The Monoamine Hypothesis Flashcards

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1
Q

What are monoamines?

A

A group of neurotransmitters containing amino acid

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2
Q

Which monoamines is the hypothesis concerned with?

A

Noradrenaline, Seretonin, Dopamine

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3
Q

What suggests that monoamines are involved?

A

Antidepressents raise the levels of them and in some cases this solves depression

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4
Q

How is seretonin said to be involved?

A

It is carried across the synapse to the post synaptic neuron by a transporter. Changes in the gene encoding of this transporter could lead to low seretonin

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5
Q

What causes the changes in the seretonin transporters?

A

Stress

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6
Q

Where are seretonin recepetors found?

A

In the central nervous system cells

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7
Q

What is the role of seretonin?

A

To regulate other neurotransmitters

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8
Q

What happens if seretonin doesn’t regulate neurotransmitters?

A

Erractic brain functioning and faulty thinking patterns occur

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9
Q

How does erratic brain functioning and faulty thinking patterns explain depression?

A

Many people with depression have inappropriate guilt and feelings of unnecessary worthlessness which is a result of faulty thinking patterns

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10
Q

What can low levels of seretonin produce?

A

Low levels of noradrenaline

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11
Q

What is noradrenaline required for?

A

To show alertness, energy, anxiety and attention to life

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12
Q

How do low levels of noradrenaline link to depression?

A

Depressed people often suffer from hypersomnia where they sleep excessively due to lack of energy, low noradrenaline can reduce energy

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13
Q

What do some antidepressents work to do?

A

Some increase noradrenaline, some increase dopamine

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14
Q

What is the role of dopamine?

A

It is related to the ability to show attention and motivation, pleasure and reward

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15
Q

What do low levels of dopamine explain in terms of depression?

A

why some people have a markedly diminished interest in activities as they don’t have dopamine to give them the feeling of pleasure

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16
Q

How does Versiani et al (1999) support the monoamine hypothesis?

A

A double blind trial of noradrenaline reuptake inhibitors (NRIs) and a placebo found an increase in the mood of depressed patients with NRIs, supports that an increase of noradrenaline is needed

17
Q

Why can drug research be problematic?

A

Because drugs containing monoamines might help treat depression but it doesn’t mean they caused it, it could be that environmental factors made NTs fall low

18
Q

What is an opposing biological explanation?

A

That increased levels of cortisol in parts of the nervous system is implicated in depression suggesting the monoamine hypothesis is incorrect

19
Q

What did Klimeck et al (1997) find when he compared the locus coeruleus of 15 dead patients with major depression with 15 who didn’t suffer?

A

The locus coeruleus is responsible for producing noradrenaline and they found differences in structure suggesting that this affects the production of NTs

20
Q

What did McNeal and Cimbolic (1986) find?

A

That patients suffering from depression show lower levels of 5-H1AA than the non depressed, this is a chemical found when seretonin is broken down suggesting low levels

21
Q

How does opipramol oppose the hypothesis?

A

It is a drug used to treat depression that has an action unrelated to monoamine neurotransmitters and suggests other factors are involved

22
Q

What have MRI scans shown that oppose the hypothesis?

A

That there are physical differences in the brain in people with depression comapred to those without, these may cause depression e.g smaller hippocampus