IBDP Biology 2025 SL&HL: C2.2 Neural signaling Study Notes

C2.2.1 – Neurons as Cells That Carry Electrical Impulses

🧬 Structure of a Neuron

Neurons are specialized cells in the nervous system that transmit electrical signals.

Each neuron consists of:

Cell body (soma): Contains the nucleus and cytoplasm.
Axon: A single, long fibre that carries impulses away from the cell body.
Dendrites: Multiple short fibres that carry impulses towards the cell body.

🔌 How Neurons Work

Neurons conduct electrical impulses along their fibres to communicate with other neurons, muscles, or glands.

The direction of the impulse is typically:

Dendrites → Cell body → Axon → Axon terminals

🧠 Example: Motor Neuron

Part	Function
Dendrites	Receive signals from other neurons
Cell body	Processes signals; contains the nucleus
Axon	Transmits the signal over long distances
Axon terminals	Pass the signal to another cell (e.g. a muscle or another neuron)

📌 Key Points:
– Neurons are cells specialized for transmitting electrical impulses.
– Axons carry signals away from the cell body, while dendrites bring them in.
– The cell body holds the nucleus and processes information before sending signals down the axon.

C2.2.2 – Generation of the Resting Potential in Neurons

🔋 What Is the Resting Potential?

The resting potential is the electrical charge difference across the plasma membrane of a neuron when it is not transmitting a signal.

It’s typically around –70 mV, meaning the inside of the neuron is more negative than the outside.

🔄 How the Resting Potential Is Generated

The sodium-potassium pump (Na⁺/K⁺ pump) is a protein in the neuron membrane that uses ATP to move ions:

3 Na⁺ (sodium ions) out
2 K⁺ (potassium ions) in

This active transport process creates a concentration gradient:

High Na⁺ outside
High K⁺ inside

⚡ Why the Inside Is More Negative

Although K⁺ is brought in, many potassium channels are open, so K⁺ leaks back out.

Large negative proteins remain inside the neuron and can’t cross the membrane.

This leads to a net negative charge inside → membrane polarization.

🧠 Key Concepts

Term	Explanation
Resting potential	Electrical charge across the membrane at rest (~–70 mV)
Membrane potential	Difference in charge between inside and outside of the neuron
Polarization	Inside of neuron is more negative than the outside
ATP use	Na⁺/K⁺ pump needs ATP to work against concentration gradients

📌 Key Points:
– The resting potential is around –70 mV.
– The Na⁺/K⁺ pump moves 3 sodium ions out and 2 potassium ions in using ATP.
– The resting potential is negative due to ion gradients and leaky potassium channels.

C2.2.3 – Nerve Impulses as Action Potentials

⚡ What Is a Nerve Impulse?

A nerve impulse is an action potential – a temporary reversal of the electrical charge across a neuron’s membrane.

It’s a rapid, electrical signal that travels along the axon or nerve fibre.

⚙️ How Is It Electrical?

It’s caused by the movement of positively charged ions (Na⁺ and K⁺).

When the neuron is stimulated:

Sodium (Na⁺) channels open
Na⁺ rushes into the cell, making the inside less negative → depolarization

Then:

Potassium (K⁺) channels open
K⁺ flows out, restoring negativity inside → repolarization

🔁 Propagation of the Impulse

The action potential moves along the axon like a wave:

One part depolarizes
It triggers the next section to depolarize

This is called propagation.

🧠 Key Concepts Table

Term	Explanation
Action potential	Rapid change in membrane potential (inside becomes positive briefly)
Depolarization	Na⁺ enters → inside becomes less negative
Repolarization	K⁺ exits → inside becomes more negative again
Propagation	Action potential spreads along the neuron like a domino effect

📊 Real Example

A typical action potential lasts ~3–5 ms and peaks at +30 to +40 mV.

Impulses can travel up to 120 m/s in myelinated axons!

📌 Key Points:
– A nerve impulse is an action potential, involving ion movement.
– Na⁺ and K⁺ ions cause depolarization and repolarization of the membrane.
– The action potential is electrical due to movement of positive ions.
– It propagates along the nerve fibre in one direction.

C2.2.4 – Variation in the Speed of Nerve Impulses

🚀 What Affects the Speed of a Nerve Impulse?

The speed of a nerve impulse can vary depending on:

Axon diameter
Presence or absence of a myelin sheath
Animal size

🔬 Comparisons of Nerve Impulse Speed

Fibre Type	Speed	Reason
Giant axons (e.g. squid)	Fast	Large diameter → less resistance to ion flow
Small, non-myelinated fibres	Slow	Narrow → more resistance; no insulation
Myelinated fibres (e.g. humans)	Very fast (up to 120 m/s)	Saltatory conduction – impulse jumps between nodes
Non-myelinated fibres	Slower	Impulse travels continuously → slower conduction

💡 Key Terms

Myelin sheath: Fatty insulating layer around axons.
Saltatory conduction: The “jumping” of impulses between nodes of Ranvier in myelinated axons.
Axon diameter: Wider axons have less resistance → faster impulse.

📉Understanding Correlations

Correlation Type	Description
Negative correlation	As one variable increases, the other decreases
Positive correlation	As one variable increases, the other also increases
Correlation coefficient (r)	Value between -1 and +1 showing strength and direction of correlation
Coefficient of determination (R²)	Indicates how much variation in one variable is explained by another (0 to 1)

📊 Example Correlations

Variables	Type of Correlation
Animal size vs conduction speed	Negative
Axon diameter vs conduction speed	Positive

If R² = 0.85 for axon diameter vs speed, it means 85% of the variation in speed is explained by axon diameter.

📌 Key Points:
– Nerve impulses travel faster in giant or myelinated axons.
– Axon diameter and myelination increase conduction speed.
– Speed is negatively correlated with animal size, but positively correlated with axon diameter.
– Correlation coefficients (r) and R² values help analyse these relationships mathematically.

C2.2.5 – Synapses as Junctions Between Neurons and Effector Cells

🧬 What Are Synapses?

Synapses are tiny gaps (junctions) between:

Two neurons
A neuron and an effector cell (e.g. muscle or gland)

Only chemical synapses are covered here (not electrical).

📩 How Do Synapses Work?

Step	Process
1	An electrical impulse reaches the axon terminal.
2	It triggers release of neurotransmitters from vesicles.
3	Neurotransmitters diffuse across the synaptic cleft.
4	They bind to receptors on the postsynaptic membrane.
5	This generates a new impulse in the next neuron or activates an effector.

🛑 Why Does the Signal Only Go One Way?

Vesicles with neurotransmitters are only in the presynaptic neuron.
Receptors for neurotransmitters are only on the postsynaptic membrane.

This ensures that signals only pass in one direction across synapses.

📘 Key Terms

Term	Meaning
Synaptic cleft	Gap between neurons at a synapse
Neurotransmitter	Chemical messenger (e.g. acetylcholine)
Presynaptic neuron	Sends the signal
Postsynaptic cell	Receives the signal
Effector cell	Muscle or gland cell that responds to a signal

📌 Key Points:
– Synapses connect neurons or neurons to effectors (muscles/glands).
– Only chemical synapses are considered.
– Signal transmission is one-way only due to vesicle and receptor placement.
– Neurotransmitters carry the signal across the synaptic cleft.

C2.2.6 – Release of Neurotransmitters from a Presynaptic Membrane

🧬 What Triggers Neurotransmitter Release?

Neurotransmitters are released from the presynaptic membrane of a neuron when a nerve impulse (action potential) reaches the axon terminal.

🔄 Step-by-Step: How Neurotransmitters Are Released

Step	Event
1	Depolarization of the presynaptic membrane occurs as the action potential arrives.
2	Voltage-gated calcium channels open in the membrane.
3	Calcium ions (Ca²⁺) rush into the presynaptic neuron from the synaptic cleft.
4	Calcium acts as an internal signal, triggering synaptic vesicles.
5	Vesicles move toward and fuse with the presynaptic membrane.
6	Neurotransmitters are released into the synaptic cleft by exocytosis.

🧪 Why Is Calcium Important?

Calcium ions (Ca²⁺) are essential signalling molecules inside the neuron.
They cause vesicle fusion with the membrane so neurotransmitters can be released.
Without calcium uptake, neurotransmission would not occur.

📌 Key Points:
– Depolarization opens calcium channels in the presynaptic membrane.
– Calcium ions enter the neuron and trigger vesicles to release neurotransmitters.
– Neurotransmitters are released by exocytosis into the synaptic cleft.
– Calcium acts as a signalling chemical inside the neuron.

C2.2.7 – Generation of an Excitatory Postsynaptic Potential (EPSP)

🔁 What Happens After Neurotransmitter Release?

Once neurotransmitters like acetylcholine (ACh) are released into the synaptic cleft, they trigger an excitatory postsynaptic potential (EPSP) in the next neuron or muscle cell.

🧪 Step-by-Step: How an EPSP is Generated

Step	What Happens
1	Acetylcholine diffuses across the synaptic cleft.
2	It binds to transmembrane receptors on the postsynaptic membrane (e.g. ligand-gated sodium channels).
3	The receptor changes shape and opens, allowing Na⁺ ions to enter the postsynaptic cell.
4	Influx of Na⁺ causes a small depolarization — this is the EPSP.
5	If enough EPSPs add up (summation), they trigger an action potential in the postsynaptic cell.

🧠 What is an EPSP?

An Excitatory Postsynaptic Potential is a temporary depolarization of the postsynaptic membrane caused by the flow of positive ions (mainly Na⁺).

It brings the membrane potential closer to the threshold needed to fire an action potential.

🧩 Why Acetylcholine?

Acetylcholine is a common excitatory neurotransmitter found in:

Neuromuscular junctions (activates muscles)
Brain and spinal cord synapses

It’s broken down quickly by acetylcholinesterase, stopping its action.

📌 Key Points:
– Acetylcholine diffuses across the synaptic cleft and binds to postsynaptic receptors.
– Sodium channels open, causing Na⁺ influx and slight depolarization.
– This is called an EPSP – it increases the chance of an action potential.
– Acetylcholine is used in many types of synapse, including neuromuscular junctions.

Additional Higher Level

C2.2.8 – Depolarization and Repolarization During Action Potentials

⚙️ What is an Action Potential?

An action potential is a rapid, temporary change in membrane potential that travels along a neuron to transmit electrical signals.

To generate an action potential, the membrane must reach a threshold potential (around –55 mV) to trigger the opening of voltage-gated ion channels.

⚡ Depolarization (Making the Inside More Positive)

Event	What Happens
1. Threshold reached	A small stimulus causes the membrane to depolarize to –55 mV.
2. Voltage-gated sodium (Na⁺) channels open	Sodium ions flood into the cell due to the electrochemical gradient.
3. Membrane potential spikes	Inside becomes more positive, rising up to +30 mV.

🔋 Repolarization (Resetting the Charge)

Event	What Happens
4. Na⁺ channels close	After peaking, the sodium channels shut.
5. Voltage-gated potassium (K⁺) channels open	K⁺ ions move out of the neuron.
6. Inside becomes negative again	The membrane repolarizes, dropping back below 0 mV.

⬇️ After-Hyperpolarization (Optional Extra Dip)

Too much K⁺ leaves the cell, briefly making the membrane more negative than resting potential (e.g. –75 mV).
This is called the after-hyperpolarization or undershoot.
It quickly returns to normal via the Na⁺/K⁺ pump and leak channels.

📊 Graph: Action Potential Stages

🔑 Key Channels Involved

Ion Channel	When It Opens	Ion Movement
Voltage-gated Na⁺ channels	When threshold is reached	Na⁺ in (depolarizes)
Voltage-gated K⁺ channels	After Na⁺ peak	K⁺ out (repolarizes)

📌 Key Points:
– Action potentials occur only if the threshold potential (~–55 mV) is reached.
– Depolarization: Na⁺ channels open → Na⁺ enters → inside becomes positive.
– Repolarization: Na⁺ channels close, K⁺ channels open → K⁺ exits → inside becomes negative again.
– Action potentials allow rapid and unidirectional transmission of nerve signals.

C2.2.9 – Propagation of an Action Potential Along a Nerve Fibre/Axon

🚀 What is Propagation?

Propagation = how an action potential travels along an axon. It doesn’t move all at once – it’s regenerated at each point along the membrane. This is possible due to local currents caused by ion diffusion.

🌊 What Are Local Currents?

Local currents are small movements of Na⁺ ions that:

Spread along the inside of the axon (cytoplasm), and
Attract ions on the outside of the membrane.

This movement depolarizes nearby membrane regions, helping them reach the threshold potential (≈ –55 mV).

⚙️ Step-by-Step: How an Action Potential Moves

Step	What Happens
1	A section of axon is depolarized (Na⁺ channels open).
2	Na⁺ floods in → inside becomes more positive.
3	Na⁺ ions diffuse along the inside of the axon to the next region.
4	This local current raises the voltage of the next segment.
5	If it reaches threshold, new Na⁺ channels open and another action potential starts.
🔁	This continues all the way down the axon.

🔄 Why Can’t It Go Backward?

After firing, that region of the axon enters a refractory period. During this time, Na⁺ channels are inactivated, so a new action potential can’t start there. This ensures one-way direction of impulse travel.

🧠 Analogy: Mexican Wave in a Stadium

Just like a wave of people stands up and sits down in sequence during a game, an action potential travels as each part of the axon “fires” and then resets.

📌 Key Points:
– Action potentials move due to local currents caused by sodium ion diffusion.
– These currents cause nearby areas to depolarize, triggering new action potentials.
– The process ensures fast, one-way signal transmission along the axon.

C2.2.10 – Oscilloscope Traces Showing Resting Potentials and Action Potentials

🧪 What is an Oscilloscope Trace?

A graphical display of voltage changes over time used to visualize nerve impulses (action potentials).

X-axis = Time
Y-axis = Membrane potential (mV)

🔋 Key Features of an Action Potential on a Trace

Phase	What Happens	Typical Voltage (mV)
Resting Potential	Na⁺/K⁺ pumps maintain –70 mV	–70 mV
Depolarization	Voltage-gated Na⁺ channels open → Na⁺ in	Up to +30 mV
Repolarization	Voltage-gated K⁺ channels open → K⁺ out	Falls toward –70 mV
Hyperpolarization	Too much K⁺ leaves temporarily	Around –80 mV
Return to Resting	Pumps restore original gradient	Back to –70 mV

📊 Interpreting the Trace:

Before spike = resting (–70 mV)
Rising curve = depolarization (Na⁺ in)
Peak = maximum voltage (+30 mV)
Falling curve = repolarization (K⁺ out)
Dip below baseline = hyperpolarization
Flat line return = back to resting potential

⏱️ Measuring Impulse Frequency (Hz or impulses/sec)

To calculate:

Measure time between peaks on the oscilloscope.
Use the formula:
Frequency (Hz) = 1 / time interval (s)

More frequent impulses = stronger stimulus or higher intensity.

📌 Key Points:
– Oscilloscopes show voltage changes during action potentials.
– Each phase on the trace corresponds to ion movements across the membrane.
– Impulse frequency can be calculated from the time between peaks.

C2.2.11 – Saltatory Conduction in Myelinated Fibres

🧠 What is Saltatory Conduction?

A fast method of transmitting nerve impulses along myelinated axons.
The action potential “jumps” from one node of Ranvier to the next.

🧪 How It Works:

Feature	Role in Saltatory Conduction
Myelin sheath	Insulates axon; prevents ion flow in these regions
Nodes of Ranvier	Gaps in the myelin where ion channels are concentrated
Na⁺/K⁺ pumps & ion channels	Only located at nodes – where depolarization happens
Jumping effect	Action potential only forms at the nodes, not along the whole axon

➡️ This speeds up transmission because less of the membrane needs to depolarize!

🚀 Why Is It Faster Than Non-Myelinated Conduction?

Non-myelinated axons: Impulse moves continuously along entire axon
Myelinated axons (saltatory): Impulse skips between nodes → less resistance, faster depolarization
Saltatory conduction = up to 120 m/s
Non-myelinated conduction = around 2 m/s

🧠 Real-World Analogy:

Imagine walking vs hopping:

Non-myelinated = walking the whole path
Myelinated = hopping between stones in a river = faster and more efficient

📌 Key Points:
– Saltatory conduction = impulse “jumps” from node to node.
– Myelin prevents ion flow except at nodes of Ranvier.
– Increases impulse speed significantly compared to continuous conduction.

C2.2.12 – Effects of Exogenous Chemicals on Synaptic Transmission

🧠 What Are Exogenous Chemicals?

Exogenous = from outside the body These chemicals can disrupt or enhance synaptic transmission by interfering with neurotransmitters.

Example 1: Neonicotinoids (Pesticides)

Feature	Details
Target	Nicotinic acetylcholine receptors in insects
Mechanism	Binds to receptor → continuous stimulation → no breakdown by enzymes
Effect	Paralysis and death of insects due to blocked synaptic transmission
Use	Widely used in agriculture as insecticides
Selective toxicity	Much less toxic to mammals → different receptor structure in vertebrates

🔒 Neonicotinoids lock the receptors open → nerve impulse can’t reset → synapse fails

Example 2: Cocaine (Drug)

Feature	Details
Target	Dopamine reuptake transporters in brain neurons
Mechanism	Blocks dopamine reuptake → dopamine stays in synaptic cleft longer
Effect	Enhanced stimulation of post-synaptic neuron → feelings of pleasure
Long-term risk	Can lead to addiction, altered brain chemistry, and tolerance

🎯 Cocaine creates an overstimulated synapse by flooding receptors with excess neurotransmitter.

⚖️ Comparison Table

Chemical	Target	Mechanism	Effect on Synapse
Neonicotinoids	Acetylcholine receptors (insects)	Overstimulate, and block receptor	Stops transmission
Cocaine	Dopamine transporters	Prevents reuptake	Enhances transmission

📌 Key Points:
– Exogenous chemicals alter synaptic transmission.
– Neonicotinoids bind irreversibly to acetylcholine receptors in insects, causing paralysis.
– Cocaine blocks dopamine reuptake, increasing stimulation of post-synaptic neurons.
– Effects vary: some enhance signals, others block them entirely.

C2.2.13 – Inhibitory Neurotransmitters and Generation of Inhibitory Postsynaptic Potentials (IPSPs)

❗ What Are Inhibitory Neurotransmitters?

Inhibitory neurotransmitters reduce the chance of a neuron firing an action potential. They create an inhibitory postsynaptic potential (IPSP). Common examples: GABA (gamma-aminobutyric acid), glycine

⚙️ How Do IPSPs Work?

Step	What Happens
1	Inhibitory neurotransmitter is released from the presynaptic neuron
2	It binds to receptors on the postsynaptic membrane
3	This opens chloride (Cl⁻) or potassium (K⁺) channels
4	Cl⁻ enters or K⁺ leaves the neuron
5	The inside of the neuron becomes more negative than usual = hyperpolarized
6	Harder to reach threshold potential → no action potential fired

📉 Excitatory vs Inhibitory Synapses

Type	Neurotransmitter	Effect on Membrane	Result
Excitatory	e.g. Acetylcholine	Depolarization (Na⁺ in)	Increases chance of action potential
Inhibitory	e.g. GABA, Glycine	Hyperpolarization (Cl⁻ in or K⁺ out)	Decreases chance of action potential

🧯 IPSPs act like a “brake” to suppress unnecessary signals.

📌 Key Points:
– Inhibitory neurotransmitters prevent action potentials by hyperpolarizing the postsynaptic membrane.
– This is done by increasing the negative charge inside the neuron (via Cl⁻ in or K⁺ out).
– IPSPs make neurons less likely to fire, balancing excitatory inputs in the nervous system.

C2.2.14 – Summation of the Effects of Excitatory and Inhibitory Neurotransmitters in a Postsynaptic Neuron

🧩 What Is Summation?

Summation = the combined effect of multiple excitatory and inhibitory neurotransmitters on a postsynaptic neuron. It determines whether the threshold potential is reached and an action potential is fired. Neurons integrate signals from many synapses at once.

🔄 Types of Summation

Type	Description
Temporal Summation	Multiple impulses from one presynaptic neuron in quick succession
Spatial Summation	Impulses from multiple presynaptic neurons firing at the same time

⚖️ Excitatory vs Inhibitory Balance

Excitatory neurotransmitters (e.g. acetylcholine) cause depolarization (EPSPs).
Inhibitory neurotransmitters (e.g. GABA) cause hyperpolarization (IPSPs).
If net depolarization reaches the threshold, an action potential occurs.
If IPSPs outweigh EPSPs, the neuron won’t fire.

Neurons act like calculators weighing up all inputs before deciding whether to “fire”.

⚡ All-or-Nothing Principle

Once the threshold potential (~ -55mV) is reached, the neuron fires an action potential.
If threshold is not reached, no impulse is generated.
There’s no partial response it’s either all or none.

🎯 Example:

Neuron A sends an EPSP (+5 mV)
Neuron B sends another EPSP (+6 mV)
Neuron C sends an IPSP (–3 mV)
→ Net change = +8 mV
→ If this reaches the threshold, the neuron fires.

📌 Key Points:
– Summation is the combining of excitatory and inhibitory signals.
– It determines whether the postsynaptic neuron reaches threshold and fires.
– The “all-or-nothing” rule ensures that only strong enough signals trigger an action potential.

C2.2.15 – Perception of Pain by Neurons with Free Nerve Endings in the Skin

🩹 What Are Free Nerve Endings?

Free nerve endings are sensory neurons found in the skin.
They are unencapsulated-meaning they are exposed nerve endings that detect pain (nociception).

⚡ How Do They Work?

These neurons have ion channels that open in response to:

High temperatures (e.g. >43°C)
Acidic pH (e.g. lactic acid)
Irritating chemicals like capsaicin (from chili peppers)

🧪 Triggering a Nerve Impulse

When the channels open, positively charged ions (like Na⁺ or Ca²⁺) enter the neuron.

This causes depolarization of the membrane.

If the threshold potential is reached (typically ~ -55 mV):

An action potential is triggered.
The signal travels along the neuron to the spinal cord and brain.

🧠 Where Is Pain Felt?

Although the receptors are in the skin, the sensation of pain is only experienced when the brain processes the signal.
Pain is a perception, not a direct property of the stimulus.

🌶️ Example: Capsaicin

Stimulus	Effect on Free Nerve Endings
Capsaicin (from chilli)	Binds to TRPV1 ion channels, making them open
Result	Na⁺/Ca²⁺ ions enter → depolarization → pain signal sent

📌 Key Points:
– Free nerve endings detect painful stimuli like heat, acid, and chemicals.
– Pain perception starts when ion channels open and positive ions enter.
– If the threshold is reached, a nerve impulse travels to the brain.
– The brain interprets this signal as “pain”.

C2.2.16 – Consciousness as an Emergent Property of Neural Interactions

💡 What Is Consciousness?

Consciousness is the awareness of self and surroundings.
It includes:

Thinking
Feeling
Perceiving
Decision-making

🔁 Emergent Property: What Does That Mean?

An emergent property is a feature that arises from the interaction of simpler parts but cannot be predicted by studying the parts alone.
Consciousness is not the function of any one neuron, but of networks of neurons working together.

🧬 How Does the Brain Create Consciousness?

The brain has ~86 billion neurons.
These neurons form complex networks and communicate using electrical impulses and neurotransmitters.
Through:

Synaptic connections
Signal integration
Feedback loops

➤ The combined activity of many neurons in multiple brain regions gives rise to conscious thought.

🧠 Brain Regions Involved in Consciousness

Region	Function
Cerebral cortex	Higher-order thinking, awareness
Thalamus	Sensory relay station
Brainstem	Maintains alertness and wakefulness
Prefrontal cortex	Decision-making, personality, attention

📘 Real-World Analogy

Consciousness is like a symphony:
Each instrument (neuron) plays its part, but only together do they produce music (consciousness).

📌 Key Points:
– Consciousness is an emergent property of neural networks.
– No single neuron produces it—it’s the result of billions of neurons interacting.
– It’s a higher-level function of the brain as a system.