neurotransmitter explanation of schizophrenia Flashcards
what is the original dopamine hypothesis?
- 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
what can sensitivity to dopamine arise from and how can this be seen?
- 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
what is the revised dopamine hypothesis?
- positive symptoms caused by excess dopamine in subcortical areas
- negative and cognitive symptoms caused by deficits of dopamine in the PFC
describe the mesocortical pathway
- VTA to the PFC
- involved with motivation and executive functioning
- deficits lead to negative and cognitive symptoms e.g. flattened mood
describe the mesolimbic pathway
- 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
what is the role that serotonin plays and how does clozapine effect serotonin?
- 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
what is the role of glutamate?
- regulatory effect on dopamine
- low levels in cerebral cortex leads to negative symptoms
- glutamate failure in basal ganglia leads to positive symptoms
what is a strength regarding antipsychotic drugs?
- 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
strength regarding the explanation of negative symptoms?
- successfully explains the negative symptoms (reduction in activity at mesocortical pathways) which other explanations struggle to account for
strength regarding post mortem studies and PET scans aswell as a study that shows this?
- 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
what does Grilly (2002) show about the explanation relating to parkinsons patients?
- parkinsons patients have low levels of dopamine
- Grilly = found that those who were taking drugs to increase activity were developing Sz symptoms
what is a weakness regarding reductionism?
- 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
what is a weakness relating to drugs such as clozapine?
- newer antipsychotic drugs such as clozapine have been found to actually increase dopamine levels
- contradicts the dopamine hypothesis
what did the study of Albert and Freidhoff find?
- some patients showed no improvement whatsoever after taking dopamine antagonists
- atypical neuropletics dont necessarily work by blocking only dopamine receptors