The Dopamine Hypothesis, Neurotransmitter explanation

Question 1

What does it believe the cause of schizophrenia to be?

Answer 1

A chemical imbalance in the brain as schizophrenia patients produce more dopamine and have increased dopamine at the synapse

Question 2

What causes the positive symptoms?

Answer 2

Increased D2 activity in the mesolimbic pathway

Question 3

What causes the negative and cognitive symptoms?

Answer 3

Decreased D1 activity in the mesocorticol pathway

Question 4

Where is the mesocorticol pathway located and why is this significant?

Answer 4

In the prefrontal cortex which finishes developing in adolescence - links to the common onset of the disorder

Question 5

How is seretonin involved?

Answer 5

It regulates dopamine and could be linked to the negative symptoms

Question 6

What is glutamate?

Answer 6

A neurotransmitter that produces psychotic symptoms when it is reduced

Question 7

How has PCP shown that dopamine is not the only neurotransmitter involved?

Answer 7

PCP acts upon NMDA receptors (glutamate receptors) as an antagonist (increasing dopamine)

Question 8

How does glutamate work in the mesocortical pathway?

Answer 8

Glutamate acts as an accelerator leading to high D1 activity but if this goes wrong and glutamate levels fall too low, D1 levels drop = negative symptoms

Question 9

How does glutamate work in the mesolimbic pathway?

Answer 9

Glutamate acts as a break and signals to GABA to inhibit D2 production, if this doesn’t work GM falls, GABA falls and D2 rises = positive symptoms

Question 10

What is a limitation of this theory?

Answer 10

Excess dopamine can also have a stimulant effect producing symptoms like high confidence and altertness which aren’t present in schizophrenia

Question 11

How could this theory be reductionist?

Answer 11

It doesn’t consider environmental factos or stressful life events that could lead to excess dopamine

Question 12

How does the use of amphetamines support this?

Answer 12

It causes excess dopamine and symptoms similar of psychosis but only the positive symptoms are produced so it isn’t fully sufficiant

Question 13

How does Lindstroem et al support it?

Answer 13

IDOPA is used by the brain to make dopamine, compared to 10 untreated schiophrenics, the normal controls used less IDOPA while the sz used it quicker

Question 14

How does Donnelly et al (1996) support?

Answer 14

Homovanillic acid is a waste product of dopamine passed out through the body and it was found that schizophrenics had more homovanillic acid than controls

Question 15

How does Naheed and Green (2007) support?

Answer 15

They found that atypical AP clozapine works by binding to seretonin receptors and dopamine receptors, its the most effective helping positive and negative symptoms

Question 16

What weakness does Carlsson et al (1999) offer?

Answer 16

He says how humans undergoing scans might feel under pressure and are likely to respond differently to normal which means any findings might not be valid

Question 17

How does Parkinsons disease provide evidence for dopamine?

Answer 17

Sufferers of Parkinson’s disease who are given Levodopa (adds to dopamine production) can experience symptoms similar to schizophrenia

Question 18

How does the glutamate aspect support it?

Answer 18

It works with the dopamine hypothesis rather than refuting it and adds to its scientific credibility