Dopamine Hypothesis Flashcards
How was the link between dopamine and schizophrenia established?
1950s research
Levodopa increased dopamine in the brain reducing Parkinson’s symptoms
Symptoms/behvaiours of schizophrenia developed
What did the research by Griffith et al. (1968) suggest?
When dopamine was increased in the brain, positive symptoms of schizophrenia appeared (sudden onset of paranoid delusions and detached emotional responses) which is supporting evidence for too much dopamine = schizophrenia symptoms
Why is the initial dopamine hypothesis considered a partial explanation?
The drugs that reduced dopamine levels had little or no effect on those suffering mainly negative schizophrenia symptoms
What receptor sites are mainly focused on within the dopamine hypothesis?
D2 Receptors
What is the name of the system that is the main focus of the dopamine hypothesis?
Limbic system as D2 receptors are mostly found in the subcortical regions
What are the names of the pathways associated with schizophrenia?
Mesolimbic Pathway
Mesocortical Pathway
What happens in the mesolimbic pathway?
Signals from the ventral tegmental area (VTA) to the nucleus accumbens
How is the mesolimbic pathway related to schizophrenia?
Too much dopamine causes overstimulation and ultimately positive symptoms e.g. hallucinations (HYPERFUNCTION)
What happens in the mesocortical pathway?
Signals from VTA to frontal lobe
Why is the mesocortical pathway important?
Associated with our emotional responses, motivation and cognition
What did Davis et al. (1991) suggest?
Too little dopamine (hypofunction) is evident in the D1 receptors in the frontal lobe of individuals with negative symptoms and cognitive impairments of schizophrenia
What is a strength of the theory that dopamine imbalances may be caused by genes?
Idea that there is a genetic predisposition as twin and family studies have indicated this (Gottesman 1991 conducted research on a variety of family members noting that as genetic similarity increased so did the probability of both individuals having schizophrenia)
Why is the theory of dopamine imbalances being caused by genes a weakness?
As the concordance rate is not 100% for identical twins and it could be much more complex e.g. the environment in which people grow up
Why has research focusing on identifying genes responsible for dopamine imbalances been disappointing?
Because a group of psychiatric genomics (300 scientists from 35 countries) reported there are 108 genetic loci associated with schizophrenia therefore indicating a more complex explanation than abnormal genes
How can we measure levels of neurotransmitters?
Through metabolites and this can be measured in cerebrospinal fluid obtained via a lumbar puncture
