The monoamine hypothesis

• Depression results from a functional deficit of monoamine transmitters, in particular serotonin (5-HT) and noradrenaline
• Drugs that deplete stores of monoamines (e.g. reserpine) can induce low mood
• CSF from depressed patients has reduced levels of monoamines or their metabolites
• Most drugs that treat depression act to increase monoaminergic transmission, but this does not mean that depression is caused by monoamine activity

Efficacy of current antidepressants

• Most classes of drug have similar clinical efficacy
• Most have a delayed onset of action (several weeks)
• Side effect profiles differ as does individual response and susceptibility to side effects
• Clearer evidence for usefulness in more severe depression
• Caution in young adults/teenagers due to transient increase in suicidal/aggressive ideas