. Many visceral reflexes (heart rate, breathing rate, swallowing, pupil dilation) also operate via reflex arcs involving the autonomic nervous system.
In a withdrawal reflex, in which order do the following components respond to a painful stimulus?
- A. Effector → receptor → sensory neurone → relay neurone → motor neurone
- B. Receptor → motor neurone → relay neurone → sensory neurone → effector
- C. Receptor → sensory neurone → relay neurone → motor neurone → effector
- D. Relay neurone → sensory neurone → receptor → effector → motor neurone
Topic 15A Practice — Comprehensive
Mixed practice across nervous communication topics.
Which correctly describes the role of the Na⁺/K⁺ ATPase pump in maintaining the resting potential?
- A. It pumps 2 Na⁺ out and 3 K⁺ in, using ATP
- B. It pumps 3 Na⁺ out and 2 K⁺ in, using ATP, maintaining higher Na⁺ outside and higher K⁺ inside
- C. It allows Na⁺ to diffuse in and K⁺ to diffuse out by facilitated diffusion
- D. It is inactive at rest; only operates after an action potential
Which correctly explains why myelinated neurones conduct action potentials faster than unmyelinated neurones of the same diameter?
- A. Myelinated neurones have more mitochondria, providing more ATP for faster ion pumping
- B. Myelinated neurones have more voltage-gated channels distributed along the whole axon
- C. The action potential jumps between nodes of Ranvier rather than propagating along the entire axon membrane, because myelin insulates the internodal segments
- D. Myelinated neurones have a larger resting potential, requiring less depolarisation to reach threshold
Describe the ionic events during a complete action potential, including the resting potential, depolarisation, repolarisation, and return to resting state. [8]
- Resting potential (−70 mV): Na⁺/K⁺ pump actively moves 3 Na⁺ out and 2 K⁺ in; K⁺ leak channels allow K⁺ to diffuse out slowly; Na⁺ channels mostly closed; large anions inside the cell; inside is −70 mV relative to outside [any 2 points for 2]
- Depolarisation: stimulus causes membrane to reach threshold (~−55 mV); voltage-gated Na⁺ channels open; Na⁺ rushes in down electrochemical gradient; inside becomes positive (to ~+30–40 mV) [any 2 points for 2]
- Repolarisation: Na⁺ channels inactivate/close; voltage-gated K⁺ channels open; K⁺ rushes out; inside becomes more negative [any 2 points for 2]
- Hyperpolarisation / return to rest: K⁺ channels close slowly; slight undershoot below −70 mV; Na⁺/K⁺ pump restores concentration gradients; membrane returns to −70 mV [any 2 points for 2]
Both insulin signalling (Topic 14) and synaptic transmission (Topic 15) involve Ca²⁺ ions as a key intracellular messenger.
(a) Describe the role of Ca²⁺ specifically at the cholinergic synapse. [3]
(b) Compare the speed of signal transmission in the nervous system with transmission via the endocrine system (hormones). Give TWO differences. [2]
(c) State TWO roles of synapses in the nervous system, other than transmission of a signal. [2]
(a) Ca²⁺ at the cholinergic synapse [3 marks]
- An action potential depolarises the presynaptic terminal, opening voltage-gated Ca²⁺ channels [1]
- Ca²⁺ enters the presynaptic terminal from the synaptic cleft [1]
- Ca²⁺ triggers synaptic vesicles to fuse with the presynaptic membrane by exocytosis, releasing acetylcholine into the cleft [1]
(b) Nervous vs endocrine: TWO differences [2 marks]
- Nervous transmission is faster (milliseconds) than endocrine (seconds to hours); nerve impulses travel along specific neurones to precisely targeted effectors, whereas hormones travel in the blood and reach all cells but only affect those with the correct receptor [1]
- Nervous signals are rapid and short-lived; hormonal signals may be slower to initiate but often longer-lasting [1]
(c) Two other roles of synapses [2 marks]
- Ensure one-way transmission of nerve impulses (vesicles only in presynaptic; receptors only on postsynaptic) [1]
- Summation of signals allows integration / filtering of weak signals; inhibitory synapses can cancel excitatory signals [1]
- Divergence/convergence for signal amplification or multiple pathways [1]
- Basis of memory and learning through new synapse formation / long-term potentiation [1]
Topic 15A — Common Mistakes
- 🔨Saying Na⁺ is pumped IN during depolarisationNa⁺ enters during depolarisation through voltage-gated channels by passive electrochemical diffusion — no pumping. The Na⁺/K⁺ pump is a background maintenance mechanism; it does NOT cause or drive depolarisation. Saying “the pump pumps Na⁺ in to cause depolarisation” is wrong.
- ⚡Confusing depolarisation (Na⁺ in) with repolarisation (K⁺ out)Depolarisation = Na⁺ rushes IN (membrane goes from −70 to +40 mV). Repolarisation = K⁺ rushes OUT (membrane returns from +40 back to ~−70 mV). Getting these reversed is a very common exam error.
- 💥Saying larger stimuli produce larger action potentialsWrong. The action potential is all-or-nothing: once threshold is reached, the amplitude is always ~100 mV regardless of stimulus strength. Larger stimuli produce more frequent action potentials, not larger ones. Amplitude is constant; frequency encodes intensity.
- 🖧Forgetting Ca²⁺ in synaptic vesicle releaseThe action potential alone does not directly cause vesicle exocytosis. The trigger is Ca²⁺ influx through voltage-gated Ca²⁺ channels opened by the arriving action potential. Leaving out Ca²⁺ from the synaptic transmission sequence typically loses 1–2 marks.
- 📉Confusing spatial and temporal summationSpatial = multiple presynaptic neurones firing simultaneously onto the same postsynaptic cell. Temporal = one presynaptic neurone firing rapidly in succession, so EPSPs overlap. The key distinguishing word is “simultaneously” (spatial) vs “rapid succession from one source” (temporal).
- 💯Saying acetylcholine is reabsorbed into the presynaptic terminalWrong. Choline (the breakdown product of ACh) is reabsorbed, not ACh itself. Acetylcholinesterase in the cleft breaks ACh into choline + ethanoate; choline is reabsorbed and used to re-synthesise ACh. Saying “ACh is recycled” is imprecise and may lose marks.
- 🔮Saying the refractory period only prevents backward transmissionThe refractory period has three roles: (1) ensures one-directional propagation (the area behind the impulse cannot re-fire), (2) limits the maximum frequency of impulses, (3) preserves discrete action potentials. Questions asking for “roles of the refractory period” expect all three.
- ❓Saying inhibitory synapses “block” the signalMore precisely, inhibitory synapses hyperpolarise the postsynaptic membrane (make inside more negative), moving it away from threshold. This makes an action potential less likely, but doesn't absolutely prevent it if enough excitatory input also arrives. The postsynaptic cell integrates both inputs; inhibition is a graded effect, not a binary block.
- 💯Confusing the dorsal and ventral rootsSensory neurones enter the spinal cord via the dorsal (posterior) root; their cell bodies are in the dorsal root ganglion. Motor neurones leave via the ventral (anterior) root. Dorsal = back = afferent = sensory; ventral = front = efferent = motor. This is classic Bell-Magendie law and is regularly tested.
- 🎭Saying synapses "slow down" transmission as a disadvantageSynaptic delay is real (~0.5 ms per synapse), but synapses serve crucial functions that outweigh this: one-way transmission, integration of signals (summation), divergence, and memory. The question of whether synaptic delay is a “limitation” depends on context — exam questions framed as “advantages of having synapses” expect the positive roles listed above.
Topic 15A is mechanism-rich and requires precise ionic language. Highest-yield items: resting potential (3 Na⁺ out / 2 K⁺ in by pump; K⁺ leak makes inside negative; Na⁺ channels closed), action potential 5 phases with correct ion movements (Na⁺ in = depolarise / K⁺ out = repolarise), all-or-nothing principle + frequency encoding, refractory period three roles, saltatory vs continuous conduction comparison, cholinergic synapse 8-step sequence with Ca²⁺ trigger, acetylcholinesterase terminates signal, excitatory (Na⁺ in) vs inhibitory (K⁺ out or Cl⁻ in), spatial vs temporal summation, four roles of synapses, reflex arc components in correct order with dorsal/ventral roots. Synoptic links: Topic 4 (ion channels / facilitated diffusion), Topic 14 (Ca²⁺ as messenger, ADH aquaporin), Topic 15B (neuromuscular junction and muscle contraction).