contemporary schizophrenia study- carlsson et al

Question 1

aim

Answer 1

review relationship between dopamine and sz by investigating involvement of other neurotransmitters such as glutamate, GABA and serotonin

Question 2

method

Answer 2

meta-analysis of 33 diff studies investigating neurotransmitter’s involvement in sz. some involved carlsson’s own studies and many involved PET scans and animal research such as rats and mice (secondary data)

Question 3

define meta-analysis

Answer 3

a review of secondary data so not a study itself

Question 4

how many carlsson studies were used in this meta-analysis

Answer 4

14

Question 5

dopamine hypothesis supported-

Answer 5

PET scans in which ppl given amphetamines have higher dopamine release in basal ganglia than controls so more likely to exhibit sz symptoms

Question 6

dopamine hypothesis criticised-

Answer 6

found not all sz have high dopamine levels, some showing dopamine levels in normal range

Question 7

role of glutamate generally

Answer 7

proposed glutamate activity provides both “an acceleration and a brake” in diff brain regions causing both positive and negative symptoms so dopamine not only explaination

Question 8

low glutamate in mesocortical pathways (cerebral cortex)

Answer 8

if glutamate levels too low, accelerator function of glutamate increasing dopamine does not work and dopamine levels drop causing negative symptoms

Question 9

low glutamate in mesolimic pathways

Answer 9

glutamate levels too low causes low levels of GABA so dopamine release not inhibited and levels become too high causing positive symptoms

Question 10

evidence of glutamate’s role in sz

Answer 10

evidence comes from drugs such as PCP which inhibits NMDA receptors (glutamate receptors) so they cause low glutamate and high dopamine causing sz sypmtoms

Question 11

what do NMDA receptor inhibitors do

Answer 11

stimulate serotonin turnover and release it more consistently than dopaminergic activity suggesting serotonin also linked to reduced glutamate levels so may contribute to formation of negative symptoms in mesocortical pathways

Question 12

nickname for PCP

Answer 12

angle dust

Question 13

Ketamine effects

Answer 13

reduces glutamate in brain and increases amphetamine induced dopamine release in humans.

Question 14

what was the role of NMDA antagonists and their slight impact on dopamine release tested on

Answer 14

rats (experimentation)

Question 15

hyper refers to….

Answer 15

excess dopamine hypothesis

Question 16

hypo refers to….

Answer 16

inhibited glutamate hypothesis

Question 17

implications of “excess dopamine” and “inhibited glutamate” hypothesise for drug therapy

Answer 17

drugs work by focusing on certain neurotransmitters rather than a combination showing certain drugs may be effective for certain individuals and not others

Question 18

which drugs does carlsson suggest would be useful

Answer 18

drugs that work with the glutamatergic system in diff ways

Question 19

conclusion

Answer 19

further glutamate deficiency study needed to help understand sz, might be a glutamate deficiency that leads to more responsiveness to dopamine, serotonin activity also important as it is thought serotonin and dopamine both contribute to pos and neg symptoms of sz