Carlsson et al (2000) Flashcards
What was the aim of this study?
To review studies into the relationship between levels of neurotransmitters, especially seretonin, dopamine and glutamate on the symptoms of schizophrenia
What does hyperdominergia and hypoglutamatergia mean?
Too much dopamine and too little glutamate
What research method does this study use?
Literary review - looks at brain scans like Brier et al (1997) and the use of recreational drugs as well as the neurochemical levels of those with sz and APs
What effect does PCP have on neurotransmission?
It acts as an antagonist on glutamate receptors - NMDA receptors, blocks them and therefore increases dopamine
Why is it believed that glutamate may play a role in schizophrenia?
Glutamate acts as a brake/accelerator on dopamine, reduced glutamate increases dopamine so it is an accelerator, if amphetamines rise dopamine, glutamate brakes it
Other than dopamine and glutamate, which other neurotransmitter is thought to be involved in schizophrenia and why?
Seretonin as NMDA antagonists increase seretonin causing negative symptoms. Monoamine agonists and NMDA antagonists work together to form pathways and impact schizophrenia
What role does dopamine and glutamate play with regard to sensory information and how may this be linked to psychosis?
They function in pathways that relate to sensory information to protect the thalamus from sensory overload. D2 receptors overact = overload
What effect does Clozapine have and what does this suggest about the cause of schizophrenia for some sufferers?
Blocks D2 receptors and seretonin receptors and reduces negative and positive suggesting that some sufferers have hyperglutamatergia
The key conclusions are:
- More research needed - GABA, acetycholine etc
- Need less dopamine but not too little
- high seretonin and high dopamine leads to positive symptoms
What did they find about the basal ganglia?
It is the brain’s reward centre where positive symptoms occur as dopamine is active there, schizophrenics show more dopamine in basial ganglia than control group
What did they find about the cerebral cortex?
Low glutamate there leads to negative symptoms, lower glutamate found in schizophrenics compared to controls
How might the study not be valid?
Glutamate and seretonin are difficult to study in the living brain, difficult to seperate functions and effects
What is the advantage of using secondary data?
- Allows for a larger pool of data
- Quicker and cheaper
- Reliable methods used: PET
What is a difficulty with the animal studies used?
They lack validity as shizophrenia is not present in animals
What application does it have?
It may help develop more effective treatment as antipsychotics don’t work for everyone
What Sendt et al (2012) find?
That drugs focusing on dopamine don’t work for many and that they need to focus on glutamate deficiency. Sendt believes that neg and cog symps come from glutamate dysfunction
What are the disadvantages associated with secondary data?
Reliability and validity is questionned as the studies had different aims, controls and samples, may be the influence of individual differences
How many studies were used and how many did Carlsson take part in?
33 studies included, 14 that he took part in
What were the results from Lodge et al (1989) relating to psychosis?
Found that glutamate activity at NMDA receptors produces psychotic reactions in rats and humans
What did Carlsson find from Miller and Abercrombie (1996) about the relationship between dopamine and glutamate?
That the release of dopamine is increased if glutamate activity is reduced
What does Carlsson conclude about the cause of schizophrenia?
That there are subpopulations of schizophrenia, can’t be a one size fits all approach, need individual treatment for sufferers as each has a different cause
Why might this study be time locked?
It took place in 1999 and reviewed research that had been conducted up to 1999 which may not be true now as it is likely that more research has been conducted
What are the issues with some of the studies used?
Laruelle et al for example was used and had never been published meaning it had never been peer reviewed suggesting that there could have been inaccuracies
What was found from studies into PCP?
PCP brings about symptoms of psychosis more than amphetamines which only increase dopamine suggesting glutamate is involved
