Carlsson et al (2000)

Question 1

What was the aim of this study?

Answer 1

To review studies into the relationship between levels of neurotransmitters, especially seretonin, dopamine and glutamate on the symptoms of schizophrenia

Question 2

What does hyperdominergia and hypoglutamatergia mean?

Answer 2

Too much dopamine and too little glutamate

Question 3

What research method does this study use?

Answer 3

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

Question 4

What effect does PCP have on neurotransmission?

Answer 4

It acts as an antagonist on glutamate receptors - NMDA receptors, blocks them and therefore increases dopamine

Question 5

Why is it believed that glutamate may play a role in schizophrenia?

Answer 5

Glutamate acts as a brake/accelerator on dopamine, reduced glutamate increases dopamine so it is an accelerator, if amphetamines rise dopamine, glutamate brakes it

Question 6

Other than dopamine and glutamate, which other neurotransmitter is thought to be involved in schizophrenia and why?

Answer 6

Seretonin as NMDA antagonists increase seretonin causing negative symptoms. Monoamine agonists and NMDA antagonists work together to form pathways and impact schizophrenia

Question 7

What role does dopamine and glutamate play with regard to sensory information and how may this be linked to psychosis?

Answer 7

They function in pathways that relate to sensory information to protect the thalamus from sensory overload. D2 receptors overact = overload

Question 8

What effect does Clozapine have and what does this suggest about the cause of schizophrenia for some sufferers?

Answer 8

Blocks D2 receptors and seretonin receptors and reduces negative and positive suggesting that some sufferers have hyperglutamatergia

Question 9

The key conclusions are:

Answer 9

• More research needed - GABA, acetycholine etc
• Need less dopamine but not too little
• high seretonin and high dopamine leads to positive symptoms

Question 10

What did they find about the basal ganglia?

Answer 10

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

Question 11

What did they find about the cerebral cortex?

Answer 11

Low glutamate there leads to negative symptoms, lower glutamate found in schizophrenics compared to controls

Question 12

How might the study not be valid?

Answer 12

Glutamate and seretonin are difficult to study in the living brain, difficult to seperate functions and effects

Question 13

What is the advantage of using secondary data?

Answer 13

• Allows for a larger pool of data
• Quicker and cheaper
• Reliable methods used: PET

Question 14

What is a difficulty with the animal studies used?

Answer 14

They lack validity as shizophrenia is not present in animals

Question 15

What application does it have?

Answer 15

It may help develop more effective treatment as antipsychotics don’t work for everyone

Question 16

What Sendt et al (2012) find?

Answer 16

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

Question 17

What are the disadvantages associated with secondary data?

Answer 17

Reliability and validity is questionned as the studies had different aims, controls and samples, may be the influence of individual differences

Question 18

How many studies were used and how many did Carlsson take part in?

Answer 18

33 studies included, 14 that he took part in

Question 19

What were the results from Lodge et al (1989) relating to psychosis?

Answer 19

Found that glutamate activity at NMDA receptors produces psychotic reactions in rats and humans

Question 20

What did Carlsson find from Miller and Abercrombie (1996) about the relationship between dopamine and glutamate?

Answer 20

That the release of dopamine is increased if glutamate activity is reduced

Question 21

What does Carlsson conclude about the cause of schizophrenia?

Answer 21

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

Question 22

Why might this study be time locked?

Answer 22

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

Question 23

What are the issues with some of the studies used?

Answer 23

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

Question 24

What was found from studies into PCP?

Answer 24

PCP brings about symptoms of psychosis more than amphetamines which only increase dopamine suggesting glutamate is involved

Question 25

How have studies shown that glutamate is involved?

Answer 25

Where NMDA antagonists are given alondside amphetamines = rapid increase in dopamine, higher than when just amphetamines given