Dopamine Hypothesis

Question 1

What is the basic concept?

Answer 1

Individuals with schizophrenia had too much dopamine and demonstrated symptoms related to high levels of dopamine

Question 2

What did J.J. Griffith et al. (1968) induce?

Answer 2

Psychosis in non-schizophrenic volunteers with the dextro-amphetamine (increase dopamine), finding that they demonstrated paranoid delusions and a detached response

Question 3

What was the initial issue?

Answer 3

It was too simple as the drugs that reduced dopamine had no effect on individuals suffering with negative symptoms

Question 4

Where are the D1-D5 receptor sites found?

Answer 4

The cerebral cortex and subcortically in the limbic system

Question 5

What is the main receptor and why?

Answer 5

D2 because it is found primarily in the subcortical regions

Question 6

What did Seeman and Lee (1975) show?

Answer 6

The impact of antipsychotic drugs on D2 receptor.

Question 7

What does the limbic system consist of?

Answer 7

A variety of subcortical structures engaged in many functions but mainly emotions, memory formation, and arousal.

Question 8

What are the two pathways leaving from the limbic sytem?

Answer 8

Mesolimibc and Mesocortical

Question 9

Mesolimbic pathway

Answer 9

Dopamine is a major neurotransmitter here. This carries signals from the ventral tegmental area to the nucleus accumbens. Too much dopamine causes positive symptoms.
Antipsychotics reduce the positive symptoms in this pathway.

Question 10

Mesocortical pathway

Answer 10

Dopamine is a major neurotransmitter here. This carries signals from the ventral tegmental area to the frontal lobe. This is vital in emotional responses, motivation, and cognition.

Question 11

What did Kenneth Davis et al. (1991) note?

Answer 11

Too little dopamine is evident in D1 receptors of the frontal lobe of individuals with negative symptoms.

Question 12

What do twin and family studies indicate?

Answer 12

There is a genetic basis for schizophrenia.

Question 13

What did Irving Gottesman et al. (1991) look at?

Answer 13

Incidence of schizophrenia in cousins, grandchildren, half-siblings, and twins. As genetic similarity increase, so did the probability of both being schizophrenia.

Question 14

What did the Schizophrenia Working Group of Psychiatric Genomics Consortium report?

Answer 14

There were 108 genetic loci associated with schizophrenia, showing that the genetic basis is complex.

Question 15

What is the problem with measuring neurotransmitters?

Answer 15

It is not easy to make direct measurements of neurotransmitters. Most of the research supporting dopamine hypothesis is based on metabolite research.

Question 16

How do we measure neurotransmitter and metabolite levels?

Answer 16

Dopamine becomes metabolised into HVA and this is measured in cerebrospinal fluid (unpleasant).

Question 17

What is the issue with measuring metabolite levels?

Answer 17

The participant’s diet and drug use may seriously affect the results and can be difficult to interpret as HVA levels vary widely, suggesting we should be cautious.

Question 18

How does the role of serotonin fit into this?

Answer 18

Serotonin is also a potential influence. Conventional antipsychotics block D2 receptors, but atypical antipsychotics block D2 and serotonin receptor equally, suggesting it is partial.

Question 19

Cause or effect issue

Answer 19

Schizophrenia could cause the dopamine imbalances.

Question 20

What did Copolov and Crook (2000) research?

Answer 20

Used PET scans and have not been able to detect differences in dopamine activity of schizophrenics and non-schizophrenics, meaning it will take some time.