Neural signalling
IB Biology SLΒ· 12 min read
1. Resting Potential Maintenanceβ β ββββ± 3 min
At rest, neurons maintain a consistent negative internal charge relative to the extracellular fluid, driven by unequal ion distribution across the axon membrane.
Resting Potential
The stable voltage difference across an inactive neuron membrane, where the inside is 70mV more negative than the outside.
The Na+/K+ ATPase pump moves 3 Na+ ions out of the neuron for every 2 K+ ions pumped in, using ATP
K+ leak channels are permanently open, allowing K+ to diffuse out of the neuron down its concentration gradient
Large negatively charged organic molecules inside the neuron cannot cross the membrane, adding to internal negative charge
Explain why the resting potential of a neuron would rise to -20mV if all K+ leak channels were blocked
- 1
First, identify the main contributor to negative internal charge at rest: outward diffusion of K+ ions via leak channels
- 2
If K+ cannot exit the neuron, the net loss of positive charge from the cytoplasm stops
- 3
The Na+/K+ pump will still generate a small net negative charge (3 positive out, 2 positive in), but this is far smaller than the contribution from K+ leakage, leading to a much less negative resting potential of ~-20mV
Which ion movement is the largest contributor to the negative resting potential?
A) Na+ pumped out by the Na+/K+ pump
B) K+ diffusing out through leak channels
C) Na+ diffusing in through open channels
D) Ca2+ entering the axon
Reveal answer
B βK+ leakage out of the neuron accounts for ~80% of the total negative resting charge.
2. Action Potential Generationβ β β βββ± 3 min
An action potential is triggered when a local depolarization raises the membrane potential above a threshold of ~-55mV, activating voltage-gated ion channels in a sequential, all-or-nothing sequence.
Depolarization: Voltage-gated Na+ channels open, Na+ rushes into the neuron, reversing membrane potential to +40mV
Repolarization: Na+ channels inactivate, voltage-gated K+ channels open, K+ rushes out of the neuron to return internal charge to negative
Refractory period: K+ channels remain open briefly, causing a small hyperpolarization before the membrane returns to resting potential
Label the 3 key phases of an action potential trace recorded on an oscilloscope
- 1
Phase 1 (Rising edge): Rapid depolarization from -55mV threshold to +40mV, caused by Na+ influx
- 2
Phase 2 (Falling edge): Repolarization from +40mV back to ~-75mV, caused by K+ efflux
- 3
Phase 3: Hyperpolarization / refractory period, before the membrane returns to the -70mV resting potential
3. Action Potential Propagation and Saltatory Conductionβ β β βββ± 3 min
Local current flow from a depolarized section of axon triggers opening of adjacent voltage-gated Na+ channels, moving the action potential forward along the axon. Myelination drastically increases propagation speed.
Two modes of action potential propagation exist in neurons:
Continuous Conduction
Occurs in unmyelinated axons, with every section of membrane depolarizing sequentially
+ Pros: No myelin required, works for small local neurons
β Cons: Slow (~1 m/s), high ATP demand for Na+/K+ pumps
Saltatory Conduction
Occurs in myelinated axons, with depolarization only happening at exposed nodes of Ranvier, 1-2mm apart
+ Pros: Very fast (~100 m/s), 100x less ATP used
β Cons: Requires glial cells to produce myelin sheath
Calculate how many times faster a myelinated axon conducting at 80 m/s is than an unmyelinated axon of the same diameter conducting at 1.5 m/s
- 1
- 2
The ratio is ~53, meaning the myelinated axon propagates signals over 50x faster than the unmyelinated equivalent.
4. Cholinergic Synaptic Transmissionβ β β β ββ± 3 min
Synapses are gaps between neurons where signals are transmitted chemically, preventing backwards propagation of action potentials and allowing for signal integration across multiple inputs.
Action potential arrives at the presynaptic axon terminal, opening voltage-gated Ca2+ channels
Ca2+ influx triggers synaptic vesicles full of acetylcholine to fuse with the presynaptic membrane
Acetylcholine diffuses across the 20nm synaptic cleft, binding to ligand-gated Na+ receptors on the post-synaptic membrane
Na+ enters the post-synaptic neuron, triggering a local depolarization that can initiate a new action potential if threshold is reached
Acetylcholinesterase breaks down acetylcholine, products are reabsorbed into the presynaptic terminal for recycling
Predict the effect of a neurotoxin that blocks all post-synaptic acetylcholine receptors
- 1
Acetylcholine will still be released from the presynaptic neuron into the synaptic cleft normally
- 2
No ligand-gated Na+ channels will open on the post-synaptic membrane, so no local depolarization occurs
- 3
The signal cannot cross the synapse, so neural transmission is fully blocked, causing paralysis of downstream effectors like muscle cells
5. Common Pitfalls
Wrong move:
Stating the resting potential is generated exclusively by the Na+/K+ pump
Why:
K+ diffusion out of the neuron via leak channels contributes ~80% of the negative internal charge, the pump only maintains concentration gradients
Correct move:
Explicitly separate the role of K+ leak channels as the main driver of negative resting potential, with the pump sustaining ion concentration differences
Wrong move:
Claiming action potential amplitude increases with stronger stimulus strength
Why:
Action potentials follow the all-or-nothing principle, so their magnitude is fixed at ~110mV total change above resting potential
Correct move:
Note that stronger stimuli only increase the frequency of action potentials, not their individual amplitude
Wrong move:
Describing saltatory conduction as ions jumping across the myelin sheath
Why:
Ions cannot cross the thick lipid myelin layer, they only move across the membrane at exposed nodes of Ranvier
Correct move:
Explain local positive current flow between adjacent nodes, with depolarization restricted exclusively to gaps in the myelin sheath
Wrong move:
Stating neurotransmitters enter the post-synaptic neuron to trigger depolarization
Why:
Neurotransmitters are large polar molecules that cannot cross the post-synaptic membrane, they only bind to external surface receptors
Correct move:
Clarify that neurotransmitters bind to extracellular domains of ligand-gated ion channels to trigger Na+ influx into the post-synaptic cell
Wrong move:
Omitting acetylcholinesterase from extended explanations of synaptic transmission
Why:
IB mark schemes award a dedicated independent mark for describing the breakdown and recycling of neurotransmitter in the synaptic cleft
Correct move:
Always include the role of acetylcholinesterase as a final mandatory step in cholinergic synaptic transmission descriptions
6. Quick Reference Cheatsheet
Process | Key Molecules | Mandatory IB Mark Scheme Points |
|---|---|---|
Resting Potential | Na+/K+ pump, K+ leak channels | -70mV, high Na+ outside, high K+ inside |
Action Potential | Voltage-gated Na+ / K+ channels | Depolarization -> Repolarization -> Refractory period, all-or-nothing |
Saltatory Conduction | Myelin sheath, Nodes of Ranvier | 50-100x faster than continuous conduction, lower ATP demand |
Synaptic Transmission | Acetylcholine, Ca2+, Acetylcholinesterase | Presynaptic Ca2+ influx, neurotransmitter diffusion across cleft, recycling |
When this came up on past exams
AI-estimated based on syllabus patterns β cross-check with official past papers for accuracy. Use only as revision-focus signals.
- 2023 Β· P2
Action potential graph analysis
- 2022 Β· P1
Synaptic transmission MCQ
- 2021 Β· P2
Resting potential explanation
What's Next
Mastering neural signalling gives you the core foundational knowledge to tackle high-weight extended response questions on nervous system function that appear in almost every IB SL Biology exam. You will build directly on these concepts to explore how recreational and medicinal drugs modify synaptic activity, a very common 6-mark essay topic. This content also links tightly to your understanding of homeostasis, as the nervous system coordinates fast, rapid responses to internal and external changes alongside the slower endocrine system. Ensure you can accurately interpret and label action potential traces, as these data analysis questions are almost guaranteed to appear on your final assessment.