colsson Flashcards
what is Carlssons’ study
- a literature review
what are the 3 aims of carlsson’s study
1- provide more of an explanation for.schizophrenia than just the dopamine hypothesis
2- look at the relationship between neurotransmitter levels of dopamine and glutamate on the symptoms of schizophrenia
3- review anti-psychotic drugs that could be more effective with fewer side effects
how many studies did Carlsson use in his literature review
- 33
- 32 published
- 1 unpublished
what 4 different types of studies were used
- previous research using rodents to test NT functioning and related brain structure
- studies with acute schizophrenia and schizophrenia in remission
- studies using PET scanning methodology
- evidence from studies looking at mice and their behaviour
Carlsson used a variety of previously conducted research investigating neurotransmitter levels in patients diagnosed with schizophrenia
true or false
- false
- neurochemical levels
what drugs known to induce symptoms of psychosis did Carlsson use
- angel dust (PCP)
- amphetamine
Carlsson used Laurelle et al in his literature review
what did Laurelle et al (1996) found
- used SPECT and PET studies to measure the release of dopamine in the basal ganglia
- found that amphetamine enhanced dopamine significantly in the basal ganglia in drug-naive patients
- correlates with positive symptoms
Carlsson used miller and abercrombie in his literature review
what did miller and abercrombie (1996) find
- a slight release of dopamine studied by microdialysis was obeserved in rats following treatment with MK-801
Carlsson used Lindstrom in his literature review
what did Lindstrom et al (1997) find
- found deviant from normal levels of dopamine in pre-frontal cortex and straitum in drug-naive schizophrenic patients following administration of radiolabelled dopa or flurodopa
- measured by PET scans
what did carlsson look into in terms of glutamate and schizophrenia
- PCP blocks glutamate receptors (NMDA)
- PCP is an antagonist (decreases effect of neurotransmitter)
- deficiency of glutamate lead to cognitive disturbances e.g. poverty of speech, negative symptoms
- glutamate deficiency in the cerebral cortex leads to negative symptoms
- glutamate deficiency in the basal ganglia leads to positive symptoms
- use of PCP is more likely to result in psychosis
what did carlsson look into in terms of glutamate and dopamine
- glutamate regulates dopamine it either acts as an accelerator or a break
- it acts as an accelerator if dopamine levels are too low it increases the levels by exiting release
- if glutamate isn’t working properly dopamine levels stay too low
- which may lead to low levels of dopamine in the meso-cortical pathway which would result in negative symptoms
- other way around for glutamate acting as a break
- high levels of dopamine in the meso-limbic pathway would result in positive symptoms
what did Carlsson look into in terms of drug therapy
- some people respond drug treatment differently e.g. because some may have abnormal levels of glutamate and some dopamine
- those who FGA didn’t work may have a more glutamate focused condition
- Clozapine which regulates dopamine and serotonin
- if serotonin is inhibited so is glutamate
- an increase in serotonin causes an increase in glutamate which reduces negative symptoms and positive symptoms if levels are reduced in the basal ganglia
what are the 3 overall findings of Carlsson
- excess dopamine as an explanation was too simplistic
- dopamine isn’t the only neurotransmitter to affect symptoms of schizophrenia e.g. GABA and glutamate
- dopamine is just easier to study in the brain
what did carlsson conclude
- schizophrenia may have different types that could be caused by abnormal levels of different neurotransmitters
- further research is needed in developing drugs that avoid negative side effects
why does Carlsson have low generalisability
- uses studies that use animal studies
- e.g. Miller and abercrombie used rats to look at the relationship between dopamine and glutamate
- humans have a more developed PFC
