IB Psychology SLTopic 1 — Mental Health DisordersPaper 1 & 2Biological approach~10 min read
Neurotransmitters and Depression
You have probably heard that depression is “a chemical imbalance in the brain”. It is one of the most repeated sentences in psychology — and one of the shakiest. This page shows you what the chemistry actually does, what the evidence really supports, and the reasoning trap that most students walk straight into.
📚 What you need to know
Neurotransmitters are chemical messengers that carry a signal across the gap between two neurons.
The gap is the synaptic cleft; the sending cell is presynaptic, the receiving cell is postsynaptic.
Serotonin (5-HT) is a monoamine involved in mood, sleep and appetite.
The monoamine hypothesis says MDD is linked to low or irregular monoamine levels.
SSRIs block reuptake, leaving more serotonin sitting in the cleft.
The 5-HTT gene controls the reuptake transporter; short and long versions behave differently.
Caspi et al. (2003) is your key study — and it is really a gene and stress study, not a pure biology one.
What actually happens at a synapse
Neurons never touch. To pass a message on, the sending neuron has to fire a chemical across a tiny gap. Learn this sequence properly, because half the marks in this topic come from describing it accurately.
🧩 Synaptic transmission, step by step
An electrical signal, the action potential, travels down the presynaptic neuron.
It reaches the end of the axon, where neurotransmitters are stored in small sacs called vesicles.
The vesicles release the neurotransmitter into the synaptic cleft.
The molecules diffuse across the gap and briefly lock into receptor sites on the postsynaptic membrane.
If enough receptors are triggered, a new action potential starts in the postsynaptic neuron.
Leftover molecules are cleared away: broken down by enzymes, or sucked back into the sending neuron by a reuptake pump.
That last step is the one the drugs target. Reuptake is basically recycling — it stops the signal repeating forever. But if you slow the recycling down, the neurotransmitter hangs around longer and keeps working.
Draw this yourself once from memory. If you can label the vesicle, the cleft, the receptor and the pump, you can answer almost any question on biological treatments too.
The monoamine hypothesis
Monoamines are a family of neurotransmitters that includes serotonin, noradrenaline and dopamine. The monoamine hypothesis says that mood disorders are related to how much of these chemicals is available in the brain, and that low or irregular serotonin in particular is linked to depressive symptoms.
The main support comes from the drugs. SSRIs block reuptake, more serotonin stays in the synapse, and many patients feel better. Working backwards from that, it looks like low serotonin must have been the problem.
The reasoning trap
“The drug raises serotonin → the drug helps → so low serotonin caused the depression”
That last arrow does not follow. Painkillers help a headache, but headaches are not caused by a shortage of painkiller. Treating a symptom successfully does not prove you have found the cause. Psychologists call this the treatment–aetiology fallacy, and dropping that phrase into an essay is an easy way to show real understanding.
The timing problem is your strongest evidence here. SSRIs raise serotonin within hours, but patients do not feel better for weeks. If low serotonin were simply the cause, why the delay? Something slower and more complicated must be going on underneath.
Genes and chemistry meet: the 5-HTT gene
The reuptake pump is built to a genetic blueprint. The 5-HTT gene (the serotonin transporter gene) comes in a short and a long version, and you inherit one from each parent. That gives three possible combinations, and this is exactly what the next study used.
🔬 Caspi et al. (2003)
The study that turned “genes vs environment” into “genes and environment”
AIM
To find out whether different versions of the 5-HTT serotonin transporter gene are linked to depression.
PARTICIPANTS
An opportunity sample of 847 people, all aged 26. They were sorted into three groups by their 5-HTT alleles: two short, one short and one long, or two long.
PROCEDURE
Participants reported the stressful life events they had been through between ages 21 and 26. The Diagnostic Interview Schedule was used to assess depression over the past year. The researchers then ran correlational analyses between stressful events and depression, allele length and depression, and perceived stress and allele length.
RESULTS
People with two short alleles reported more depressive episodes after stressful life events than the other two groups. People with two long alleles reported fewer depressive symptoms overall.
CONCLUSION
Short alleles seem to raise vulnerability to stress-induced depression; long alleles seem to offer some protection, possibly through a steadier serotonin supply.
Read the result carefully. Having two short alleles did not cause depression by itself. It only made a difference once stress had happened. That is the diathesis–stress model in action: a vulnerability plus a trigger. This is the single most useful sentence you can memorise for this whole option.
Evaluating the neurochemical explanation
Strengths
Limitations
Clear research support, and a plausible physical mechanism you can actually describe.
The evidence is not conclusive — the drugs work, but that does not prove the original cause.
Practical value: SSRIs are cheap, widely available and effective for many people.
SSRIs do not work for everyone. Research suggests only around a third of patients respond well.
Uses objective methods, clinical data and replicable findings, which supports psychology as a science.
Caspi’s study is correlational, and self-reported life events may be remembered inaccurately.
Caspi’s design shows biology and environment can be studied together rather than separately.
Biologically reductionist: depression is not a “one size fits all” chemical fault, and cause and effect between serotonin and MDD is still not established.
EXAM ANSWER
Discuss one biological explanation for one disorder. [22 marks]
A “discuss” question wants balance. Plan it as four moves before you write a word.
Move 1 — set the claim out clearly
The monoamine hypothesis: MDD is linked to low or irregular serotonin at the synapse.
Move 2 — explain the mechanism
Serotonin crosses the cleft, binds to receptors, then gets recycled by the reuptake pump. SSRIs block that pump so more stays available.
Move 3 — evidence
Caspi et al.: two short 5-HTT alleles plus stressful life events predicted more depressive episodes; two long alleles predicted fewer symptoms.
Move 4 — the counter-argument
Drug success does not prove chemical cause, and SSRIs take weeks to lift mood despite raising serotonin in hours.
Conclude: a real contributing factor, not a complete explanationbalance is not sitting on the fence — it is showing you know the limits of the evidence
Linking to the concepts
Causality: correlational designs can show a relationship between serotonin and mood, but cannot prove which one came first.
Perspective: cognitive factors (faulty thinking) and sociocultural ones (poverty, abuse, difficult relationships) also predict MDD, so depression should be viewed holistically.
Reductionism: reducing MDD to one neurotransmitter gives scientific clarity but loses the person’s actual life.
💡 Exam tips
Describe the synapse in order. Examiners give credit for accurate sequencing, and it costs you nothing to learn.
Use the phrase “linked to” rather than “caused by” when talking about serotonin. It is more accurate and safer.
The 2 to 6 week delay before SSRIs lift mood is the sharpest single criticism of the hypothesis. Have it ready.
Caspi works for the biological approach, for research methods (correlational study), and for diathesis–stress. Get full value out of it.
An opportunity sample of 847 people all aged 26 is a nice sampling point — large, but narrow in age.
If you are short on time, one well-explained study beats three name-dropped ones.
⚠ Common mix-ups
“SSRIs give you more serotonin.” They do not add any. They stop what is already there from being reabsorbed.
Mixing up presynaptic and postsynaptic. Pre = sending, post = receiving. The reuptake pump is on the presynaptic side.
Saying the short allele causes depression. In Caspi’s data it only mattered when stressful events had also happened.
Calling Caspi an experiment. It is correlational, so no cause and effect can be claimed.
Confusing serotonin with dopamine. Both are monoamines, but dopamine is the one you use for reward and addiction.
Writing “chemical imbalance” as if it were proven fact. It is a hypothesis with mixed support — treat it that way.
Up next: What Animal Studies Tell Us About Depression — if we cannot ethically give a human depression to study it, what can rats and dogs tell us instead, and how far should we trust it?
Want this explained one-to-one?
Book a free session with an experienced IB Psychology tutor and get your trickiest topics made simple.
