biochemical expo of depression

Question 1

biochemical expo of depression basic summary
(monoamine hypothesis)

Answer 1

-too little monoamine
-serotonin: controls nt and happiness
-noradrenaline:alertness, concentration, reducing energy
-dopamine:pleasure, motivation,sense of reward
-monoamine oxidase: breaks down into waste so not enough nts
-5-HTT gene is associated with not enough serotonin and shortened alleles when stressed so genetic predisposition

Question 2

og dopamine hypothesis

Answer 2

The OG dopamine hypothesis states that the brain of schizophrenic patients produce more dopamine than the brain of a normal person
Through further research it is now thought that schitzophrenics have an abnormally high number of D2 receptors
Dopamine activity is associated with exploratory, outgoing, pleasure-seeking behaviors
This over-activity of dopamine-controlled synapses is associated with auditory hallucinations and paranoia (positive symptoms)

Question 3

dopaminergic in what pathways

Answer 3

Dopaminergia= dopamine activity

Excess dopamine (hyperdopaminergia) in the mesolimbic pathway may contribute to the positive symptoms of sz
Lower dopamine(hypodopaminergia) in the mesocortical pathway may be responsible for the negative symptoms of sz

Question 4

glutamate in dopamine hypothesis

Answer 4

Glutamate

Low levels of glutamate have been linked to development of psychotic symptoms
When we reduce glutamate, dopamine levels rise
Glutamate doesn’t necessarily conflict with dopamine hypothesis, but rather adds to it
High dopamine= low glutamate

Question 5

Van Rossum (1967)

Answer 5

Van Rossum (1967) made a significant link between overstimulation of dopamine receptors and sz (particularly D2 receptor) There is a link but it is only a correlation, not necessarily causation

Question 6

Carlsson et al (2000)

Answer 6

Carlsson et al (2000) Looked at whether JUST dopamine causes sz. Animal studies showed that NMDA antagonists reduced levels of glutamate but did not always increase dopamine not just dopamine that is involved in sz but other nt Aswell=too simplistic. Research on animals so cannot generalise to humans and sz as we cannot communicate with them only measure nt levels so cannot measure sz symptoms

Question 7

Amphetamines and LSD effect on dopamine

Answer 7

Amphetamines and LSD boost dopamine (dopamine agonists) giving some symptoms of sz drugs that increase dopamine give symptoms/ increase symptoms suggestion high dopamine leads to positive symptoms

Question 8

Falkai et al (1988)

Answer 8

Falkai et al (1988) Autopsies have shown that people with sz have a larger number of dopamine receptors otoh no cause and effect

Question 9

diathesis stress model

Answer 9

Social and environmental factors seem to trigger sz, so bio expo is insufficient. Stressful events in life can trigger the production of excess dopamine. Other factors play a role not just dopamine. Diathesis stress model is better- biological predisposition, environmental trigger

Question 10

depression types

Answer 10

An affective disorder, which is on a continuum. Patients can have it to a greater or lesser degree
Unipolar depression
Bipolar- mood fluctuates between manic episodes and depressive episodes, these are often separated with periods of normality
Postpartum- major depression within 4 weeks of delivery of a child
Seasonal- symptoms for 2 years, only in one season

Question 11

depression features

Answer 11

1 in 5 people report experiencing a common mental health problem (like anxiety and depression) in any given week in england
Common, globally it is estimated 5% of adults suffer from depression WHO 2020
The common cold of mental illness
Most common in young adulthood

Question 12

depression symptoms

Answer 12

-Depressed mood or irritable most of the day, nearly everyday,for 2 weeks as indicated by either subjective report or observation from others
-Decreased interest or pleasure in activities, most of each day
-Significant weight change(5% both ways) or change in appetite
-Change in sleep: hypersomnia or insomnia
-Change in activity: psychomotor activity or retardation
-Fatigue or loss of energy
-Guilt/worthlessness: feeling worthless or excessive or inappropriate guilt
-Concentration: dimished ability to think or concentrate, or more indecisiveness
Suicidality, thoughts of death/ suicide/ suicide plan

Question 13

serotonin in depression

Answer 13

Serotoin
Controls activity of other nts
Too low other nts will be too, specifically other monoamines
Leads to erratic brain activity because nts are trying to adapt= problems concentrating
Responsible for happiness/mood, regulating sleep and appetite = not enough means low mood, insomnia, changes in appetite

Question 14

noradrenaline depression

Answer 14

Noradrenaline

Responsible for alertness, attention to life (surroundings), reducing energy
Low = poor concentration, lack of energy/fatigue, loss of interest in activities

Question 15

dopamine depression

Answer 15

Dopamine

Linked with pleasure,motivation,sense of reward(enjoyment)
Low= lack of interest/pleasure gained from activities; low energy due to not being motivated

Question 16

Monoamine oxidase
depression

Answer 16

Monoamine oxidase

Breaks down nt into waste product
People with depression get rid of nt too quickly so dont have enough left to feel them

Question 17

gemes and chromosomes in depression

Answer 17

5-HTT gene associated with serotonin
Shortened alleles of this gene is associated with not producing enough serotonin when stressed
Genetic predisposition to lower levels of monoamines

Question 18

Drevets et al (1999)

Answer 18

Drevets et al (1999) found a reduced potential in serotonin to bind to receptors in
unmedicated depressed patients. This shows that reduced monoamines/reduced binding of
monoamines to receptors are a possible cause of depression

Question 19

Bunney et al (1970)

Answer 19

Bunney et al (1970) found that urinary levels of noradrenaline decreased during episodes of
depression, suggesting reduced noradrenaline in depressed patients.

Question 20

Delgado (2000)

Answer 20

Delgado (2000) found that monoamine depletion did not make symptoms worse in depressed
patients not taking medication. This means that low levels of serotonin are not sufficient an
explanation of where the depression came from.

Question 21

Angoa-Perez (2014)

Answer 21

Angoa-Perez (2014) found that mice without the gene for tryptophan did not show signs of
depression. This means that low levels of monoamines (which tryptophan are a precursor for)
are not sufficient an explanation of where the depression came from.