Monoamine hypothesis and Biological treatment for depression

What is the biological explanation of depression

The monoamine hypothesis

What does the monoamine hypothesis claim to be the cause of depression

Less monoamine molecules are available for binding to receptors than needed, meaning they fail to regulate the limbic system- the centre for emotion in the brain

How may having too much monoamine oxidase cause depression

The monamines would be broken down too quickly by this enzyme so the brain would run out

What are the three main monoamines that may influence depressive symptoms

Dopamine, serotonin, norepinephrine (noradrenaline)

What is the role of serotonin

Regulating mood, well-being, stomach-functioning and other monoamine neurotransmitters

Which depressive symptoms may be directly caused by a lack of serotonin

Reduced appetite, low mood, illogical thinking patterns

How did Wender and Klein’s study support the monoamine hypothesis

A drug that lowered noradrenaline levels of animals made them sluggish and inactive- symptoms associated with depression

What is the role of noradrenaline

Regulating heart rate, concentration, attention, energy, alertness

What depressive symptoms may be caused by a lack of noradrenaline

Disruption of sleep patterns and lack of energy

What is the role of dopamine

Regulating motivation, reward, pleasure

What depressive symptoms may be caused by a lack of dopamine

Reduced attention, motivation and interest in pleasure

How is the successful use of drug treatments a strength of the monoamine hypothesis

If the drugs work then the theory has predictive validity as it suggests that increasing monoamine levels may reduce depressive symptoms

How does Meyer’s research support the monoamine hypothesis

He found that depressed patients who had not taken antidepressants for 5 months had significantly higher monoamine oxidase levels in all brain areas than clinically normal controls, which suggests they had lower levels of monoamines

How is therapeutic delay a weakness with the monoamine hypothesis

If low levels of monoamines were the sole cause of depression then drug treatment should be effective immediately

What is the biological treatment for depression

Drug treatment: SSRIs, MAOIs, SNRIs and NaSSAs

What do MAOIs stand for?

Monoamine oxidase inhibitors

How were MAOIs discovered

By accident when researchers noticed that an anti-tuberculosis drug had the side effect of improving mood

What do MAOIs do

Inhibit monoamine oxidase, which breaks down serotonin after reuptake. This increases availability of serotonin for future release into the synapse, therefore improving mood levels. MAOIs increase all monoamine neurotransmitters, including dopamine and noradrenaline

Give an example of a MAOI

Phenezine

What do SSRIs stand for

Selective serotonin reuptake inhibitors

When were SSRIs developed and why were they necessary

1980s because MAOIs are effective but have bad side effects

What do SSRIs do

Inhibit reuptake of serotonin by blocking the serotonin transporters so more serotonin is available in the synapse to bind with the post-synaptic neuron

What is the most commonly prescribed type of antidepressant in the UK

SSRIs

Give an example of an SSRI

Fluoxetine

What do SNRIs stand for

Serotonin-noradrenaline reuptake inhibitors

What do SNRIs do

Block reuptake of both serotonin and noradrenaline (in a similar way to SSRIs)

Give an example of a SNRI

Duloxetine

What do NaSSAs stand for

Noradrenergic and specific serotonergic antidepressants

Give an example of a NaSSA

Mirtazapine

Who are NaSSAs used for

People who have not benefited from SSRIs or SNRIs because they were ineffective or had intolerable side effects (e.g. sexual dysfunction)

How do NaSSAs work

They inhibit reuptake of serotonin and noradrenaline (like SNRIs but to a lesser extent) but also block certain types of serotonin and noradrenaline receptors to enable an increase in activity of the key receptor that improves mood

What is the key receptor that NaSSAs work to increase the activity of

5-HT1A

How is the existence of opipramol a weakness to the monoamine hypothesis

It alleviates depressive symptoms but doesn’t contain any mechanisms that effect monoamines so monoamines can’t be the only cause of depression

What does Kirsch believe about antidepressants

They are only effective due to the placebo effect

What did Verisani find from his double blind trial of noradrenaline reuptake inhibitors (NRIs)

The NRIs improved mood of depressed patients more than a placebo drug