Biological Explanation for Unipolar Depression - Monoamine Hypothesis Flashcards
What are monoamines?
Group of NTs which contain amino acids
Serotonin, dopamine, norepinephrine
What are neurotransmitters?
Chemicals responsible for sending messages around the brain
What is depression caused by?
Caused by a decrease in the monoamines in the CNS
Believed to be inherited
What does serotonin do?
Regulates our mood
Associated with feeling happy
Sends messages around the brain to signal our mood
How does the reuptake of serotonin work?
Not enough receptors on the postsynaptic neuron so not enough receptors for serotonin molecules to bind to
They are reabsorbed into the pre-synaptic neuron and therefore there are fewer messages
Serotonin levels may also be low if enzymes destroy them in the synapse
Low messages from serotonin = low mood
What do low levels of serotonin lead to?
Leads to disturbances in sleep and appetite
Particularly seen in the Raphe Nuclei area of the brain
What is the importance of serotonin?
Serotonin is the gatekeeper - serotonin levels are important for other NTs
How can low levels of serotonin affect norepinephrine levels?
Low levels of serotonin can lead to low levels of norepinephrine
Leads to decreased energy levels and also decrease in concentration
Increase in guilt and anxiety
How can low levels of serotonin affect dopamine levels?
Low levels of serotonin can lead to low levels of dopamine
Reduces motivation, reward and pleasure, anhedonia
What is the supporting evidence/strengths of the monoamine hypothesis as a biological explanation for unipolar depression?
Drevets et al (1999)
Delgado (2000)
Decrease dopamine levels
Post-mortems
Psychology in society
What is the refuting evidence/weaknesses of the monoamine hypothesis as a biological explanation for unipolar depression?
Thase et al (2002)
Pharmacological agents
Antidepressant drugs
Reductionism
Diathesis-stress model
Why is Drevets et al (1999) supporting evidence of the monoamine hypothesis as a biological explanation for unipolar depression?
Drevets found that serotonin levels were reduced in the raphe nuclei of unmedicated patients with depression compared to controls using PET scans
This evidence therefore supports the hypothesis, showing that lower levels of serotonin are linked to depression. Furthermore, the research uses a control group and PET scans making the evidence more objective.
Why is Delgado (2000) supporting evidence of the monoamine hypothesis as a biological explanation for unipolar depression?
Delgado claims that the use of drugs such as SSRIs (specifically work to increase serotonin levels) are effective, resulting in a reduction of symptoms
This evidence therefore supports the hypothesis because it shows that by increasing the level of serotonin there is a reduction in symptoms of depression supporting that neurotransmitters are the sole cause of depression.
Why is decreased dopamine levels a strength of the monoamine hypothesis as a biological explanation for unipolar depression?
Decreased levels of dopamine in the nucleus accumbens has been found in animals exhibiting ‘learned helplessness’ (depressive behaviour)
This evidence therefore supports the hypothesis as dopamine levels relate to depression and the findings can be generalised to humans. However, animals’ brains are different to human brains.
Why is post-mortems a strength of the monoamine hypothesis as a biological explanation for unipolar depression?
Post-mortem studies show that people who have experienced multiple depressive episodes have fewer norepinephrinergic neurons than people who have no depressive history
This evidence therefore supports the hypothesis, because it suggests that norepinephrine levels are lower in people with depression which may have been caused by low levels of serotonin. This suggests that the monoamine hypothesis is valid in its claims.
Why is psychology in society a strength of the monoamine hypothesis as a biological explanation for unipolar depression?
The development of antidepressants such as SSRIs has been significant in treating patients with depression
Previously patients locked away or treated using more controversial techniques such as ECT
This evidence therefore supports the hypothesis, because SSRIs are created to specifically target serotonin, which indicates that serotonin levels have an effect on depression.
Why is Thase et al (2002) refuting evidence of the monoamine hypothesis as a biological explanation for unipolar depression?
Thase found that depressed patients (especially those with severe depression) had increased levels of norepinephrine
This evidence therefore refutes the hypothesis because the monoamine hypothesis suggests that low levels of serotonin causes low levels of norepinephrine. This means that it questions the validity of the findings, suggesting that norepinephrine levels (as a result of serotonin levels) may not influence depression in the way it stated.
Why is pharmacological agents a weakness of the monoamine hypothesis as a biological explanation for unipolar depression?
Experiments with pharmacological agents that cause the depletion of monoamines have shown that this depletion doesn’t cause depression in healthy people nor does it worsen the symptoms of depressed patients
This evidence refutes the hypothesis as it contradicts the idea that lower levels of monoamines cause depression as the study showed that its didn’t affect a healthy person or make the symptoms worse for depressed patients.
Why is antidepressant drugs a weakness of the monoamine hypothesis as a biological explanation for unipolar depression?
Antidepressant drugs such as SSRIs which increase the levels of biochemicals immediately can take weeks before they effectively alleviate the symptoms of depression
This is a weakness because it shows that increasing the levels of serotonin is not the only factor in preventing symptoms as it takes weeks to work. However, it does stop the symptoms eventually showing that while not fully effective they do still work
Why is reductionism a weakness of the monoamine hypothesis as a biological explanation for unipolar depression?
Monoamine hypothesis focuses specifically on the natural levels of monoamines in the brain and ignores other possible external factors which may also alter the chemical balance in the brain such as substance misuse
This is a weakness as it ignores the possibility that the levels of neurotransmitters in the brain be altered by another factor. Furthermore, a person may seek out other ways of altering their levels of NTs by using drugs which can cause symptoms of depression.
Why is diathesis-stress model a weakness of the monoamine hypothesis as a biological explanation for unipolar depression?
Serves to explore how biological or genetic traits (diathesis) interact with environmental influences (stressors) to explain the onset of mental illnesses
A biological predisposition for depression may be triggered by an external factor such as losing a job
This is refuting evidence because the monoamine only focuses on biological factors such as neurotransmitter levels as being the sole cause of depression. However, the diathesis-stress model argues biological and genetic factors could contribute to depression.
