PSY2003 W1 Schizophrenia 1 - R

Question 1

Dopamine hypothesis, Van Rossum in 1967

Seeman and Kapur (2000)

Answer 1

Drugs have different strengths at the receptor.
The strength (potency) depends on the dissociation constant at D2 (the break down) related to the realise rate of drugs from the D2 receptor (DA D2 Release clozapine and quetiapine more rapidly than other antipsychotic drugs).

Question 2

Post-Mortem studies - dopamine hypothesis

Seeman and Kapur (2000)

Answer 2

Found more D2 receptors in the striata of patients with schizophrenia but they were majoritevely treated with antipsychotics (raising the risk of those drugs contirbuting in the increase of D2 receptors)

Question 3

Abi-Dargham et al

Seeman and Kapur (2000)

Answer 3

: revealed an increase in DA D2 receptors because there is no possible why to show a greater increase without having higher number of D2 receptors.

Question 4

Is the dopamine dysregulaiton hypothesis a good explanation for Schizophrenia

Seeman and Kapur (2000)

Answer 4

The hypothesis of dopamine dysregulation is a good explanation for the psychotic episode however the other psychological and cognitive abnormalities remain unclear.

Question 5

Increased baseline occupancy of D2 receptors by dopamine in Schizophrenia

Abi-Dargham et al., (2000)

Answer 5

increase of the use D2 receptors by DA in schizephenia.
Compared how available D2 receptors before and during pharmacologically induced acute dopamine depletion.

Question 6

What results were a good predictor of what?

Abi-Dargham et al., (2000)

Answer 6

Larger increase in D2 receptor availability in schizophrenic patients predicted a better treatment response for positive smptoms to the antipsychotic drugs (which elevated synaptic dopamine)

Question 7

Dopamine dysregulation - enzyme

Abi-Dargham et al., (2000)

Answer 7

Evidence shows a dysregulation of dopaminergic transmission in schizophrenia. Increase uptake in consistent with increased activity of dopa decarboxylase (= enzyme involved in dopamine synthesis)

Question 8

What was used to measure the dopamine depletion

Abi-Dargham et al., (2000)

Answer 8

SPECT (single-photon computerized emmission tomography) and IBZM (D2 receptor antagonist)

Question 9

What was used/How did they ‘delete’ dopamine?

Abi-Dargham et al., (2000)

Answer 9

Dopamine depletion was achieved by administrating tyrosine hydroxylase inhibitor a-MPT for 2 days. Indirect measure of the propotion of D2 receptors occupied by dopamine in baseline state (‘unmasking receptors’)

Question 10

What happened after MPT exposure?

Abi-Dargham et al., (2000)

Answer 10

D2 receptors were significantly more available after a-MPT exposure compared to baseline, specifically in phrenic patients.

Question 11

What was a-MPT’s effect on symptoms?

Abi-Dargham et al., (2000)

Answer 11

exposure induced a significant reduction in severity of positive symptoms.

Question 12

What predicted good response of positive symptoms with exposure to a-MPT

Abi-Dargham et al., (2000)

Answer 12

High synaptic dopamine levels but it induced a nonsignificant increase in negative symptoms.

Question 13

What did dysregulation of dopamine transmission predict?

Abi-Dargham et al., (2000)

Answer 13

of better response of positive symptoms to treatment.

Question 14

What may be related to the larger occupancy of D2 receptors by dopamine in patients versus wontrol

Abi-Dargham et al., (2000)

Answer 14

may be related to higher levels of free dopamin ein the vicinity of D2 receptors hgiher affinity of D2 receptors for dopamine or some combination of both factors

Question 15

Was there a correlation between severity of positive symptoms and occupancy of strital D2 receptors by dopamine

Abi-Dargham et al., (2000)

Answer 15

No correlation

Question 16

Positive Symptoms

Pinel, J. Biopsychology

Answer 16

Represent an excess of typical function:
Delusions (being controlled, persecuted, of grandeur)
Hallucinations,
Inappropriate affect (failure to react with appropriate emotion to positive or negative events),
Disorganized speech or thought (illogical thinking, beliefs)
Odd behaviour (difficulty with everyday tasks, hygiene and talking rhymes).

Question 17

Negative Symptoms

Pinel, J. Biopsychology

Answer 17

Represent a reduction or loss of typical function:
Affective flattening (diminished emotional expression),
Avolition (reduction of motivation),
Catatonia (motionless).

Question 18

Adoption studies

Pinel, J. Biopsychology

Answer 18

risk of schizophrenia is higher if the biological parents had the disorder whilst there was no risk if the adoptive parents had the disorder.

Today, it is believed you inherit a potential for schizophrenia, but it is only activated by experience.

Question 19

Schizophrenia - Multiple causes

Pinel, J. Biopsychology

Answer 19

Genetic susceptibility
Early experience (birth complication, maternal stress, prenatal infections, Socioeconomic factors, urban birth childhood adversity)
Thought to alter typical neurodevelopment leading to schizophrenia if you are genetically susceptible.

Question 20

Typical Anti-psychotics

Pinel, J. Biopsychology

Answer 20

first generation of anti-psychotic drugs.

Question 21

Atypical anti-psychotics

Pinel, J. Biopsychology

Answer 21

second generation antipsychotic are often the drugs of choice for treatment. Effective against schizophrenia but yet do not bind strongly to D2 receptors. (e.g. clozapine has an affinity for D1 receptor, D4 receptors and several serotonin and histamine receptors.)

Question 22

Schizophrenia and brain structure changes

Pinel, J. Biopsychology

Answer 22

1st generation of studies reported enlarged ventricle and fissures which reduced brain volume. A study also found that the hippocampus, amygdala, thalamus and nucleus accumbent were smaller in those with schizophrenia.