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DOPAMINE HYPOTHESIS

DOPAMINE HYPOTHESIS

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DOPAMINE HYPOTHESIS. LEARNING OBJECTIVES. By the end of the lesson your goal is to be able to Describe the role of Dopamine (DA) in schizophrenia and you should be able to Outline evidence to support this hypothesis You could even be able to Evaluate the Dopamine Hypothesis. - PowerPoint PPT Presentation

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Page 1: DOPAMINE HYPOTHESIS

DOPAMINE HYPOTHESIS

Page 2: DOPAMINE HYPOTHESIS

LEARNING OBJECTIVESBy the end of the lesson your goal is to

be able to• DescribeDescribe the role of Dopamine

(DA) in schizophreniaand you should be able to• OutlineOutline evidence to support this

hypothesisYou could even be able to• EvaluateEvaluate the Dopamine Hypothesis

Page 3: DOPAMINE HYPOTHESIS
Page 4: DOPAMINE HYPOTHESIS

Lets remind ourselves how neurotransmitters work

1

2

5

4

3

Page 5: DOPAMINE HYPOTHESIS

Lets remind ourselves how neurotransmitters work

Page 6: DOPAMINE HYPOTHESIS

DOPAMINE HYPOTHESIS

The Dopamine hypothesis states that the brain of schizophrenic patients produces moremore dopamine than normal brains.

Evidence for this comes from studies with drugs post mortems pet scans

Page 7: DOPAMINE HYPOTHESIS

Dopamine Hypothesis

Although the original Dopamine Hypothesis states that the brain of schizophrenic patients produces more dopamine than the brain of a “normal” person.

It is now thought that schizophrenics have an abnormally high number of D2 receptors.

Page 8: DOPAMINE HYPOTHESIS

Normal Level of Dopamine In The

Human Brain

Elevated Level of Dopamine In The Brain of a Schizophrenic Patient

(specifically the D2 receptor)

Neurons that use the transmitter ‘dopamine’ fire too often and transmit too many messages.

There may be an excess of DA receptors at the synapse in schizophrenics

Lowering DA activity helps remove the symptoms of schizophrenia

Page 9: DOPAMINE HYPOTHESIS

ROLE OF DRUGS

Amphetamines (agonists) lead to increase in DA levelsLarge quantities lead to delusions and hallucinationsIf these drugs are given to schizophrenic patients their symptoms get worse

Page 10: DOPAMINE HYPOTHESIS

Randrup et al

Rats given amphetamines developed schizophrenia type symptoms

Page 11: DOPAMINE HYPOTHESIS

Parkinson’s disease• Parkinson’s sufferers have low

levels of dopamine • L-dopa raises DA activity • People with Parkinson's develop

schizophrenic symptoms if they take too much L-dopa

–Chlorphromazine (given to schizophrenics) reduces the symptoms by blocking D2 receptors

Page 12: DOPAMINE HYPOTHESIS

Seidman (1990)Post-mortem (after death) examinations have found that

people with schizophrenia have a larger than usual number of dopamine receptors.

Increase of DA in brain structures and receptor density (left amygdala and caudate nucleus putamen)

Concluded that DA production is abnormal for schizophrenia

What is a strength and weakness of a post-mortem study?

Post-mortems

Page 13: DOPAMINE HYPOTHESIS

Lindstroem et al (1999)• Radioactively labelled a chemical L-Dopa • administered to 10 patients with

schizophrenia and 10 with no diagnosis• L-Dopa taken up quicker with

schizophrenic patients• Suggests they were producing more DA

than the control group

PET SCANS

Page 14: DOPAMINE HYPOTHESIS

Gjedde and Wong (1987)There are more than twice as many

dopamine receptors in schizophrenics compared to controls.

Farde et al. (1990)There is no difference in the number of

dopamine receptors between schizophrenics and controls.

PET Scans

What is the main strength of a PET scan?

What conclusions can be drawn from the research findings?

Page 15: DOPAMINE HYPOTHESIS

Schizophrenia or Faulty Chemicals?

Faulty chemicals cause schizophrenia but

schizophrenia may cause faulty chemicals

Chickens hatch from

eggs, but a mother chicken

must keep an

egg warm in order for

it to hatch

The Chicken or the Egg?Which Came First?

Drugs may influence other systems that impact on schizophrenia so we cannot be 100% sure about their effects

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There are lots of problems with the dopamine hypothesis!

• Read your handout carefully.

• There is a lack of correspondence between taking phenothiazines and signs of clinical effectiveness. It takes 4 weeks to see any sign that the drugs are working when they begin to block dopamine immediately. We cannot seem to explain this time difference.

• It could be that the development of receptors in one part of the brain may inhibit their development in another.

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Other EVALUATION POINTS• Type 1 cases respond well to conventional anti-psychotic

drugs. Drugs such as CHLOPROMAZINE: Only effective at relieving the Positive Symptoms of the Illness.

• Not good at explaining negative symptoms. Therefore suggested that Type 2 is related to a different kind of abnormality such as brain structure.

• PET scans have suggested that drugs did not reduce symptoms of patients diagnosed with disorder for 10 yrs or more

• There may be other neurotransmitters involved.• Possible that social and environmental factors trigger the

condition.

Page 18: DOPAMINE HYPOTHESIS

ACTIVITY• Describe and evaluate the dopamine Describe and evaluate the dopamine

hypothesis as an explanation of hypothesis as an explanation of schizophrenia schizophrenia

•You must comment on how the evidence you use supports or challenges the DA hypothesis. • You should comment on evidence both for and against the hypothesis. • You could use your own skills and knowledge to make additional critical and evaluative points.