Carlsson et al (Contemporary Study) - AO1 Flashcards
From which sources did Carlosson gather the data for his review on the role of neurotransmitters in SZ?
Carlsson gathered his data on the role of neurotransmitters in SZ from the following sources:
- Carlsson’s own research
- Work of others
- Animal research (rodents)
- PET scans
- Parkinson’s and Huntington’s patients
Which original theory of neurotransmitters and SZ does Carlsson investigate in his review?
Carlsson investigates the role of dopaminergic dysfunction (dopamine hypothesis) in his review. Evidence for dopaminergic dysfunction comes from brain scans - PET scans show an increase in dopamine in SZ patients which correlates with the positive symptoms of the disorder
Which newer theory does Carlsson also investigate in his review?
Carlsson also investigates the theory of hypoglutamatergia as a cause of SZ. Glutamate is a neurotransmitter responsible for 90% of synaptic connections and bonds to NMDA receptors. The theory of hypoglutamatergia suggests that SZ patients have a defect/deformity at the NMDA receptors which glutamate stimulates. This means that glutamate cannot properly by absorbed and stimulate the receptors, leading to glutamate levels in SZ patients being low
How has the drug PCP (‘angel dust’) helped to form the hypothesis of hypoglutamatergia?
Users of PCP (‘angel dust’) were observed to act as if they have SZ. PCP acts on NMDA receptors to block the effects of glutamate
What were the three main aims of Carlsson’s review?
The three main aims of Carlsson’s review were:
- To present the current view of the relationship between SZ and dopaminergic dysfunction
- To explore the rival theory of hypoglutamatergia
- To explore new drugs that reduce levels of relapse and negative side effects
Carlsson’s method was to build up a body of knowledge about dopamine and glutamate in relation to SZ. Of what areas was Carlsson’s secondary research made up?
Carlsson’s secondary research was made up of the following areas:
- Brain scans
- Animal studies
- Recreational drug research (PCP)
- Antipsychotic drug research
What were Carlsson’s findings regarding PCP research?
Regarding PCP research, Carlsson found:
- That PCP acts as an antagonist of NMDA receptors, inhibiting glutamate and resulting in psychosis in its users
- That glutamate deficiency was more likely to result in psychosis than hyperdomaminergia
What were Carlsson’s findings regarding brain scans focussing on hypoglutamatergia
Regarding brain scans focussing on hypoglutamatergia, Carlsson found:
- Hypoglutamatergia in the cerebral cortex may lead to negative symptoms of SZ
- Hypoglutamatergia in the basal ganglia may lead to positive symptoms of SZ
What were Carlsson’s findings regarding research into antipsychotic drugs (clozapine)?
Regarding antipsychotic drugs, specifically clozapine, Carlsson found:
- Clozapine is a highly effective drug for SZ;
- Clozapine has few reported side effects
- Clozapine reduces levels of dopamine and serotonin (antagonist) and increases levels of glutamate (agonist)
- However, Carlsson found that clozapine was more effective in patients who had previously responded to treatment
What were Carlsson’s findings regarding research into animal studies?
Regarding research into animal studies, Carlsson found:
- Research done on mice has shown that administering NMDA agonists (e.g. PCP) in the late- or post-foetal stage of pregnant mice increases neuronal death in their offspring, linked to adult SZ behaviour
- The offspring showed severe symptoms such as disturbed social function and an inability to adapt to predictable future stressors that overlap with SZ
What did Carlsson conclude about why some patients may respond better to some drug treatments than others?
Carlsson explained the fact that some patients respond better to some drugs than others by suggesting this may be because some people’s SZ is more dopaminergic and others’ symptoms are more glutamatergic.
The treatment-resistant patients who don’t respond to typical antipsychotics which reduce dopamine might have a more glutamatergic condition
What did Carlsson conclude about the interaction between glutamate and dopamine?
Carlsson suggested that glutamate appears to regulate the behaviour of dopamine. Carlsson describes how glutamate acts as an ‘accelerator’ or ‘break’ for dopamine (increasing or decreasing dopamine activity)
What research back’s up these conclusions about the interaction between glutamate and dopamine?
Miller and Abercrombie showed that the release of dopamine is increased if glutamate activity is reduced through the blocking of NMDA receptors
