1. Contemporary study for schizophrenia
Carlsson et al. (1999/2000)

2. Background – APRC template on learning space to make notes
DA hypothesis? Recap what does this explanation suggest?
Carlsson et al. believe that there is more to psychotic functioning than excess of dopamine at the synapse.
They suggest that other neurotransmitters are implicated and the interactions between neurotransmitters are just as important than the dopamine present.
Once we cover this study it can be used when your write about biological explanations of SZ.

3. Aims
1. Main aim in their review was to show neurotransmitters functioning between neutrons in specific brain areas
2. They also wanted to use what is know about neurotransmitter functioning and psychosis to build on the body of knowledge of this topic and move beyond the oversimplification of the dopamine hypothesis
3. To use their understanding of psychosis and links to neurotransmitter functioning to produce new antipsychotic drugs that could be more effective with fewer side effects
Application of the third aim? Positive implications of this for those with SZ?
Why is it important to reduce side effects?
Compliance will lead to less relapse and more long term treatment of symptoms without risk of serious side effects such as extra pyramidal symptoms.

4. Method Review Meta-analysis – 33 studies
Review methods and findings of studies
To build body of knowledge of neurotransmitter functioning and psychotic symptoms

5. Group work – results
Using the shared document work in pairs/groups to summarise each section of the results. Be prepared to feedback to the rest of the class.
You may find that you have to do a bit of research around each section to fully understand the results. Use the resources on the learning space.
1. Glutamate has a role is SZ? Explain this ensure you can explain the following: What is glutamate? What is PCP? NMDA receptor? Psychotogenic?
2. Glutamate and dopamine release. How do these two neurotransmitter interact and relate to one another? Ensure you can explain what glutamate is and NMDA antagonists. Monoamine agonists? PCP?
3. Thalamic filter – how can sensory load in the thalamus be changed? Two experimental models of Sz: hyperdopaminergia and hypoglutaminergia. How do these model change the way researchers think about drug therapy?

6. Conclusions and discussion.
How useful are drugs relating to dopamine? Carlsson et al. Explain that drugs have been developed that can stabilise The dopaminergic system without lowering levels of dopamine too far.
Why is this a concern?
Extrapyramidal side effects
There may be sub populations of those with SZ and there may be different causes of SZ within these sub populations.
Implications in terms of treatment? Individual differences?
Glutamate deficiency as an explanation - further research should be conducted
E.g. Why do Psychotic episodes seem to mean lasting deterioration in the patient.
Glutamate deficiency may lead to more ruesponsiveness to DA leading to excess of DA
Serotonin over activity may help explain SZ symptoms. Serotonin and dopamine contribute to positive and negative symptoms.
Research into other neurotransmitter is needed – e.g. GABA, acetylcholine and neuropeptides

7. Evaluation – table on learning space

8. Issues and debates – discuss
Which issues and debates are more relevant to this research?
The development of psychological knowledge over time
Ethical issues
Socially sensitive research
Usefulness
Practical issues on the design and implementation of research
Reductionism
Comparisons between themes (e.g. Different explanations)
Psychology as a science
Nature/nurture
Culture
Social control

9. Using the resource on the learning space write out a PEC for each point. Add a counterargument if appropriate (I.e. Reductionism.
Issues and debates
Understanding of how psychological knowledge has developed over time
Use of psychological knowledge – implications?
Psychology as a science – scientific studies, high level of control, IV and evidence
Therefore based on Reductionist research – strength and weakness
Ethics of using animals in research
Sufficient similarities In neurotransmitter functioning between animals and humans for this to be valid?