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Schizophrenia: brain chemicals
How might neurotransmitters be implicated in mental illness?
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Today’s session
You will learn about Context
Commenting on evidenceSynaptic transmissionDrug treatments for psychological disorders
SchizophreniaThe dopamine hypothesis of schizophrenia
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Neurones
Sou
rce:
sci
ence
pho
to li
brar
y
Neuronal cell bodies
Synapses occur at the junctions
Axons
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Synapses
Neurones transmit signals electrically along their axons
The synapses (junctions between neurones) transmit signals chemically
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Synapse
Vesicles filled with neurotransmitter
Location of receptors (post-synaptic density)
Synaptic cleft
Sou
rce:
neu
rosc
ienc
e.w
ustl.
edu
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Vesicles release neurotransmitter into synaptic cleft
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Neurotransmitter binds to receptors & activates them
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Enzymes are released to break down the neurotransmitter
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Excess neurotransmitter is taken up by the pre-synaptic neurone
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Vesicles are replenished with new & reused neurotransmitter
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The dopamine hypothesis
Schizophrenia is caused by excessive activity at synapses that use dopamine as their primary neurotransmitter
This causes abnormal functioning of DA-dependent brain systems, resulting in schizophrenic symptoms
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Biology and Schizophrenia
Consistent evidence for abnormal brain functioning in S patients but no single factor identified. Two syndromes? Cause & effect issues everywhere Confounding effects of drug treatment
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What could be done to make dopamine synapses less active?
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Antipsychotic medication
Neuroleptics (e.g. chlorpromazine) bind to DA receptors without activating them
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Effectiveness
Older (typical) drugs (e.g. chlorpromazine) Short term beneficial effect in 75% of
patients (Davis et al, 1989) Long term beneficial effect in 55-60%
(Davis et al, 1993) Most effective against positive symptoms High risk of side effects
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Side effects
Extrapyramidal side effects (EPS) Parkinson’s-type symptoms Postural & motor abnormalities
Other side effects Sedation Weight gain Seizures
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What implications arise from the side effects of antipsychotic drugs?
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Effectiveness
Newer (atypical) drugs (e.g. clozapine) As effective as typical drugs on positive
symptoms; better for negative symptoms (Bilder et al, 2002)
More effective with treatment-resistant patients (DeNayer et al, 2003)
Less risk of EPS, but other side effects may occur (e.g. blood disorders)
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Typical vs. atypical
DA receptor
tightly bound; slow release
from receptor
loosely bound; fast release
from receptor
Drug