P2 - Abnormal - Biological Treatments

Question 1

what antidepressants do we look at

Answer 1

SSRIs - selective serotonin reuptake inhibitors

Question 2

how do SSRIs work?

Answer 2

block reabsorption of serotonin in the brain, making more serotonin available to stimulate the post-synaptic neuron

Question 3

what is the issue with SSRIs

Answer 3

they dont work for 30% of individuals with depression

Question 4

what is treatment resistant depression

Answer 4

tried two different SSRIs, and there is no reduction in symptoms

Question 5

what is serotonin

Answer 5

neurotransmitter that regulates the mood, sleep and other functions such as body temperature. It is released from nerve terminals, binding to serotonin receptors on nearby cells in the brain.

Question 6

what is neurotransmission

Answer 6

 When a neuron is in a resting state, inside of cell is negatively charged
 When a neuron is stimulated, inside becomes positively charged, causing an action potential
 Creates an electrical impulse that travels down the axon carrying information
 When it reaches end of neuron, it triggers release of neurotransmitter stored in vesicles.
 Neurotransmitter released through axon terminal into synapse chemically
 After crossing the synapse, neurotransmitters bind to receptor sites on post-synapse
 The chemical causes next neuron to be positively charged and message is now electric

Question 7

what study supports SSRIs

Answer 7

Arnone et al (2013)

Question 8

what is the aim of Arnone

Answer 8

to investigate the role of SSRIs in neurogenesis and role in reducing symptoms of depression

Question 9

what was the procedure of Arnone

Answer 9

lab
Participants were recruited at Uni of Manchester, 64 medication-free, unipolar depressed participants
Condition 1: half participants prescribed citalopram
Condition 2: half participants received no treatment
Results would be compared to 66 healthy control participants.
All participants had MRI to measure grey matter concentration in their hippocampi. All participants with depression had reduced amounts of grey matter in their hippocampi.

Question 10

what were the findings of Arnone

Answer 10

After 8 weeks, results showed participants with citalopram had an increase in grey matter and experienced a decrease in depressive symptoms.

Question 11

what was the conclusion of Arnone

Answer 11

Citalopram increases grey matter which correlates with a decrease in depressive symptoms.

Question 12

strengths of arnone

Answer 12

lab experiment and highly controlled
+ creates insight into cause of SSRI efficiency and provides information regarding depressive etiology
+ MRI scanning is unbiased
+ high ecological and temporal validity
+ control group

Question 13

weaknesses of Arnone

Answer 13

• Unethical to withhold treatment suffering from depression
• Only looked at short term effects, does the treatment lose efficacy?
• Small sample size
• Cannot generalise to other cultures.

Question 14

strengths of SSRIs

Answer 14

+ affordable treatment
+ easily integrated into your daily routine
+ can be quick to work

Question 15

weaknesses of SSRIs

Answer 15

• Side effects include nausea, insomnia, dry mouth and blurred vision.
• Doesn’t help with the cause/underlying problems
• May be difficult to withdraw yourself from antidepressants

Question 16

what is ketamine

Answer 16

 Increasing neural connections
 Targets different systems that SSRIs do
 Rapid effects on neuroplasticity
 Triggers mechanisms to maintain healthy circuits

Question 17

what is glutamate

Answer 17

most common excitatory neurotransmitter, which facilitates neuro network connections and ‘turning on’ of neurons and neural networks.

Question 18

how is ketamine used in high doses

Answer 18

 High doses = glutamate antagonist (blocks glutamate, which facilitates neural connections), making it an effect anaesthetic and moving into a state of immobility leaving individuals unable to see, hear, or feel pain.
 Disconnects the limbic system from the cortex so we are unable to communicate with ourselves – good for field hospitals

Question 19

how is ketamine used in low doses

Answer 19

 Low doses = glutamate production is enhanced. ‘sub-anaesthetic’
 Increases release of AMPA receptors which enhance synaptic connectivity and plasticity

Question 20

what is the research used for ketamine

Answer 20

Siegel et al (2021)

Question 21

what is seigels aim

Answer 21

to investigate efficacy of a longer infusion of ketamine in regard to reducing depressive symptoms and link to neural network activity

Question 22

what is the procedure of siegel

Answer 22

Procedure: University of Washington
23 individuals with treatment resistant depression + 27 matched non-depressed participants
Measured depressive symptoms using MADRS (diagnostic questionnaire which measures severity of depressive episodes) at baseline, 24hrs, 2 weeks and 8 weeks
Also measured resting state fMRI to examine changes in brain’s regions associated with drepressive etiology.

Question 23

what is seigel’s findings

Answer 23

All participants had reduced scores on MADRS
Ketamine condition: significantly decrease in hyperconnectivity (unrational emotions which make symptoms worse) and increase in connectivity between limbic system and frontal areas of the brain (connecting rational thoughts with emotion, which is easier to overcome).
Individuals who had a smaller right hippocampus at baseline had largest reduction in depressive symptoms as it created more networks to help with depression

Question 24

what is seigel’s conclusions

Answer 24

An infusion of ketamine had a sustained response in treatment resistant depression and normalises hyperconnectivity in the limbic system and frontal lobe.

Question 25

strengths in seigel

Answer 25

+ provides insight into understanding the network correlates of depressive etiology and treatment

+ high in temporal validity, technology was used more recently and the people studied are similar those to have grown up with technology, therefore its high in population validity

Question 26

weaknesses in seigel

Answer 26

• 8 weeks isnt long enough, people could relapse after the trial
• There was only 23 indviduals which is a small sample size.

Question 27

biological treatments critical thinking

Answer 27

 Reductionism – it would be reductionist to assume so, and researchers need to consider other explantations
 How effective is a treatment that allows relapse? Short solution to address depressive treatments quickly but doesn’t help long term
 Assumptions – doesn’t consider extraneous variables
 Individual differences – people respond differently to treatments
 Chiao and Blizinsky (2010) that the 5-HTT gene is higher in East Asia, but collectivist nature adds as a buffer
 Kirsch 2015 – SSRIs are overhyped and any benefits are due to the placebo effect