Contemp (Sz)- Carlsson (1999) Flashcards
Aims?
1) Consider drug treatments targeting NTs + improve these
2) Produce new anti- psychotic drugs w fewer side effects
3) Use knowledge of NT functioning to find new hypothesis for Sz aside from Dop Hyp. Consider relationship btwn NT lvls-incl Dop + Glut w symptoms of Sz
Define ‘glutamate’
A neurotransmitter nerve cells use to send messages to other nerve cells that controls memory and learning.
What was used in sample?
32 studies investigating neurochemical levels in patients with schizophrenia.
Animal research-rodents
Carlsson involved in 14
33 studies, 32 published, 1 unpublished/ under peer review
Method and data used?
Literature review
Secondary data
Procedure?
Reviewed 32 pieces of research into the relationship between neurotransmitters and schizophrenia- all patients w acute episodes of Sz, patients in studies complained abt tm side effects of Sz antipsychotics
Considered evidence from studies on the use of recreational drugs known to induce psychosis and studies into the effectiveness of drugs used to treat schizophrenia and their method of action on the brain
What were the 3 parts to the results of Carlsson’s study?
1) The Dopamine hypothesis revisited (evidence from PET scans)
2) Beyond Dopamine- Glutamate, (evidence from animal studies)
3)Glutamate Dopamine interaction
Describe results 1)
1) Dopamine as an explanation for schizophrenia
- Evidence from PET scans support the dopamine hypothesis as patients with SZ showed more dopamine activity than a healthy control group - especially in the basal ganglia
Describe results 2)
2) Glutamate as an explanation for schizophrenia
- Evidence supports the role of hypoglutamergia(too little glutamate) in the development of psychotic symptoms
Miller and Abercrombie (1996) show that the release of dopamine is increased if glutamate activity is reduced through blocking NMDA receptors with PCP
- Glutamate failure in the cerebral cortex may lead to negative symptoms whereas failure in the basal ganglia may lead to positive symptoms
Lodge (1989)- incr glutamate activity at NMDA receptors causes positive symptoms in rats and humans
S& Carlsson (1990)- mice given drugs to decr motor activity,if you then give a further drug (MK801) it will improve motor activity but incr dopamine and glutamate which leads to positive Sz symptoms- suggests lower lvls of glutamate & dop led to lower motor activity & less Sz symptoms
Describe results 3)
Conclusion
Carlsson concluded that further research is needed in developing drugs to treat schizophrenia that avoid negative side effects
This should be done by considering more neurotransmitters than dopamine in the development of the disorder
Schizophrenia may have different types that could be caused by different neurotransmitters eg GABA (controlling gluatamate, may cause issues w glutamate and then dopamine)
Look at antipsychs targeting pre-synapse rather than post-synapse- glutamate has more effect at pre-synaptic neuron
GRAVE- G
P - High
E - Used 32 pieces of research looking at the different types of schizophrenia
E - Therefore this represents all/most patients with schizophrenia eg catatonic, paranoid
P - Low
E - Study uses research from 20 years ago where data would be ‘time-locked’ to that era’s society where behaviour of schizophrenia
E - Therefore it would not represent people with schizophrenia and their symptoms today
P- Low
E- Animal research
E- Animal studies aren’t generalisable to human populations as animals are more susceptible to training and following researcher demands, literature review doesnt represent Sz patients
GRAVE- R
P- Low
E- Secondary data used as its a literature review so different researchers used diff procedures to study network interactions in Sz, so not using the same/ any standardised procedures
E- W, lower test-retest and inter rater as Carlsson couldnt be sure that they all gained their findings and similar findings in the same way for future research for NTs and Sz
GRAVE-A
P- Yes
E-Sendt (2012) supports application saying we need more research into glutamate
E- S, create better treatments/ develop better drugs using different NTS to target different symptoms eg positive
GRAVE- V
P - Low
E - Secondary data of 32 studies that involve animal research
E - Wouldn’t know about subjectivity or researcher bias in whether the animals were actually displaying symptoms of schizophrenia which decreases credibility
P-Low
E- Carlsson was involved in 14/33 of the studies chosen in his lit review
E- W, could’ve included studies with research favouring his hypothesis (researcher bias), skewing the findings for Sz
GRAVE-E
P - Good
E - Uses secondary data from 32 other studies in the public domain
E - Therefore no ethical considerations to be made and no ethical guidelines broken
P - Good
E - Uses animals in research
E - More ethical to use for extensive research with things such as drugs than humans
