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Neurones
Sou
rce:
sci
ence
pho
to li
brar
y
Neuronal cell bodies
Synapses occur at the junctions
Axons psyc
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Synapses
Neurones transmit signals electrically along their axons
The synapses (junctions between neurones) transmit signals chemically
Most drugs act by interfering with events at the synapse
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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
psyc
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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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Drug Therapies
Increase synaptic activity by: Causing more neurotransmitter to be
released Introducing a chemical that acts like the
neurotransmitter Preventing breakdown of neurotransmitter Preventing reuptake of neurotransmitter
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Drug therapies
Decrease activity by: Increasing rate of neurotransmitter
breakdown Blocking off receptors
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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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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
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