NT's SZ

Question 1

What are the 4 neurotransmitters mentioned in this cause of SZ?

Answer 1

-Dopamine
-Glutamate
-Serotonin
-GABA

Question 2

Dopamine function and behaviours (5)

Answer 2

-pleasure, satisfaction and motivation
-reward pathway
-Factor in addiction
-High levels improve focus
-once past point can turn into manic behaviour

Question 3

Glutamate (2)

Answer 3

-Memory, cognition, learning and processing info
-Low levels = anxiety

Question 4

GABA(5)

Answer 4

-Calming effect
-controls anxiety stress and fear
-lessens ability for nerve cells to send or receive messages
-regulates other NT’s
-Calms firing neurons in CNS

Question 5

Serotonin(2)

Answer 5

-Body functions: mood, sleep, digestion,
-Happiness and well-being

Question 6

What are 8 AO1 points to use in an essay?

Answer 6

-Dopamine hypothesis
-D1 and D2 receptors
-Mesolimbic and meso-cortical pathway
-serotonin imbalance
-Gaba
-Glutamate
-Basal ganglia and c.cortex
-example eg drugs/parkinsons

Question 7

Dopamine hypothesis

Answer 7

-Excess dopamine (imbalance)
-Messages from neuron fire too often
-High DA
-Positive sympt
-Hallucinations and delusions

Question 8

D1 and D2 receptors

Answer 8

-D2 receptors meso-limbic pathway. Too many or too sensitive on post-synaptic. More D absorbed. Manic beh. Attention and perception issues.
-Not enough D1 receptors in the meso-cortical pathway. Lack activation. Can’t communicate to PFC through cortical, slows down. neg symtp like disordered thnking

Question 9

Meso-limbic and meso-cortical pathway

Answer 9

-Meso-limbic: too much DA. Pos symtp like hallucinations. Reward pathway so if pleasure then activated. D released
-Meso-cortical: low DA. negative and cognitive symptoms (disordered speech) links to PFC, slows everything down

Question 10

Serotonin

Answer 10

-Imbalance.
-Regulates body temp, sleep, mood and appetite.
-More recent anti-psychotics target serotonin and also are better
-Regulates D in meso-limbic
-Neg symptoms like depression, withdrawal

Question 11

Gaba

Answer 11

-No regulation of other NT’s
-More severe sympt
-calms CNS
-More anxiety

Question 12

Glutamate (4)

Answer 12

-Deficiencies
-Cog and neg sympt
-learning and memory
-leads to insomnia, problems concentrating, exhaustion, poverty of speech

Question 13

Basal ganglia and C.cortex (2)

Answer 13

-low glut in BG. leads to pos symtpoms
-low glut in c.cortex leads to negative

Question 14

Example

Answer 14

Parkinsons
-Low DA leads to parkinsons. high DA leads to SZ. Those with parkinsons taking drugs to inc dopamine, showed symptoms of SZ

Question 15

Evidence to use for NT’s (3+ 3-)

Answer 15

+Lindstroem et al
+Randrup and Munkvan
+Falkai
-Carlsson
-Angrist
-Noll

Question 16

Lindstroem et al (6)

Answer 16

-Supports
-Radioactively labelled L-DOPA (produces dopamine0
-Gave to 10 SZ and 10 non SZ.
-PET scans to trace L-DOPA.
-Taken up quicker in meso-limbic pathway of SZ’s
-More D2 receptors and produce more D

Question 17

How good is the research for Lindstroem?

Answer 17

-PET scans.
-correlations no c&e.
-Only look at post diagnosis when T starts
-Carlsson said stress and anxiety could impact, change NT and distort
-Lowers cred
BUT
-scientific and obj data. Can’t be argued. Improves validity. Live activity, can see uptake of D

Question 18

Randrup and Munkvan

Answer 18

-Amphetamines are agonists which worsen SZ symtp. Similar to paranoid SZ
-They release dopamine
-Gave rats amphetamine and they developed SZ like symptoms.

Question 19

How good is the research for randrup and munkvan?

Answer 19

-Animal studies: can’t tell rat is hallucinating. what seems to be psychotic in rats may not be in humans.
-But can generalise as bio similarities in brain and NT’s function. scientific cred, cause and effect.

Question 20

Evidence to contrast Randrup and Munkvan

Answer 20

Angrist: treated with single shot of amphetamines showed reduction in neg symtpoms like withdrawal. supports glutamate as amphetamines inc glutamate.

Question 21

Falkai

Answer 21

-Post mortem. found SZ patients more D2 receptors than usual in left amygdala & mesolimbic pathway. Supports that DA production abnormal for SZ

Question 22

How good is the research for Falkai?

Answer 22

-Retrospective as post mortem
-Don’t know what behaviour or symptoms were like

Question 23

Carlsson

Answer 23

-Supports dopamine but in review suggests more than just excess DA.
-Deficiency of glutamate
-Stress and anxiety could impact and change NT levels

Question 24

How good is the research for Carlsson?

Answer 24

-meta analysis. researcher bias as can choose studies to use which support idea. Used many of his own studies so reduces credibility.

Question 25

Noll 2009

Answer 25

-1/3 patients dont respond to drugs which block dopamine. Other NT’s involved.
-Clozapine has weakest dopamine antagonist effects but is effective for those who don’t respond to drugs

Question 26

Credibility (strengths)

Answer 26

-Drugs to treat SZ reduce dopamine, side effects like Parkinsons which lacks DA. Supports that major contributor
-DA can explain why dev sympt when never met someone withSZ. Learning requires exposure or positive reinforcement
-Animal studies
-Brain scans

Question 27

Comparisons (5)

Answer 27

-Drugs block DA quick but sympt reduce slowly. expect to reduce as soon as dopamine. more effect on pos
-one level of explanation. may be multiple facotrs. eg family influence, other stresses. Drugs only effective for 65%
-only study post diagnosis, DK if cause or conseq. Start drugs straight away. Impact on NT’s
-only explains pos sympt.
-not only NT. serotonin, gaba and glutamate. reductionist. can explain indiv diffs if look at all NT’s.

Question 28

Alt explanation

Answer 28

-Brain structure (ventricles, redcued vol) and social causation (psychosocial stressors trigger SZ)

Question 29

Conclusions

Answer 29

-Stress diathesis provides best explanation - bio and environment
-Treatments, some only focus on dopamine. 15% SZ non-responsive to drugs