Carlsson et al (1999) Flashcards
what is the method for the study?
There is no method as it is a literature review which means that they look at different research and compile it and figure out what is the main cause for their question. This review looks at 33 studies (32 published, 1 unpublished)
the background of the study
it considers two areas of developing SZ. Hyperdopaminergia - too much dopamine and hypoglutamatergia - too little glutamate. many drugs that treat SZ tackle Dopamine and have bad side effects for the patient so the study is trying to research what is the main cause for the disease and what could we do to make better drugs.
The aims of the study
to use what is known about neurotransmitter functioning and provide a better explanation for SZ than simply the dopamine hypothesis.
what is the dopamine hypothesis?
That in people with SZ there is too much dopamine in the brain, especially in the basal ganglia. They found this due to the drug amphetamine - this increases dopamine in the brain and increases SZ symptoms. Those with Sz have more dopamine than healthy people in a control group.
Evidence from studies using PET scans
what is the glutamate hypothesis?
they came up with this due to the dopamine hypothesis being too simplistic. Glutamate is a NT that is important in memory, cognition, and mood regulation. Lodge et al (1989) -PCP (drug) is a NMDA inhibitor (a type of glutamate receptor) and produces psychotic symptoms like SZ in rodents and humans showing that glutamate does play a role in positive symptoms of SZ.
evidence from studies using Animals and Humans
how do glutamate and dopamine work together?
glutamate regulates he behaviour of dopamine Carlsson describes it as a brake or accelerator of dopamine (decreasing or increasing dopamine activity)
what did miller and abercrombie find?
show the release of dopamine is increased when glutamate is reduced as it blocks the NMDA receptors that glutamate binds to.
what is hypoglutamatergia and how does it effect SZ? what does it mean if it is in different areas in the brain?
it means low levels of glutamate
in NMDA receptors in cerebral cortex= negative symptoms of SZ.
in basal ganglia = positive symptoms of SZ
what is the thalamic filter?
it is between the stratum and cerebral cortex and it filters off excess NT to stop the cerebral cortex from overloading.
what did Carlsson conclude?
that dopamine is too much of a simple explanation of SZ there needs to be a needs to be researched more and develop new drugs to tackle both dopamine and glutamate.
