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PSYC10003 · Mind, Brain and Behaviour 1

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Chapter 7 of 13 · PSYC10003

Neurons, Synapses and Neural Communication

Week 7 teaches the cellular basis of behaviour: neuron structure, the resting membrane potential, the all-or-none action potential and its propagation, and chemical synaptic transmission via neurotransmitters. It links excitatory and inhibitory signalling (EPSPs and IPSPs, glutamate and GABA) to how the brain integrates information, and covers agonist/antagonist drug action. The examinable skill, within the 25% Behavioural Neuroscience block, is sequencing the events of an action potential with the correct voltages and describing how a signal crosses the synapse.

In this chapter

What this chapter covers

  • 01Neuron structure: dendrites → soma → axon (myelin sheath) → terminal buttons
  • 02Resting membrane potential ≈ −70 mV; threshold of excitation ≈ −50 mV; peak ≈ +40 mV
  • 03Action-potential sequence: Na⁺ in (depolarisation) → K⁺ out (repolarisation) → hyperpolarisation/refractory
  • 04All-or-none law and the rate law (stimulus strength coded by firing frequency)
  • 05Saltatory conduction: the action potential jumps between nodes on myelinated axons
  • 06Synaptic transmission: vesicle release → diffusion across the cleft → receptor binding → reuptake
  • 07EPSP (glutamate, depolarising) vs IPSP (GABA, hyperpolarising); neural integration at the axon hillock
  • 08Receptors as lock-and-key; agonists activate, antagonists block
Worked example · free

Ordering the action potential and reading a synaptic input

Q [4 marks]. (a) Put these events in the correct order and give the approximate membrane potential at each labelled point: threshold reached; peak of the action potential; resting potential; sodium channels open and Na⁺ flows in; potassium flows out. (b) A neurotransmitter binding opens channels that let positive ions in, depolarising the postsynaptic membrane. Name this potential and state its effect on the likelihood of firing. Name a transmitter that does this. (4 marks)
  • +1Start at rest and trigger the rise. Resting potential ≈ −70 mV; a stimulus opens Na⁺ channels and Na⁺ flows in, depolarising the membrane toward 0.
  • +1Cross threshold to the peak. When depolarisation reaches threshold ≈ −50 mV an action potential is triggered; Na⁺ continues in and the potential rises to a peak ≈ +40 mV.
  • +1Fall back down. At the peak Na⁺ channels become refractory and K⁺ flows out, repolarising the membrane; it briefly overshoots below −70 mV (hyperpolarisation/refractory period) before returning to rest. Full order: resting (−70) → Na⁺ in / depolarisation → threshold (−50) → peak (+40) → K⁺ out / repolarisation → hyperpolarisation → resting.
  • +1Read the synaptic input. A depolarising input that makes firing more likely is an excitatory postsynaptic potential (EPSP); it increases the chance the postsynaptic neuron reaches threshold. The primary excitatory transmitter is glutamate (contrast an IPSP, which hyperpolarises and is driven by GABA).
(a) Order: resting potential (−70 mV) → Na⁺ channels open, Na⁺ in / depolarisation → threshold (−50 mV) → peak of the action potential (+40 mV) → K⁺ flows out / repolarisation → hyperpolarisation → back to −70 mV. (b) An excitatory postsynaptic potential (EPSP); it increases the likelihood of an action potential; glutamate is the primary excitatory transmitter.
Sia tip — Memorise the three voltages as a story: rest −70, fire at −50, top out at +40, then K⁺ brings you back down. Sodium in goes up, potassium out comes down. Ask Sia to scramble the steps and have you re-order them with voltages — a dependable Behavioural Neuroscience item.
Glossary

Key terms

Resting membrane potential
The neuron's polarised state at rest, about −70 mV inside relative to outside, maintained by ion distributions across the membrane.
Action potential
The rapid, all-or-none change in membrane potential when a neuron fires: Na⁺ influx depolarises to about +40 mV once threshold (about −50 mV) is reached, then K⁺ efflux repolarises.
All-or-none law / rate law
An action potential fires fully or not at all (fixed amplitude); because amplitude is fixed, stimulus strength is coded by the frequency of firing (the rate law).
Saltatory conduction
Faster propagation along myelinated axons, where the action potential jumps between the unmyelinated nodes rather than travelling continuously.
EPSP vs IPSP
An excitatory postsynaptic potential depolarises the membrane and increases the chance of firing (glutamate); an inhibitory postsynaptic potential hyperpolarises it and decreases the chance of firing (GABA).
Agonist vs antagonist
A drug that activates a receptor like the natural transmitter is an agonist; one that binds and blocks the receptor, preventing activation, is an antagonist.
FAQ

Neurons, Synapses and Neural Communication FAQ

What causes the rising and falling phases of the action potential?

The rising phase (depolarisation) is caused by sodium (Na⁺) rushing into the cell once channels open; the falling phase (repolarisation) is caused by potassium (K⁺) leaving as its channels open and sodium channels become refractory. A brief hyperpolarisation follows before the neuron returns to about −70 mV.

What does 'all-or-none' mean, and how is stimulus strength encoded?

All-or-none means an action potential either fires at full amplitude or not at all — a stronger stimulus does not make a bigger spike. Instead, stimulus strength is encoded by how frequently the neuron fires: the rate law. This is a common MCQ point.

How does a signal cross the synapse?

The action potential reaching the terminal triggers synaptic vesicles to fuse with the presynaptic membrane and release neurotransmitter into the cleft; the transmitter diffuses across and binds receptors on the postsynaptic membrane, producing an EPSP or IPSP. Leftover transmitter is cleared by reuptake, and the presynaptic cell influences the postsynaptic cell only chemically.

What is the difference between glutamate and GABA?

Glutamate is the brain's primary excitatory neurotransmitter — it produces EPSPs that depolarise the postsynaptic membrane and increase firing. GABA is the primary inhibitory neurotransmitter — it produces IPSPs that hyperpolarise the membrane and decrease firing. A neuron sums all its EPSPs and IPSPs (neural integration) and fires only if net excitation passes threshold.

How do drugs act as agonists or antagonists?

Receptors are selective (lock-and-key). An agonist mimics the natural transmitter and activates the receptor; an antagonist binds and blocks it so the natural transmitter cannot act. Drugs can affect any stage — synthesis, release, receptor binding or reuptake — which is why they change psychological function.

Study strategy

Exam move

Commit the action-potential trace to memory as three numbers (−70 rest, −50 threshold, +40 peak) and two ions (Na⁺ in = up, K⁺ out = down), then be able to narrate the sequence including hyperpolarisation and the refractory period. Keep the synaptic sequence as a five-step chain (arrival → vesicle fusion → release → binding → reuptake) and pair EPSP/IPSP with glutamate/GABA and depolarise/hyperpolarise. Finish with agonist vs antagonist. These are among the most predictable MCQs in the Behavioural Neuroscience block, so drill the ordering rather than re-reading prose. Confirm exam details on Canvas.

Working through Neurons, Synapses and Neural Communication in PSYC10003? Sia is AskSia’s AI Psychology tutor — ask any PSYC10003 Neurons, Synapses and Neural Communication question and get a clear, step-by-step explanation grounded in how PSYC10003 is taught and assessed. Read this chapter free, then take your hardest questions to Sia.

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