18331273
Description
Mind Map by Katie Greensted, updated more than 1 year ago
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Created by Katie Greensted
almost 5 years ago
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Evaluation: Neurotransmitters as an
Explanation for Schizophrenia (the
Dopamine Hypothesis)
- Introduction
- The dopamine hypothesis suggests that
schizophrenia may be caused by an
increased level of dopamine at the
dopamine synapse. At the synapse,
vesicles hold dopamine neurotransmitters
until an electrical impulse is sent down the
axon, triggering the vesicles to release the
dopamine into the synaptic gap.
- This idea is supported by
research on amphetamines,
which are drugs found to cause
excess dopamine levels,
resulting in psychotic symptoms
similar to those of Sz.
- Timmons and Hamilton found that high doses
of amphetamines resulted in acute psychosis
resembling schizophrenia in clinically normal
people, suggesting that hyperdopaminergia is
linked to symptoms of Sz.
- Contrastingly, Depatie and Lal found that increased
dopamine levels does not always link to psychotic
symptoms. They found that a drug which is a dopamine
agonist (stimulates the release of dopamine) does not
induce Sz symptoms in non-psychotic patients, nor did it
exacerbate them in psychotic patients. This suggests that
dopamine may not be the primary cause of schizophrenia
and its symptoms.
- Contrastingly, Depatie and Lal found that increased
dopamine levels does not always link to psychotic
symptoms. They found that a drug which is a dopamine
agonist (stimulates the release of dopamine) does not
induce Sz symptoms in non-psychotic patients, nor did it
exacerbate them in psychotic patients. This suggests that
dopamine may not be the primary cause of schizophrenia
and its symptoms.
- However, many of the symptoms amphetamines
produce are more symptoms of mania rather
than schizophrenia, such as overconfidence and
high alertness, which could suggest that the
evidence does not fully support the explanation.
- Timmons and Hamilton found that high doses
of amphetamines resulted in acute psychosis
resembling schizophrenia in clinically normal
people, suggesting that hyperdopaminergia is
linked to symptoms of Sz.
- Dopamine is an excitatory neurotransmitter which is
involved in guiding attention, perception and
thinking, and is also linked to pleasure and addiction.
It is suggested that positive symptoms of Sz, such as
delusions, are linked to excess dopamine activity in
the mesolimbic system, whereas negative symptoms,
such as flat affect, may result from
hypodopaminergia (low dopamine levels) in the
mesocortical pathway.
- This idea is supported by
research on amphetamines,
which are drugs found to cause
excess dopamine levels,
resulting in psychotic symptoms
similar to those of Sz.
- The dopamine hypothesis suggests that
schizophrenia may be caused by an
increased level of dopamine at the
dopamine synapse. At the synapse,
vesicles hold dopamine neurotransmitters
until an electrical impulse is sent down the
axon, triggering the vesicles to release the
dopamine into the synaptic gap.
- Higher density of/more receptors.
- A higher density of receptors would
mean more are being triggered by
the dopamine neurotransmitters
binding to them, and more sensitive
receptors may mean that receptors
are triggered more easily and
frequently.
- Janowski et al gave identical doses of amphetamines to
schizophrenic patients and normal controls and found
that low doses produced a slight increase in psychological
agitation, but substantially exacerbated symptoms
among schizophrenic patients. This supports the idea
that people with schizophrenia may be more sensitive to
dopamine uptake.
- However, research has found that there is no
difference in the number of dopamine receptors
in those with schizophrenia and those without,
refuting the idea that the density of receptors
influences higher dopamine levels and therefore
schizophrenia.
- However, research has found that there is no
difference in the number of dopamine receptors
in those with schizophrenia and those without,
refuting the idea that the density of receptors
influences higher dopamine levels and therefore
schizophrenia.
- Janowski et al gave identical doses of amphetamines to
schizophrenic patients and normal controls and found
that low doses produced a slight increase in psychological
agitation, but substantially exacerbated symptoms
among schizophrenic patients. This supports the idea
that people with schizophrenia may be more sensitive to
dopamine uptake.
- A higher density of receptors would
mean more are being triggered by
the dopamine neurotransmitters
binding to them, and more sensitive
receptors may mean that receptors
are triggered more easily and
frequently.
- Reduced enzyme activity
- Enzymes break down excess
neurotransmitters in the synapse
ready for reuptake to occur. If
enzyme activity is reduced, excess
dopamine will be left in the synapse
and may continue to bind with
receptors.
- Wise and Stein found abnormally low levels of DBH in
the brain fluid of schizophrenic patients who died in
accidents, which is the enzyme which breaks down
dopamine after its release. This suggests that low
enzyme activity may be linked to higher levels of
dopamine in the synapse, and therefore perhaps
schizophrenia.
- Wise and Stein found abnormally low levels of DBH in
the brain fluid of schizophrenic patients who died in
accidents, which is the enzyme which breaks down
dopamine after its release. This suggests that low
enzyme activity may be linked to higher levels of
dopamine in the synapse, and therefore perhaps
schizophrenia.
- Enzymes break down excess
neurotransmitters in the synapse
ready for reuptake to occur. If
enzyme activity is reduced, excess
dopamine will be left in the synapse
and may continue to bind with
receptors.
- GABA Deficiency
- GABA is an inhibitory
neurotransmitter which
blocks dopamine from
working, amongst other
neurotransmitters.
- Low levels of GABA means that
dopamine levels will not be
being regulated as well and
therefore levels will be higher,
possibly inducing schizophrenic
symptoms.
- Low levels of GABA means that
dopamine levels will not be
being regulated as well and
therefore levels will be higher,
possibly inducing schizophrenic
symptoms.
- GABA is an inhibitory
neurotransmitter which
blocks dopamine from
working, amongst other
neurotransmitters.
- Criticisms
- The dopamine hypothesis has been criticised
for being too simplistic as it only bases its
theory on a single neurotransmitter. Other
people argue that there may be other
important neurotransmitters, such as
glutamate, which also play a role in the
development of schizophrenia.
- Carlsson reviewed evidence surrounding the
dopamine hypothesis and suggested that other
neurotransmitters, such as glutamate, should be
taken into account when considering the causes of
schizophrenia.
- Javitt and Zukin found that PCP blocks glutamate receptors
and creates schizophrenic symptoms, and that drugs which
increased glutamate levels reversed this effect. This provides
evidence which suggests glutamate may also have a role in
schizophrenia. However, these studies were done on animals
so lack generalisability to humans.
- Carlsson reviewed evidence surrounding the
dopamine hypothesis and suggested that other
neurotransmitters, such as glutamate, should be
taken into account when considering the causes of
schizophrenia.
- However, as the dopamine hypothesis is a
reductionist theory, it fails to look at other,
non-biological factors that may have an
influence on the cause of schizophrenia.
For example, it cannot explain why certain
groups in society are more likely to
develop schizophrenia than others.
- Veling et al showed that Moroccan immigrants were more likely to
be diagnosed with Sz than Turkish immigrants, and this correlated
with the amount of discrimination felt by each group. This
suggests environmental factors, such as the social causation
hypothesis, influence the development of Sz, but the dopamine
hypothesis ignores this.
- Veling et al showed that Moroccan immigrants were more likely to
be diagnosed with Sz than Turkish immigrants, and this correlated
with the amount of discrimination felt by each group. This
suggests environmental factors, such as the social causation
hypothesis, influence the development of Sz, but the dopamine
hypothesis ignores this.
- The dopamine hypothesis has been criticised
for being too simplistic as it only bases its
theory on a single neurotransmitter. Other
people argue that there may be other
important neurotransmitters, such as
glutamate, which also play a role in the
development of schizophrenia.
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