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Clinical Psychology
Contemporary study: Carlsson et al. (2000)
- 2 things to know
- Papers 2 and 3
Overview
Recall questions on why the simple dopamine hypothesis was insufficient, the role of glutamate, and the therapeutic implications.
What you need to know
Answer each one before you reveal it.
What evidence pointed to glutamate involvement in schizophrenia?
Questions from this subtopic
Each one with the model answer underneath.
- 1
What was the aim of Carlsson et al.'s (2000) work on schizophrenia?
Model answer
To re-evaluate the neurochemical basis of schizophrenia, moving beyond the classic dopamine hypothesis to consider how several neurotransmitter systems interact, and what this means for treatment.
- 2
What research method did Carlsson et al. (2000) use?
Model answer
It was a review that drew together findings from animal studies and human pharmacological research on neurotransmitter interactions.
- 3
What was Carlsson et al.'s central argument about the cause of schizophrenia?
Model answer
That schizophrenia is not caused by dopamine alone but by interactions within networks of neurotransmitters, including glutamate, GABA and serotonin, that regulate one another.
- 4
According to Carlsson et al. (2000), how does glutamate relate to dopamine in schizophrenia?
Model answer
Glutamate normally helps to control dopamine activity, so reduced glutamate function at NMDA receptors (hypoglutamatergia) can lead to dysregulated dopamine and psychotic symptoms.
- 5
What were the therapeutic implications of Carlsson et al.'s (2000) review?
Model answer
That new drugs could target glutamate and other transmitter systems rather than dopamine alone, potentially treating a wider range of symptoms with fewer side effects.
- 6
What did Carlsson et al. (2000) argue about schizophrenia and dopamine?
Model answer
That the simple dopamine hypothesis is insufficient, and that glutamate and other transmitter systems interact with dopamine to produce symptoms.
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