neurotransmitter explanation of schizophrenia Flashcards

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1
Q

what is the original dopamine hypothesis?

A
  • hyperactivity of dopamine transmission
  • hypersensitivity of D2 receptors in the brain so a larger effect is caused by dopamine
  • causes positive symptoms such as hallucinations
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2
Q

what can sensitivity to dopamine arise from and how can this be seen?

A
  • genetic inheritance to brain lesioning and therefore biochemical abnormalities should be detectable
  • postmortem examinations have shown the brains of people with Sz have higher density of dopamine receptors
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3
Q

what is the revised dopamine hypothesis?

A
  • positive symptoms caused by excess dopamine in subcortical areas
  • negative and cognitive symptoms caused by deficits of dopamine in the PFC
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4
Q

describe the mesocortical pathway

A
  • VTA to the PFC
  • involved with motivation and executive functioning
  • deficits lead to negative and cognitive symptoms e.g. flattened mood
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5
Q

describe the mesolimbic pathway

A
  • VTA to basal ganglia
  • involved with goal orientation, reward and attention
  • excess dopamine in these areas leads to positive symptoms such as hallucinations and delusions
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6
Q

what is the role that serotonin plays and how does clozapine effect serotonin?

A
  • plays a role in mood and the sleep wake cycle
  • in areas with low serotonin there was high dopamine linking to positive symptoms
  • clozapine = affects the D1 and D4 receptors
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7
Q

what is the role of glutamate?

A
  • regulatory effect on dopamine
  • low levels in cerebral cortex leads to negative symptoms
  • glutamate failure in basal ganglia leads to positive symptoms
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8
Q

what is a strength regarding antipsychotic drugs?

A
  • block the activity of dopamine by reducing the stimulation of the dopamine system
  • helps reduce symptoms of hallucinations and delusions
  • strengthens the case of dopamine being a contributing factor
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9
Q

strength regarding the explanation of negative symptoms?

A
  • successfully explains the negative symptoms (reduction in activity at mesocortical pathways) which other explanations struggle to account for
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10
Q

strength regarding post mortem studies and PET scans aswell as a study that shows this?

A
  • have shown that dopamine receptors are greater in number or are hypersensitive
  • Falkai et al = studied autopsies and found that people with Sz have larger number of receptors
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11
Q

what does Grilly (2002) show about the explanation relating to parkinsons patients?

A
  • parkinsons patients have low levels of dopamine
  • Grilly = found that those who were taking drugs to increase activity were developing Sz symptoms
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12
Q

what is a weakness regarding reductionism?

A
  • attempts to explain a complex disorder using the smallest unit of explanation and fails to consider any social factors
  • things are usually interactionist e.g. may be genetic predisposition that is triggered by social factors
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13
Q

what is a weakness relating to drugs such as clozapine?

A
  • newer antipsychotic drugs such as clozapine have been found to actually increase dopamine levels
  • contradicts the dopamine hypothesis
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14
Q

what did the study of Albert and Freidhoff find?

A
  • some patients showed no improvement whatsoever after taking dopamine antagonists
  • atypical neuropletics dont necessarily work by blocking only dopamine receptors
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