Bio-Dopamine hypothesis Flashcards

1
Q

What is dopamine and where is it found?

A

A NT which is a chemical in the brain which influences our behaviour
Found in limbic system which includes the hypothalamus and the amygdala thought to be related by our emotional life
people with S have shown extreme emotional disturbance

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2
Q

How does dopamine work?

A

Released and binds to the receptors which carries on the impulse
then NT goes back up and reabsorbed into the neuron

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3
Q

What has reseach suggested about dopamine receptors?

A

increased number and abnormally high numbers of d2 receptors in the brain
shown though post mortems

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4
Q

What are phenothiazines?

A

anti-phsychotic drug that had been found to reduce the symptoms of S reduces D activity by blocking D receptors
stops dopamine working by binding the receptor and carrying on the impulse

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5
Q

What are the roles of amphetamines and LSD?

A

Drugs such as amphetamines and LSD are known to have effects on dopamine levels
drugs can induce states very similar to S in individuals
Randrup and Munkvad gave amphetamines to rats and observed similar behaviour to S

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6
Q

What is L-DOPA?

A

can induce symptoms resembing paranoid S in parkinsons patients

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7
Q

What has mesolimbic and mesocortical got to do with S?

A

Thought that high levels of D is the mesolimbic D system are the cause of positive symproms whereas high levels in mesocortical dopamine system are associated with negative symptoms

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8
Q

Eval for dopamine?

A
Too simplistic x 2
Practical applications
Cause and effect
Other neurotransmitterd may be involved 
Drug companies may have inappropriately promoted D hypothesis
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9
Q

Why is it too simplistic?

A

antipsychotics take weeks to worrk although they reduce D levels by blocking D2 receptors v quickly. You would expect that as soon as the D levels are reduced the symptoms should reduce immediately
may be that dopamine is the first step in the chain reaction of S symptoms and reducing levels leads to reduction in symptoms

ignores alternative expls

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10
Q

What prac apps?

A

drug treatments, phenothiazines aim to reduce d levels

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11
Q

Why is cause and effect an issue?

A

Cannot be sure that high D levels are the cause
you do not test S until it has developed eg pet scan
so how can you esablish cause and effect

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12
Q

How may other NT’s be involved?

A

atypical antipsychotic is thought to have an influence on serotonin activity
and its suggested that atypical antips are more effective than typical that only influence D levels

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13
Q

Why may drug companies cause problems?

A

Healy suggested that D hyp is promoted this is because if they can promote that D is the cause then people can buy drugs
peoples health is put at risk and influenced by a drug companies want to make a profit

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14
Q

Researchers

A

Randrup and Munkvad
Iversen
Kessler
Wong

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15
Q

What did Randrup and Munkvad do?

A

Gave amphetaimes to rats and observes behaviour similar to S

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16
Q

What did Iverson do?

A

reported post mortems on people who has S

found excess D levels in limbic system suggesting involvement of the NT

17
Q

What did Kessler do?

A

used PET scans and MRI and found people with S had elevated D levels in basal forebrain

18
Q

What did Wong do?

A

found 2/3 increased in density of D receptor sites in the people with S who had never been treated