biological explanation of schizophrenia (neurotransmitters) Flashcards

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1
Q

what antipsychotic drug was found in the 1950s

A

chlorpromazine

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2
Q

what is a disadvantage of the use of chlorpromazine?

A

induces tremors and muscle rigidity which are symptomatic of Parkinson’s disease - caused by low levels of dopamine

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3
Q

hyperdopaminergia

A

excess dopamine in the synapse

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4
Q

what is one suggested cause of excess dopamine? hint: enzyme

A

low levels of beta hydroxylase, enzyme which breaks down dopamine, may be responsible for a build up of excess dopamine in synapse.

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5
Q

what is another suggested cause of excess dopamine?

A

proliferation of D2 receptors on the postsynaptic cells may be responsible for hyperdopamingeric activity.

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6
Q

who suggested dopamine deficiency (hypodopamingeria)?

A

Kenneth Davis et al (1991)

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7
Q

what did Kenneth et al (1991) suggest?

A

positive symptoms of SZ resulted from excess dopamine activity in mesolimbic pathway, whereas negative symptoms result from hypodopaminergia, meaning a lack of dopamine activity in the mesocortical pathway.

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8
Q

What new antipsychotic was found in the 2000s?

A

Clozapine

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9
Q

which receptors does Clozapine bind to?

A

D1 and D4 but weakly to D2 receptors

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10
Q

How does clozapine reduce SZ symptoms?

A

binds to serotonin receptors and greatly reduces both positive and negative symptoms of SZ, it was hypothesised that negative symptoms may be caused by irregular serotonergic activity.

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11
Q

what does serotonin do in mesolimbic pathway?

A

regulates dopamine levels

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12
Q

who proposed Dopamine dysregulation?

A

Shitij Kapur (2009)

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13
Q

What did Shitij say about Dopamine dysregulation?

A

suggested dopamine dysregulation in the striatum as the common pathway to psychosis. They focuses on interactions between genetic, environmental, and socio-cultural factors and believe the dopamine hypothesis should be softened and viewed as an explanation of ‘psychosis proneness’ and not an explanation of SZ

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14
Q

supporting study of neurotransmitters as an explanation of SZ (rats)

A

Tenn et al (2003) found that rats giving amphetamine injections showed SZ-like symptoms e.g. social withdrawal. Dopamine antagonists were successful in reversing these effects.

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15
Q

suggest and explain a competing argument for Tenn et al (2003)

A

Lana Depatie et al (2001) showed that apomorphine, a dopamine agonist which stimulates D2 receptors, does not induce psychotic symptoms in non-psychotic clients. Therefore, it challenges the suggestion that excess dopamine is responsible for positive symptoms.

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16
Q

what is a weakness of neurochemical explanations of SZ

A

it does not take into account social factors, and why certain groups in society, such as second generation immigrants are more likely to be diagnosed with schizophrenia.

17
Q

describe a supporting study that links to second generation immigrants

A

Wim Veiling et al (2008) showed that Moroccan immigrants were more likely to be diagnosed with schizophrenia than Turkish immigrants. This correlated with the amount real or perceived discrimination faced by each group./ This suggests that environmental factors such as social stress may interact with internal neurochemistry making some people more prone to psychosis.

18
Q

Describe a supporting study of the role of D2 receptors as an explanation of schizophrenia

A

chlorpromazine acts as an antagonist at many dopamine receptors, especially D1 and D2, and has an antipsychotic effect…

e.g. haloperidol is a dopamine antagonist with a narrower range of biochemical effects yet is more effective in reducing SZ symptoms. This suggests that excess activity on specific but not all dopamine receptor is implicated in the development of symptoms.

19
Q

explain how the role of neurotransmitters can have application to drug treatment

A

it has led to effective drug treatments for people with schizophrenia. e.g. research has demonstrated that dopamine antagonists that bind to D2 receptors like haloperidol can reduce positive symptoms while atypical drugs such as clozapine have been successful in treating positive and negative symptoms. This suggests that excess activity on specific but not all dopamine receptors is implicated in the development of symptoms.