Biological explanation of depression (neurotransmitters)

Question 1

What is the Monoamine Hypothesis?

Answer 1

• A biological explanation for depression is the monoamine hypothesis. They are a group of neurotransmitters that include Serotonin, Noradrenaline and Dopamine which regulate mood.
• Low levels of monoamine neurotransmitters may cause unipolar depression.
• Among the monoamines, serotonin is particularly important. One of its jobs is to regulate the other neurotransmitters. Without the regulation provided by serotonin, brain functioning becomes erratic.

Question 2

What does the hypothesis propose?

Answer 2

The monoamine hypothesis proposes that depression results in a chemical imbalance in the monoamine neurotransmitters in the brain specifically serotonin and noradrenaline.

Question 3

What is serotonin?

Answer 3

A chemical created by the body that works as a neurotransmitter. it is responsible for managing mood.

Question 4

What is noradrenaline (norepinephrine)?

Answer 4

it is a catecholamine hormone and neurotransmitter with multiple roles including maintaining concentration.

Question 5

What role does serotonin play?

Answer 5

• Serotonin controls sleep which links to insomnia and hypersomnia which are symptoms of unipolar depression.
• When serotonin levels are low, levels of noradrenaline drop and noradrenaline provides attention and reward. Low levels of noradrenaline are linked to a lack of pleasure.
• Low levels of serotonin also cause dopamine levels to drop and dopamine is related to alertness and energy. Low levels of dopamine are linked to anxiety.

Question 6

What was noticed in the 1950s?

Answer 6

it was noticed the the drugs that decreased these amine neurotransmitters brought about symptoms of depression, so it was assumed that depression was caused by low levels of these neurotransmitters, particularly serotonin. drugs were later developed that increased their availability in the synapse and which alleviated some of the symptoms.

Question 7

The 5-HTT gene.

Answer 7

• A particular gene called 5-HTT has been linked to regulating serotonin levels.
• People with variations of the 5-HTT gene that are under-active seem more likely to suffer depression after stressful life events.
• Rosenthal’s diathesis-stress model explains that a gene that produces a mental disorder can be “triggered” by a stressful environment.

Question 8

What was the problem with the antidepressant drugs?

Answer 8

The level of noradrenaline and serotonin increase within hours of the administration of these antidepressant drugs, the symptoms often do not improve for a period of up to six weeks in some cases.

Question 9

What challenges did this cause the monoamine hypothesis?

Answer 9

This led to a more complex alternate explanation, which suggested that the low levels of noradrenaline and serotonin led to changes in the neuro-circularity of the brain specifically causing an up regulation in the sensitivity of the receptor sits on the synapses in relevant pathways.

Question 10

What happens due to the low levels of noradrenaline and serotonin?

Answer 10

There is too little stimulation i n the postsynaptic receptors so to compensate for this more receptors are made but when more neurotransmitters become available through the administration of antidepressant drugs , there is a down-regulation where the receptors are desensitised. which can account for the delay in the effect of the drug as this interferes with allevation of symptoms.

Question 11

What problem may the receptor experience that is not due the the low levels of neurotransmitters?

Answer 11

The problem with the receptors could be when they pick up the neurotransmitters when they cross the synapse from one neuron to another. If there aren’t enough receptors – or if the receptors aren’t working properly – this will have the same effect as a lack of the neurotransmitter.

Research focuses on a protein called monoamine oxidase A (MAO-A), which is a chemical that removes monoamines from the synapse.

This is an important brain function called “re-uptake” that recycles neurotransmitters when they don’t appear to be needed.
If there is too much MAO-A in the synapse, it will remove monoamines that are needed, starving the brain of serotonin, noradrenaline and dopamine, leading to symptoms of depression.

This is the basis for a lot of antidepressant drugs, which reduces the activity of MAO-A, leading to more monoamine activity and a reduction in the symptoms of depression.

Question 12

What happens when serotonin levels are too low or high?

Answer 12

Serotonin controls the levels of noradrenaline so when there are low levels of serotonin, the levels of noradrenaline are affected. if these are too low the person will experience feelings of depression, it’s too high then they may experience bipolar depression.

Question 13

Supporting evidence - STRENGTH

Answer 13

• If there are monoamine deficiencies and there’s a drug that replaces them, this is evidence for the hypothesis.
• The monoamine hypothesis is backed up by the beneficial effects of antidepressant drugs which boost monoamine activity (flooding the synapse with monoamines – Versiani et al., 1999) or inhibit monoamine reuptake (preventing MAO-A from removing too many monoamines).
• Similarly, drugs that specifically prevent the reuptake of serotonin reduce depressive symptoms.

-E.g., SSRIs are effective in dealing with unipolar depression and work by inhibiting the reuptake of serotonin, which increases the levels.

• Post-mortem studies of patients who committed suicide (e.g. Mann, 2003) show reduced levels of serotonin and an increased number of serotonin receptor sites (i.e. the brain was starved of serotonin and adapted by increasing its serotonin receptors to process as much of it as possible). However, other post-mortem studies contradict the link between suicide and serotonin and furthermore, not all suicides are caused by depression.

Question 14

Challenging evidence - WEAKNESS

Answer 14

Although antidepressants alter monoamine activity immediately, the symptoms of depression may take weeks to disappear. Furthermore, some drugs affect depression but their action is not related to monoamine neurotransmitters.

• However, this focus on drugs suffers from the treatment aetiology fallacy: the cure is not necessarily the cause.
• Just because drugs work by re-balancing the brain’s chemistry does not mean the brain chemistry was the cause in the first place.
• Thase et al. (2002) found that depressed patients (especially those with severe depression) had increased levels of noradrenaline. This is the opposite of what the Monoamine Hypothesis predicts.

Question 15

Other explanations - WEAKNESS

Answer 15

• Biological evidence is usually in the form of an observed correlation and correlations do not show cause.
• There is a cause and effect problem – low levels of monoamines may be a symptom of unipolar depression rather than the cause.
• It is unclear whether unusual brain activity (low levels of serotonin, excessive MAO-A activity) causes depression or whether depression causes unusual brain activity – or whether an unknown third factor is causing the brain activity AND the depression.
• E.g. MRI scans show that depressed people have a smaller hippocampus so it may be a brain structure rather than brain function which is causing the unipolar depression.

Question 16

Usefulness - STRENGTH or WEAKNESS

Answer 16

• Biological explanations have led to the development of antidepressant drugs.
• However, these drugs do not work for all people who suffer from depression: 10-30% of people with severe depression do not respond to medication.
• Critics in the Recovery Movement reject the biological explanation and the dependency on drugs, which they argue do more harm than good and only create profits for “Big Pharma” (the medical drugs industry).

Question 17

Testable - STRENGTH or WEAKNESS

Answer 17

• Reductionism – reducing depression to the level of neurotransmitters has allowed research and drug treatments to be developed.
• However, the focus on only biological factors ignores the role of psychological and environmental factors. For example, poor people are much more at risk from depression.
• Psychologists must consider more than one level of explanation; the biological explanation alone is too reductionist (simplistic).

Question 18

An example of a strength paragraph of the monoamine hypothesis.

Answer 18

One strength of the monoamine hypothesis as a biological explanation of depression is that it is supported by research evidence. This explanation argues that depression is caused by low levels of monoamine neurotransmitters. Monoamines are a group of neurotransmitters that include Serotonin, Noradrenaline and Dopamine. Among the monoamines, serotonin is particularly important as this regulates the other two neurotransmitters. Research evidence highlights that the explanation is valid. For instance, Post-mortem studies of patients who committed suicide (e.g. Mann, 2003) show reduced levels of serotonin and an increased number of serotonin receptor sites (i.e. the brain was starved of serotonin and adapted by increasing its serotonin receptors to process as much of it as possible). This adds support for the depletion of monoamine neurotransmitters being implicated in the cause of depression. However, other post-mortem studies contradict the link between suicide and serotonin and furthermore, not all suicides are caused by depression. This is problematic as…

Question 19

An example of a conclusion to the monoamine hypothesis

Answer 19

The monoamine hypothesis is overly simplistic but has proven resilient, reappearing over the years in more refined forms. It seems certain that levels of monoamine neurotransmitters are linked in some way to depression, which is supported by research evidence. However, research evidence has also challenged this theory and has highlighted the dangers in inferring the role of neurotransmitters from the effects of antidepressants. It may be that neurotransmitters, to some extent, are implicated in the development of depression, but other causes may also play an important role.