QCE Psychology - Unit 3 - Brain function

Neurotransmission and neurodegenerative disease

Learn action potentials, synaptic transmission, excitation and inhibition, major neurotransmitters, and evidence-based comparisons of Parkinson's and Alzheimer's diseases.

Part of the free QCE Psychology notes library for Unit 3: Brain function.

Updated 2026-08-08 - 5 min read

Neural communication is electrochemical: electrical change carries a signal along a neuron, then chemical transmission crosses most synapses. The exam skill is to explain the sequence and connect disrupted transmission to behaviour without assuming that one neurotransmitter has one simple function.

From resting potential to action potential

A neuron's membrane maintains an unequal distribution of ions. When depolarisation at the axon hillock reaches threshold, voltage-gated channels create an action potential. It is an all-or-none event: stronger stimulation is represented mainly by action-potential frequency and the number of recruited neurons, not by a taller action potential.

The signal propagates along the axon. Myelin allows saltatory conduction between nodes of Ranvier, increasing speed. A refractory period helps ensure one-way propagation and limits firing frequency.

The chemical synapse in seven moves

1. an action potential reaches the presynaptic terminal
2. voltage-gated calcium channels open
3. calcium entry triggers vesicle fusion
4. neurotransmitter is released into the synaptic cleft
5. neurotransmitter binds to receptors on the postsynaptic membrane
6. receptor activity changes the likelihood that the postsynaptic neuron will fire
7. the signal ends through reuptake, enzymatic breakdown or diffusion

An excitatory effect increases the likelihood of postsynaptic firing; an inhibitory effect decreases it. Glutamate is the principal excitatory neurotransmitter in the CNS, while GABA is the principal inhibitory neurotransmitter. The final effect depends on receptor type, location and network state, not only the transmitter's name.

Major neurotransmitters: functions, not slogans

| Neurotransmitter | Important associations | Why oversimplification fails | | --- | --- | --- | | Acetylcholine | skeletal-muscle activation, attention, learning and memory | effects differ between neuromuscular and brain systems | | Epinephrine | arousal and stress response, especially as a hormone in the body | central and peripheral actions differ | | Norepinephrine | arousal, attention, vigilance and stress response | both too little and excessive activity can impair performance | | Dopamine | movement, motivation, reward learning and cognitive control | it is not simply “the pleasure chemical” | | Serotonin | mood regulation, sleep, appetite and other functions | low mood cannot be diagnosed from a simple “chemical imbalance” claim |

A drug may act as an agonist, increasing or mimicking neurotransmitter action, or an antagonist, reducing receptor action. Changing transmission can be therapeutic, harmful or unintended because the same signalling system contributes to several functions.

Parkinson's disease

Parkinson's disease involves progressive loss of dopamine-producing neurons, especially in the substantia nigra, disrupting basal-ganglia circuits that support movement selection. Common motor features include bradykinesia, rigidity, resting tremor and postural instability; non-motor features can also occur.

Treatments manage symptoms rather than restoring every lost neuron. Levodopa increases dopamine synthesis; dopamine agonists stimulate dopamine receptors; deep-brain stimulation can alter dysfunctional circuit activity for selected patients. Each has limitations and possible adverse effects.

Alzheimer's disease

Alzheimer's disease is a progressive neurodegenerative disorder associated with impaired memory and cognition. Pathology includes amyloid plaques, tau-related neurofibrillary tangles, synaptic dysfunction and neuronal loss. Early impairment commonly affects episodic memory, but progression can affect language, reasoning, orientation and daily functioning.

Cholinesterase inhibitors can increase the availability of acetylcholine and temporarily support symptoms for some patients. Other medicines may target different disease processes or symptoms, but treatment effectiveness and eligibility vary. A complete answer distinguishes proposed biological mechanisms, observed symptoms and treatment goals.

Worked comparison

How to evaluate a neurotransmitter claim

Ask four questions:

• What pathway and receptor are involved?
• Is the evidence correlational, experimental or clinical?
• Does the intervention change symptoms, underlying disease, or both?
• What alternative pathways and side effects matter?

A treatment response can support a mechanism but does not prove a single-cause explanation. Behavioural neuroscience informs psychology by constraining explanations with biological evidence while recognising levels from molecules to social context.

Try it yourself

Common exam traps

• reversing presynaptic and postsynaptic structures
• saying stronger stimuli produce larger action potentials
• equating excitation with a pleasant feeling or inhibition with inactivity
• presenting dopamine or serotonin as having only one function
• confusing symptom management with a cure
• using Parkinson's and Alzheimer's interchangeably because both are neurodegenerative

Sources

• QCAA Psychology 2025 v1.3 syllabus
• OpenStax Psychology 2e: Cells of the Nervous System
• National Institute of Neurological Disorders and Stroke: Parkinson's disease
• National Institute on Aging: What happens to the brain in Alzheimer's disease?

Finished reading? Practise this topic free

Open Psychology past questions with this Unit 3 topic carried into the question bank, then save your progress for the next review.

Practise this topic free. Free to start. No payment details are required. Exact question coverage depends on the available past-paper syllabus mapping.