Neurotransmission, the seven named neurotransmitters, and Parkinson's and Alzheimer's disease (QCE Psychology Unit 3)

What this dot point is asking

Unit 3 Topic 1 (Brain function) in the 2025 syllabus ends with four linked dot points on neurotransmission, all of which can be examined in the external assessment:

1. describe neurotransmission, with reference to action potentials and synaptic transmission;
2. contrast excitatory and inhibitory neurotransmitters, for example glutamate and GABA;
3. describe the physical and psychological function of acetylcholine, epinephrine, norepinephrine, dopamine and serotonin;
4. explain the impact of interference in neurotransmitter function, with reference to Parkinson's disease and Alzheimer's disease, considering causes, symptoms and treatments.

Expect to describe a process in sequence, to match a neurotransmitter to a function in a scenario, and to reason from a neurotransmitter problem to its symptoms and treatment.

The answer

Neurotransmission: the action potential

A neuron sends information along its length as an electrical signal. At rest, the inside of the neuron is negatively charged compared with the outside (the resting potential). When the neuron receives enough stimulation to reach its threshold, channels in the axon membrane open and positively charged ions rush in, briefly reversing the charge: this is the action potential. The change travels down the axon like a wave, and the membrane quickly returns to rest behind it.

Key features:

• All-or-none: a neuron either fires a full action potential or does not fire at all. Stronger stimuli are signalled by firing more often, not by bigger action potentials.
• Myelin speeds transmission, because the signal jumps between the gaps in the myelin sheath.

Neurotransmission: synaptic transmission

The synapse is the junction between neurons: the axon terminal of the presynaptic neuron, the tiny synaptic gap, and the receptor sites on the dendrite of the postsynaptic neuron. Transmission across it is chemical:

1. The action potential arrives at the axon terminal.
2. Vesicles release neurotransmitter molecules into the synaptic gap.
3. The neurotransmitter diffuses across and binds to receptor sites shaped to fit it (often described as a lock-and-key fit).
4. Binding produces an excitatory or inhibitory effect on the postsynaptic neuron.
5. The neurotransmitter is cleared from the gap, by reuptake into the presynaptic neuron or breakdown by enzymes, so the signal stops.

So transmission is electrical within a neuron and chemical between neurons.

Excitatory and inhibitory neurotransmitters

• An excitatory neurotransmitter makes the postsynaptic neuron more likely to fire an action potential. Glutamate (Glu) is the main excitatory neurotransmitter in the brain and is central to learning and memory.
• An inhibitory neurotransmitter makes the postsynaptic neuron less likely to fire. GABA is the main inhibitory neurotransmitter; it dampens neural activity, which is why low GABA activity is linked to anxiety.

Whether a neuron fires depends on the balance of excitatory and inhibitory input it receives at that moment.

The five named neurotransmitters

Interference in neurotransmitter function: Parkinson's disease

• Cause. Parkinson's disease is a progressive neurodegenerative disease in which dopamine-producing neurons in the substantia nigra (in the midbrain) die. These neurons send dopamine to the basal ganglia, which help coordinate smooth voluntary movement. The reason the neurons die is not fully understood; age is the biggest risk factor, and genetic and environmental factors both contribute. Symptoms usually appear only after a large proportion of these neurons has been lost.
• Symptoms. The main symptoms are motor: tremor when the limb is at rest, muscle rigidity, slowness of movement (bradykinesia) and problems with balance and posture. Non-motor symptoms are common too, including depression, anxiety, sleep problems and a reduced sense of smell, and some people develop cognitive decline in later stages.
• Treatments. There is no cure; treatments manage symptoms. Levodopa (L-dopa) is the main drug: dopamine itself cannot cross the blood-brain barrier, but L-dopa can, and the remaining neurons convert it into dopamine. Other drugs mimic dopamine (dopamine agonists) or slow its breakdown. Deep brain stimulation, in which electrodes are implanted in the basal ganglia circuit, can reduce motor symptoms in some people. Exercise and physiotherapy help maintain movement.

Interference in neurotransmitter function: Alzheimer's disease

• Cause. Alzheimer's disease is a progressive neurodegenerative disease in which neurons are damaged and die. Two abnormal proteins accumulate: amyloid plaques between neurons and neurofibrillary tangles (of a protein called tau) inside them. Damage typically begins in the hippocampus and nearby areas and spreads through the cortex. Neurons that produce acetylcholine are among those lost, reducing the acetylcholine available for memory and attention. Age is the biggest risk factor, and some genes raise risk.
• Symptoms. Early on, memory for recent events is impaired (difficulty forming new explicit memories), with repeated questions and misplaced items. As the disease progresses, people experience disorientation, language difficulties, poor judgement, and changes in mood and personality, and eventually need help with daily care.
• Treatments. There is no cure. Cholinesterase inhibitors block the enzyme that breaks down acetylcholine, so more acetylcholine remains active at synapses; they can modestly improve or stabilise symptoms for a time. Another drug, memantine, regulates glutamate activity in moderate to severe disease. Newer antibody drugs that target amyloid have been approved in some countries for early disease, with modest effects and significant side-effect risks. Non-drug support (routines, cognitive stimulation, and support for carers) is an important part of care.