Carlsson et al. 1999/2000

Carlsson et al. 1999/2000

"Network interactions in schizophrenia-therapeutic limitations" Contemporary study for clinical psychology  Related to SZ 

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Pie de foto: : THE MAN HIMSELF

Background

This study was a review rather than an experiment Obtained evidence about role of neurotransmitters in sz from: carlsson's own work, work of others, animal research, PET scans, patients with Parkinson's or Huntington's Research shows that sz can be caused by a dopaminergic dysfunction (the dopamine hyp.) - evidence from PET scans showing high levels of dopamine in those with sz - positive symptoms correlate  Evidence that dopamine interacts with other neurotransmitters eg glutamate 

Glutamate - most common neurotrasmitter, found in 90% of synapses, involved in learning and memory, regulates development and creation of nerves, bonds to NMDA receptors Dopamine - controls reward and pleasure centres, responsible for pleasure & addiction & movement & motivation, dopamine producing actions are repeated

Leiberman and Weinberger

Leiberman:    Idea that glutamate deficiency or a defect in its receptors could lead to sz. Discovered this by observing people taking PCP which acts on NMDA (glutamate) receptors, producing  positive sz symptoms. Implies that those with sz either have a defect in the receptor so glutamate cannot be transported properly or a glutamate deficiency Weinberger: Found evidence that  NMDA is altered by PCP and when it is blocked (as a result) people experienced sz

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Pie de foto: : LEIBERMAN

Aim and Method

Aim: Review how neurotransmitter functioning and psychosis provide explanations for sz Use understanding to produce new anti-psychotic drugs that could be more effective with fewer side effects Method:  Review methods and findings in other studies in this area.  Build body of knowledge from this about dopamine and sz

Findings

PCP -  Acts as an antagonist of a glutamate receptor Glutamate deficiency more likely to result in psychosis (Moghaddam & Adams) Glutamate failure -  In the cerebral cortex may lead to negative symptoms In the basal ganglia could lead to positive symptoms

Clozapine is highly effective - Fewer reported side effects Reduced levels of dopamine and serotonin More effective for those who haven't previously responded to treatment  Animal studies -  Research done on mice in 2009 shows NMDA antagonsits in late/post foetal stage increases neuronal death --> adult sz-like behaviour  Leading to symptoms such as disturbed social functioning, inability to adapt to stressors which overlap with sz symptoms

Conclusions

Further research is needed in developing drugs to treat sz to avoid negative side effects Drug therapies need to consider the role of other neurotransmitters - different types of sz could be due to different neurotransmitter abnormalities 

Evaluation

StrengthsSECONDARY DATA - can assess reliability and validity individually or as a whole, larger sample sizes, better research (pick out best), don't need money or resources PET scans - objective, scientific, valid, reliable, widely usedANIMAL RESEARCH - More data obtained - an test drugs on animals whereas you can't on humans, primates are quite similar (share a lot of DNA), okay if following ethical guidelines 

WeaknessesSECONDARY DATA - Can't be sure of research details, can have low validity and different objective for experiment (leading to a different interpretation of data), selection biasPET SCANS - require interpretation, invasive, radioactive, expensive = only scan a few, claustrophobic --> stress --> neurotransmitters unbalanced ANIMAL RESEARCH - unethical, can't observe cognitive function very well, rats are not similar to us, lacks generalisability