carlsson contemporary study for SZ Flashcards
How is PCP a cause of SZ?
powerful antagonist on glutamate NMDA receptors by binding to NMDA and blocking it’s functioning.
drugs like PCP and ketamine produce psychotic symptoms by activating glutamate receptors called NMDA. which is supported by lodge et al 1989 who found that glutamate activity at NDMA receptors caused psychosis
glutamatergic failure in the ___ ___ may lead to negative symptoms of SZ such as ___.
cereal cortex
social withdrawal, thought deletion, inability to feel pleasure.
Positive symptoms of SZ can be cause by …
glutamatergic failure in the basal ganglia.
What does amphetamine do?
It enhances the release of dopamine triggering negative feedback leading to strong overweight of the brake so even more dopamine is released exciting neurones.
Outline 3 details of Lindostroem’s study.
Administered radioactive L-dopa to 10 Sz patients and 10 controls. He used PET scans to measure the reuptake of dopamine.
Outline details and findings of Laurelle’s study
Sz patients in remission had normal levels of dopamine. this explains why SZ patients in remission complain of nasty side effects because they have normal levels of dopamine and are taking a drug which is reducing their levels of dopamine even more. this causes (hypodopaminergia)
- hadn’t been peer reviewed
Outline miller and Abercrombie
Used rodents. Inhibited NMDA receptors with antagonists (inhibiting the effects of glutamate). psychotic side effects of pop can be reduced by a chemical called LY354740 which increases the glutamate activity (has no effect on dopamine) and dopamine levels reduce. this supports the idea that glutamate acts as a brake and accelerator of dopamine.
Give details on carlssons study.
Literature review, secondary data , involved positive and negative symptoms as well as ppts in remission and animal studies.
What is the application of carlssons study
Improvement of drug treatment. Ie clozapine is a SGA which binds to dopamine and serotonin but is a weak dopamine antagonist. TGA are needed to target NT other than dopamine ie glutamate. Improving symptoms for 15% of patients resistant to treatment. also focusing on reducing the negative side effects which reduce patient quality of life.
what is hyperdopaminergia
SZ is caused by high levels of dopamine
what is hypoglutamatergia
SZ is caused by low levels of glutamate
what is glutamate
this is a NT which is involved in learning and memory. it is an excitatory NT in the brain. too much glutamate is linked to Parkinson’s and huntington disease. it is needed to make other NT such as GABA the calming NT which is linked to sleep, relaxing and anxiety regulation.
it acts as a direct brake and accelerator of dopamine. low levels of glutamate causing high levels of dopamine and vice versa. receptors are NMDA
is is linked to both positive and negative symptoms of SZ
overactivity of dopamine in the ___ ___ pathway can lead to positive symptoms of SZ
mesolimbic pathway
under activity of dopamine in the ___ ___ pathway can lead to negative symptoms of SZ
Mesocortical pathway
give details on clozapine
this is an atypical drug treatment that has better results with patients resistant to treatment. it is a SGA as it targets serotonin rather then just dopamine alone (it reduces serotonin and dopamine levels). has less negative side effects.