One Biological Explanation for Uni-polar Depression

Question 1

what is the biological explanation of uni-polar depression (upd) ?

Answer 1

neurochemical

Question 2

who came up with the monoamine depletion hypothesis ?

Answer 2

Joseph schildkraut (1965)

Question 3

what did schildkraut argue ?

Answer 3

upd is caused by low levels of the monoamine neurotransmitters

Question 4

what are the monoamine neurotransmitters ?

Answer 4

1) serotonin
2) dopamine
3) noradrenaline

Question 5

what is serotonin ?

Answer 5

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

Question 6

what is noradrenaline ?

Answer 6

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

Question 7

what are receptor sites ?

Answer 7

areas on the post-synaptic neuron that allow neurotransmitters to lock onto the membrane

Question 8

what is down-regulation ?

Answer 8

it is a homeostatic mechanism where the brain produces less of something in response to an increase.

Question 9

where in the brain are monoamine neurotransmitters known to regulate functions ?

Answer 9

the brain’s limbic system (the emotional centre that form connections with other areas of the brain, like the frontal cortex):

• amygdala
• hypothalamus
• hippocampus

Question 10

what did the original hypothesis focus on and what was wrong with it ?

Answer 10

it focused only on serotonin (low levels of serotonin causes depression) - this ignored the substantial evidence for the role of noradrenaline

Question 11

what was the developed monoamine depletion hypothesis called and what did it claim ?

Answer 11

the permissive hypothesis - states that it is the balance of serotonin and noradrenaline that causes depression (serotonin usually controls the level of noradrenaline but low levels of serotonin ‘permits’ noradrenaline levels to drop too - causing depression)

Question 12

overall, what does the permissive hypothesis state ?

Answer 12

serotonin is a necessary condition for depression but not sufficient on its own.

Question 13

why was the monoamine depletion hypothesis quickly challenged and why?

Answer 13

because it was too simplistic - drugs were developed that had antidepressant properties that didn’t increase levels of monoamine neurotransmitters, suggesting there was more causing depression than these alone

Question 14

what does the receptor sensitivity hypothesis argue ?

Answer 14

that depression is caused by changes in the sensitivity of post-synaptic receptors

Question 15

what usually occurs with receptors when there is a depletion of neurotransmitters ?

Answer 15

up-regulation - neurons compensate for the reduction in neurotransmitter stimulation by increasing the sensitivity of receptors and -over the long term - producing more of them

Question 16

instead of up-regulation, what happens in depression ?

Answer 16

down-regulation - serotonin and noradrenaline post-synaptic receptors become even more sensitive (supersensitivity) to the reduced stimulation than normal

Question 17

what does BDNF stand for ?

Answer 17

brain-derived neurotrophic factor

Question 18

what is BDNF ?

Answer 18

a chemical that ‘feeds’ neurons the nutrients they need to survive, grow and function efficiently

Question 19

what does BDNF play a key role in ?

Answer 19

neuronal plasticity

Question 20

what is neuronal plasticity ?

Answer 20

the ability of the brain to form new synapses

Question 21

what are the conditions of BDNF in people with upd ?

Answer 21

they have low levels of BDNF in the hippocampus and prefrontal cortex

Question 22

what is BDNF’s close relationship with symptom severity ?

Answer 22

the lower the levels of BDNF, the more severe the symptoms (negative correlation)

Question 23

what has the BDNF hypothesis allowed researchers to find and how ?

Answer 23

a link between depression and stress - this is because the gene for BDNF may be ‘switched-off’ under stress

Question 24

when the BDNF gene is ‘switched-off’, what can this lead to ?

Answer 24

it can lead to the neurons that are fed by BDNF being left vulnerable to atrophy (shrinkage) or apoptosis (cell death) - both of which are observed in depression

Question 25

what is the support for the BDNF hypothesis ?

Answer 25

there are two main sources of supporting evidence:
1) sen et al. (2008) have found a negative correlation between blood serum levels of BDNF (abnormally low) and the severity of depressive symptoms
2) post-mortem studies such as Martinowich et al. (2007) found abnormally low levels of BDNF in the hippocampus and prefrontal cortex.
THIS EVIDENCE SHOWS A CLEAR ASSOCIATION BETWEEN BDNF LEVEL AND DEPRESSIVE SYMPTOMS.

Question 26

what is the evidence against the monoamine hypothesis ?

Answer 26

weakness is that the monoamine hypothesis cannot explain the common experience of therapeutic delay - antidepressants often take 4-6 weeks for improvement to show (this is hard to explain when levels of serotonin and noradrenaline increase immediately and are at the normal level after one week).

Question 27

what is the competing argument to the weakness of the monamine hypothesis ?

Answer 27

therapeutic delay is explained with receptor sensitivity - antidepressants causes increased levels in serotonin and noradrenaline in the synapse - leads to corresponding down-regulation in post-synaptic receptors (fewer produced), to compensate for increased stimulation. but this process is not immediate - it takes several weeks and correlates closely with symptom improvement

Question 28

how has treatment aetiology fallacy developed when researching neurochemical explanations of upd ?

Answer 28

treatment aetiology fallacy - historically, the biochemical explanations derive from observations of how antidepressant medications affected depression. E.g., it was noted that post-synaptic neurons were down regulated by antidepressants that increased serotonin - researchers assumed that if a biochemical treatment treated depression then depression must have a biochemical cause

Question 29

why is treatment aetiology fallacy a weakness of all neurochemical explanations of upd ?

Answer 29

it may not be necessarily true - an antidepressant drug could work by correcting a biological process that is disturbed by a psychological factor(e.g.,stress) - SO TREATMENT IS BIOLOGICAL BUT THE CAUSE IS PSYCHOLOGICAL, A TREATMENT AETIOLOGY FALLACY.

Question 30

what is an application of neurochemical explanations ?

Answer 30

application to treatment - as our understanding of the biochemistry of depression develop, so do the drugs to treat it - E.g., recent drug treatments target both serotonin and noradrenaline level (like duloxetine) as opposed to serotonin only (like fluoxetine). THEREFORE, BIOCHEMICAL EXPLANATIONS ARE USEFUL BECAUSE TREATMENTS BASED ON THEM MAY IMPROVE QUALITY OF LIFE AND REDUCE DISTRESS.