carlsson contemporary study for SZ Flashcards

1
Q

How is PCP a cause of SZ?

A

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

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2
Q

glutamatergic failure in the ___ ___ may lead to negative symptoms of SZ such as ___.

A

cereal cortex
social withdrawal, thought deletion, inability to feel pleasure.

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3
Q

Positive symptoms of SZ can be cause by …

A

glutamatergic failure in the basal ganglia.

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4
Q

What does amphetamine do?

A

It enhances the release of dopamine triggering negative feedback leading to strong overweight of the brake so even more dopamine is released exciting neurones.

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5
Q

Outline 3 details of Lindostroem’s study.

A

Administered radioactive L-dopa to 10 Sz patients and 10 controls. He used PET scans to measure the reuptake of dopamine.

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6
Q

Outline details and findings of Laurelle’s study

A

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
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7
Q

Outline miller and Abercrombie

A

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.

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8
Q

Give details on carlssons study.

A

Literature review, secondary data , involved positive and negative symptoms as well as ppts in remission and animal studies.

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9
Q

What is the application of carlssons study

A

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.

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10
Q

what is hyperdopaminergia

A

SZ is caused by high levels of dopamine

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11
Q

what is hypoglutamatergia

A

SZ is caused by low levels of glutamate

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12
Q

what is glutamate

A

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

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13
Q

overactivity of dopamine in the ___ ___ pathway can lead to positive symptoms of SZ

A

mesolimbic pathway

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14
Q

under activity of dopamine in the ___ ___ pathway can lead to negative symptoms of SZ

A

Mesocortical pathway

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15
Q

give details on clozapine

A

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.

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16
Q

give the findings of Lodge

A

Lodge et al 1989 shows that PCP can induce psychosis by inhibiting the action of glutamate in the brain because it is a powerful antagonist on one of the glutamate receptor subtypes. Therefore suggesting that glutamate deficiency should be studied further to explain the disorder.

17
Q

how does Carlson use pet scans

A

Carlsson points out that PET scans provide evidence to show that high levels of dopamine related to psychosis (Research from Breier et al 1997) This supports the oldest biological explanation for schizophrenia ( The dopamine hypothesis . PET scans are known to be a very reliable

18
Q

why might Carlsson be reductionist

A

Crippa et al 2015 suggests that other neurotransmitters including nitric oxide and anandamide are linked to psychosis as well as dopamine and glutamate. Therefore Colsons research can be seen as reductionist as it ignores some possible neurotransmitter interactions.