# Neural signalling

> IB Biology SL · IB Diploma Biology Standard Level
> Source: https://www.owlsprep.com/study/ib-biology-sl-u3-neural-signalling/

This module covers core neural signalling concepts including resting potential maintenance, action potential generation, propagation, and cholinergic synaptic transmission, fully aligned to IB SL Biology assessment criteria.

**Prerequisites:** [Phospholipid bilayer structure and passive/active membrane transport](https://www.owlsprep.com/study/ib-biology-sl-u2-membrane-transport/); [Function of transmembrane protein pumps and channel proteins](https://www.owlsprep.com/study/ib-biology-sl-u2-membrane-proteins/)

## Learning objectives

- Explain how resting potential is maintained across the neuron axon membrane
- Describe the full sequence of events that generate an action potential
- Outline action potential propagation including saltatory conduction in myelinated neurons
- Explain the stepwise process of cholinergic synaptic transmission

## Resting Potential Maintenance

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.

*Notation:* $V_m = -70mV$

- 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

**Worked example:** 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

**Check your understanding**

1. 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

   *Why:* K+ leakage out of the neuron accounts for ~80% of the total negative resting charge.

## Action Potential Generation

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

> **tip**
>
> IB mark schemes almost always award a dedicated mark for stating the all-or-nothing principle: action potentials do not vary in amplitude, only frequency changes with stimulus strength.

**Worked example:** 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

## Action Potential Propagation and Saltatory Conduction

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.

**Comparing methods**

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
  - 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
  - Cons: Requires glial cells to produce myelin sheath

**Worked example:** 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. $$Speed ratio = \frac{80 \ m/s}{1.5 \ m/s}$$
2. The ratio is ~53, meaning the myelinated axon propagates signals over 50x faster than the unmyelinated equivalent.

## Cholinergic Synaptic Transmission

Synapses are gaps between neurons where signals are transmitted chemically, preventing backwards propagation of action potentials and allowing for signal integration across multiple inputs.

**Exam command terms**

IB exam command terms for this topic have strict mark requirements:

- **Outline synaptic transmission** — You must list at least 4 sequential steps to earn full marks

- **Explain the role of acetylcholinesterase** — You must state it breaks down acetylcholine in the cleft to prevent continuous post-synaptic stimulation

- 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

**Worked example:** 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

## Common pitfalls

- **Wrong:** Stating the resting potential is generated exclusively by the Na+/K+ pump
  - Why it fails: K+ diffusion out of the neuron via leak channels contributes ~80% of the negative internal charge, the pump only maintains concentration gradients
  - Correct: Explicitly separate the role of K+ leak channels as the main driver of negative resting potential, with the pump sustaining ion concentration differences
- **Wrong:** Claiming action potential amplitude increases with stronger stimulus strength
  - Why it fails: Action potentials follow the all-or-nothing principle, so their magnitude is fixed at ~110mV total change above resting potential
  - Correct: Note that stronger stimuli only increase the frequency of action potentials, not their individual amplitude
- **Wrong:** Describing saltatory conduction as ions jumping across the myelin sheath
  - Why it fails: Ions cannot cross the thick lipid myelin layer, they only move across the membrane at exposed nodes of Ranvier
  - Correct: Explain local positive current flow between adjacent nodes, with depolarization restricted exclusively to gaps in the myelin sheath
- **Wrong:** Stating neurotransmitters enter the post-synaptic neuron to trigger depolarization
  - Why it fails: Neurotransmitters are large polar molecules that cannot cross the post-synaptic membrane, they only bind to external surface receptors
  - Correct: Clarify that neurotransmitters bind to extracellular domains of ligand-gated ion channels to trigger Na+ influx into the post-synaptic cell
- **Wrong:** Omitting acetylcholinesterase from extended explanations of synaptic transmission
  - Why it fails: IB mark schemes award a dedicated independent mark for describing the breakdown and recycling of neurotransmitter in the synaptic cleft
  - Correct: Always include the role of acetylcholinesterase as a final mandatory step in cholinergic synaptic transmission descriptions

## 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 |

## 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.

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