Clinical: Carlsson Et Al Flashcards
What was the aim of Carlsson et al’s review?
To review the evidence for and against the dopamine hypothesis and consider the role of other neurotransmitters (role of glutamate)
What was the result of the review conducted by carlsson et al on the dopamine hypothesis?
It supported it. Schizophrenic participants had higher dopamine activity than the healthy control group.
What did the review conducted by carlsson et al discover about glutamate?
Found that drugs like ketamine produce psychotic symptoms that activate glutamate receptors called NMDA.
Glutamate activity at NMDA receptors produces psychotic reactions in rats and humans.
What does glutamate do?
Glutamate uptake keeps brain chemistry stable. Levels of glutamate mustn’t be too high (hyperglutaminergia) or too low (hypoglutaminergia)
Controls memory and learning.
What did Carlsson find about the relationship between dopamine and glutamate?
Glutamate regulates the behaviour of dopamine. It can accelerate it or slow it down.
The release of dopamine is increased if glutamate activity is reduced by blocking NMDA receptors.
Evaluate the generalisability of Carlsson et al’s review.
+ Used 33 studies= good representation of status quo.
- All around 2000, may be time locked.
-Animal studies included (not entirely generalisable to humans)
Evaluate the reliability of Carlsson et al’s review.
+Lab experiments using standardised PET brain scanning techniques (standardised and replicable)
-One hadn’t been peer reviewed
Evaluate the application of Carlsson et al’s review.
Improved dopaminergic drugs that have fewer side effects based on a better understanding of dopamine pathways and how they affect other neurotransmitters.
Evaluate the validity of Carlsson et al’s review.
- Other treatments like clozapine focus on glutamate levels which reduce symptoms and side effects of Sz
+ Dopamine and Glutamate hypothesis are linked, Carlsson agreed with this and concluded that further research was necessary.
Evaluate the effects of Carlsson et al’s review.
+ No human ethical issues other than the use of PET scans
- Animal studies that involved injecting drugs into rodents to induce Sz symptoms (no protection from harm)
What are the benefits of using secondary data?
+ Cost and time efficient
+ Large sample due to multiple studies
What was Carlsson et Al’s conclusion?
There are different groups of schizophrenic patients whose symptoms have different biological explanations.
Lack of glutamate might cause patients to have an exaggerated response to dopamine at the post synapse.
