Dopamine and Schizophrenia Essay

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What is the prevalence of Schizophrenia?
1% (Carlson, 2017), termed ‘split mind’- Bleuler (1911), Age of onset around adolescents-early 30s (Hafner et al, 1993)
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Information about symptoms?
Positive (hallucinations, delusions, thought disorders), negative (flat affect, anhedonia, poverty of speech) and cognitive (newer category, includes poor learning, memory, thinking, and attention)
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What have explanations been suggested?
. One biological approach is the dopamine hypothesis which states that deficits in dopamine regulation leads to schizo
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What will this essay argue?
dopamine hypothesis is still relevant, however may need to be updated to include other factors.
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How will this essay do this?
critically evaluating evidence supporting the hypothesis (dopamine agonists, antagonists, and abnormal transmission) as well as arguing that other factors may lead to the development of schizo (glutamate, environment)
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Dopamine is a neurotransmitter that is synthesised from?
DOPA by dopa decarboxylase in part of the dopamine synthesis
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Weinberger (1988)
): There is an overactivity of dopamine in the midbrain (specifically linked to D2 receptors and likely to be the mesolimbic pathway), consequently causing reduced dopamine levels in prefrontal regions of the brain
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Overactivity in the midbrain --> positive symptoms
Underactivity in prefrontal regions -> negative and cognitive symptoms
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Specific receptors of dopamine have been linked to what?
to schizo. D1 and D2; both located in midbrain and D2 is important for regulating dopamine release.
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What is a dopamine agonist?
o Agonists are structurally similar to a neurotransmitter. This allows it to enter and activate the neurotransmitter’s receptor
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What do agonists increase?
the amount of neurotransmitter available, therefore if we give a dopamine agonist to an animal/person then it will increase the amount of dopamine. One common indirect dopamine agonist is amphetamine.
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We can report what?
the effects and see if they were similar to effects/symptoms of schizo. If they are it provides supporting evidence for dopamine hypothesis, making it still relevant
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Griffith et al 1972
7 human participants were given 10mg of amphetamine every hr for 5 days. Within 2-5 days they were all reporting delusions and electric dynamo thought control- all similar to symptoms in schizo
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What are dopamine antagonists?
o Antagonists have the opposite effect of an agonist. These block the receptor and often have a different structure to the neurotransmitter.
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As a result what?
As a result the neurotransmitter cannot enter the receptor, meaning there is a reduction in the neurotransmitter
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For Schizo, if we look at what?
DA antagonist and find a reduction in symptoms we can infer that dopamine is a primary cause of schizo, making the hypothesis still relevant
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Many antipsychotics are what?
Dopamine antagonists, meaning they aim to reduce dopamine
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Creese et al 2010
states that typical antipsychotic drugs reduce positive symptoms of schizo as they reduce dopamine levels
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Strange 2008
that typical antipsychotic drugs such as chlorpromazine and haloperidol significantly reduce the positive symptoms of schizophrenia by acting on the dopamine receptors.
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However, what about the negative symptoms?
Newer atypical antipsychotics are used to treat both + and – symptoms.
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As well as acting on dopamine, they also are serotonin antagonists. What does this suggest?
serotonin is involved in the – symptoms, something the dopamine hypothesis fails to account for, suggesting that although it is still relevant it needs to be updated (Winans, 2003)
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Abnormalities in dopamine transmission, there is evidence that?
people with schizophrenia have abnormalities in dopamine transmission, suggesting that these abnormalities are the cause of the disorder
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Laurelle et al (1996)
gave people small doses of amphetamine to instigate dopamine release in the brain.
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The amount of dopamine that was released?
measured and they found that dopaminergic neurons of a person with schizophrenia released higher quantities of dopamine than a neurotypical individual.
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What did they find?
They found that the increase in dopamine was correlated with the increase in reported symptoms, and this association supports dopamine hypothesis
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Seeman conducted what?
post-mortem studies of schizophrenic and healthy control’s brains.
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What did they find?
schizophrenics had 60-110% more d2 receptor sites compared to healthy control; attributed to abnormal dopamine transmission supporting the dopamine hypothesis
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Wong et al (1986)
PET scans, found that there was increase in D2 receptor sites, similar study to Seeman (2000); all suggested that there was more dopamine in schizophrenic’s brains, all support the dopamine hypo for + symptoms
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What is glutamate hypothesis?
o The hypothesis states that schizo is caused by reduced function of NMDA glutamate receptors. This results in reduced glutamate transmission causing the symptoms of schizophrenic
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Kim (1980)
Reduced glutamate in cerebrospinal fluid in schizophrenic patients -> reduced glutamate functioning -> symptoms. But this has never been replicated
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Krystal (1994)
When ketamine, a NMDA antagonist, is given to in controlled conditions to people it produced similar symptoms as schizophrenia (positive + negative); hallucinations, delusions, flat affect
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Harrison et al (2003)
Genes that are linked to schizo also appear to influence NMDA receptor sites
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Clinton and Meador-Woodruff (2004)
Postmortem studies show there are differences in glutamate receptor binding in prefrontal cortex, thalamus, and hippocampus of schizophrenic.
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Maybe schizo is caused by what?
both dopamine and glutamate deficits? Dopamine is probably still important, but the hypothesis should be updated to account for the glutamate
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What are environmental factors?
People that are born in winter/spring are more likely to be schizophrenic (Kendell & Adams, 1991
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What was argued?
seasonality effects occur due to the higher risk of viral infection in pregnant females during winter
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Brain development of the fetus may be affected by what?
toxins that are produced by the virus
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What does the mother's antibodies do?
Attack the fetus rather than virus leading to abnormal brain development
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Mednick et al 1990
After an influenza epidemic, where virus levels are much higher, there is a subsequent increase in schizophrenic people. Supports that virus may lead to abnormal brain development in the fetus
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Susser et al 1996
increase risk of schizophrenia being developed in offspring whose mothers were malnourished during pregnancy.
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Davis and Bracha (1996)
Malnourishment of the pregnant female leads to a thiamine deficiency in the fetus, that lead to abnormal brain development, especially after the mother began eating normally suddenly.
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Kangui et al (2001)
More likely to have a schizophrenic baby if mother is underweight, linked to above point of issues with malnourishment
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Substance abuse: Zammit et al (2009)
maternal use of substances including tobacco, cannabis, and alcohol, all increased the risk of the baby developing schizophrenia. Tobacco was biggest risk factor, even when it was second hand smoking (e.g. from the father or a close family member).
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What they provide?
don’t necessarily go against the dopamine hypothesis; however they provide evidence that the hypothesis alone does not explain schizo, therefore it needs to be updated
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the dopamine hypo is still heavily supported (evidence) - Other factors should be taken into account (other transmitters such as glutamate and serotonin
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- The hypothesis is still relevant, however should be updated to account for the other factors + environmental influences - Possible that environmental influences cause the abnormal brain development that leads to dopamine being different
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Card 2


What is the prevalence of Schizophrenia?


1% (Carlson, 2017), termed ‘split mind’- Bleuler (1911), Age of onset around adolescents-early 30s (Hafner et al, 1993)

Card 3


Information about symptoms?


Preview of the front of card 3

Card 4


What have explanations been suggested?


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What will this essay argue?


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