Carlsson et al (1999) - Contemporary Study on Sz Flashcards
Why did Carlsson carry out this review?
Challenging his original hypothesis from the 1960s
What is a review?
Using primary and secondary data
What did Carlsson suggest about glutamate?
Glutamate also important in the onset of Sz not just dopamine as original hypothesis suggested
What is glutamate?
Excitatory neurotransmitter
Linked to learning and memory
What was the aim of Carlsson’s review?
To investigate the role of glutamate and other neurotransmitters in the onset of Sz
To develop new improved antipsychotics with less side effects and more effective
How may studies did Carlsson use in his review?
33 studies all relating to the role of glutamate in Sz
14 studies Carlsson carried out himself
Who were the studies used in Carlsson’s review carried out on?
Large number carried out on rodents
People with acute Sz
People with Sz in remission
People using recreational drugs e.g. PCP (angel dust)
What did a lot of the studies used in Carlsson’s review use to analyse behaviour?
A lot of the studies used PET scans to analyse behaviour
What did Carlsson find about drug users and Sz?
Drug users using PCP started to have psychotic symptoms similar to Sz
PCP stimulates NMDA receptors (glutamate receptors)
What did Carlsson find about glutamate?
Glutamate appears to be important in the onset of Sz
Evidence from PCP users
What did Carlsson find about glutamate and dopamine?
Less glutamate regulates the production of dopamine
Increases levels of dopamine
What did Carlsson find about specific areas of the brain and symptoms of Sz?
Specific areas linked to different symptoms
Cerebral cortex linked to negative symptoms
Basal ganglia linked to positive symptoms
What did Carlsson find about the original antipsychotic medication?
Lowers dopamine but didn’t work for all patients in reducing symptoms
Glutamate must also need addressing
What were the conclusions of Carlsson’s review?
Two explanations for Sz need to be considered:
hypoglutamatergia (too little glutamate ) leads to hyperdopaminergia (too much dopamine)
Future research must address other neurotransmitters too e.g. GABA and serotonin
