biological explamation of schizophrenia: the function of neurotransmitters Flashcards
(28 cards)
1
Q
define neurotransmitter
A
- body’s chemical messengers
- molecules used by ns to transmit messages between neurons
2
Q
define dopamine
A
- nt made in your brain
- plays as a ’reward center’/sense of pleasure
3
Q
define hyperdopaminergia
A
- overactive
- having too much dopamine activity
4
Q
define hypodopaminergia
A
- under active
- having too little dopamine activity
5
Q
define dopamine agonist
A
- drugs that activate certain types of cells in brain
6
Q
define mesocortical pathway
A
- neural connection between ventral tegmental area and frontal cortex
7
Q
define mesolimbic pathway
A
- begins in the ventral tegmental area and connects nucleus accumbens, amygdala, hippocampus and prefrontal cortex
8
Q
define glutamate
A
- most abundant excitatory nt in brain and cns
9
Q
define antagonist
A
- chemical/medication that attached brain receptors and inhibits an antagonist from reacting
10
Q
define amphatamine
A
- stimulant drugs that speed up messages between brain and body
11
Q
what is the dopamine hypothesis
A
- original dopamine hypothesis states that the brain of schizophrenic patients produces more dopamine than the brain of a “normal” person
- through further research, it’s now thought that schizophrenics have an abnormally high number of D2 receptors
12
Q
how is dopamine linked to schizophrenia?
A
- dopamine (da) is a neurotransmitter
- high levels of dopamine in the brain
- too many d2 receptors at synapses
- linked to schizophrenia symptoms
- contributes to the illness
13
Q
what happens when there’s a change in the mesolimbic and mesocortical pathways? (dopamine hypothesis)
A
- increased mesolimbic activity → positive symptoms
- decreased mesocortical activity → negative symptoms
14
Q
how does dopamine activity affect attention and schizophrenia symptoms?
A
- dopamine neurons firing too often → too many messages
- certain D2 receptors guide attention
- lowering DA activity helps reduce schizophrenia symptoms
15
Q
how does amphetamine (agonists) affect dopamine and schizophrenia symptoms?
A
- amphetamine increases dopamine levels
- large quantities → delusions and hallucinations
- giving amphetamines to schizophrenic patients worsens symptoms
16
Q
what is the role of glutamate in schizophrenia? (glutamate hypothesis)
A
- theory from 1980s, now widely supported
- glutamate, major excitatory neurotransmitter, activates neurons
- decreased glutamate activity → schizophrenia symptoms
- phencyclidine (PCP) blocks NMDA receptors, causing symptoms
- glutamate normally lowers dopamine levels, controlling dopamine release
17
Q
supporting: post mortem (Falkai et al)
A
- autopsies found that people with schizophrenia have more dopamine receptors than usual
- increased dopamine in brain structures (left amygdala, caudate nucleus, putamen)
- suggests abnormal DA production in schizophrenia
18
Q
supporting: lindstroem et al
A
- radioactively labelled a chemical called L-DOPA (chemical for dopamine production)
- administered to ten untreated patients with schizophrenia and control group of 10 people
- used PET scans to trace what happened to the L-DOPA
- L-DOPA taken up faster in schizophrenia patients
- suggests higher dopamine production in schizophrenia compared to controls
19
Q
supporting evidence: Snyder
A
- chlorpromazine acts as an antagonist at many dopamine receptors (especially d1 and d2) and has an antipsychotic effect
- haloperidol is a dopamine antagonist with fewer effects but more effective at reducing symptoms
- suggests excess activity on specific dopamine receptors contributes to schizophrenia symptoms
20
Q
other things: haloperidol
A
- dopamine antagonists like haloperidol bond to d2 receptors
- they successfully reduce positive symptoms of schizophrenia
21
Q
supporting: tenn et al
A
- rats given 9 amphetamine injections over 3 weeks showed schizophrenia-like symptoms
- dopamine antagonists (drugs blocking d1 receptors) successfully reversed these symptoms
22
Q
other: pre scanning (weakness)
A
- using pet scanning affect the validity of neurotransmitter research
- pet scanning might cause pressure on ppts
- feeling pressured could make people respond differently than normal
- this can lead to inaccurate findings and affect validity
23
Q
other: pet scans (weakness)
A
- pet scans show blocking dopamine receptors doesn’t always remove symptoms
- drugs blocking dopamine don’t reduce symptoms in people with schizophrenia for 10+ years
24
Q
strength amphetamines
A
- amphetamines produce symptoms similar to excess dopamine
- this is called amphetamine psychosis
- the symptoms are similar to the positive symptoms of schizophrenia
25
weakness antipsychotic drugs
- **antipsychotic drugs** block dopamine receptors quickly
- but it takes a few days to reduce symptoms
- suggests **other factors** beyond neurotransmitters are involved in schizophrenia
- doesn't fully explain the development of schizophrenia
26
opposing: depatie and lal
- giving drugs that increase dopamine production doesn't create schizophrenia symptoms
- this suggests **excess dopamine** isn't the only cause of schizophrenia
27
other things: incomplete
- neurotransmitter explanation can be said to be **incomplete**
- it ignores other possible causes like **early childhood experiences or cognitive processes**
- not the only explanation for schizophrenia
- **liverpool university (2012)** found **childhood trauma** makes you three times more likely to develop schizophrenia
- suggests a strong **environmental** factor, not just neurotransmitters
28
opposing: wim veling et al
- **moroccan immigrants** were more likely to be diagnosed with schizophrenia than **turkish immigrants**
- this correlated with the level of **discrimination** faced by each group
- suggests that **environmental factors** like **social stress** may interact with **neurochemistry**, making some more prone to psychosis
