Contemporary Study: Carlsson et al 2000
Aims:
Presented evidence for and against the dopamine hypothesis of schizophrenia.
Aimed to include a consideration of the role of other neurotransmitters like glutamate,
serotonin and GABA.
They wanted to explore new antipsychotics, especially for people who are ‘treatment-
resistant’ or who experience extreme side effects.
The Dopamine Hypothesis Revisited:
PET studies show that the drug
Glutamate-dopamine Interaction:
amphetamine enhances schizophrenic-
Hypoglutamatergia in the cerebral cortex
like symptoms in people with
may lead to negative symptoms of
schizophrenia more than controls.
schizophrenia.
The explanation is insufficient as it does
But in the subcortical basal ganglia could
not apply to all people with
be responsible for positive symptoms.
schizophrenia.
Proposal that dopamine and glutamate
Beyond Dopamine:
pathways interact and affect the
Unlikely that dopamine is the only
striatum.
neurotransmitter in the brain associated
The Thalamic Filter:
with schizophrenia.
Area of the brain involved in the
Glutamate induces schizophrenic-like
suggested ‘psychotogenic pathway’ -
symptoms and is a powerful antagonist of
brain system which governs a psychotic
NDMA receptors - a type of glutamate
response.
receptor.
Thalamus may be turned on or off
Decrease glutamate increases dopamine.
depending on which way the pathway is
Glutamatergic Control of Dopamine
activated.
Release:
Comparing 2 models:
Affects the release of GABA producing
Hyperdopaminergic model - traditional
the opposite effect.
view of the role of dopamine when
Acts like a ‘brake’ and reduces dopamine
increased produces psychotic symptoms.
activity.
Hypoglutamatergic model - glutamate
Low glutamate may increase/decrease
can produce an increase/decrease in
dopamine.
dopamine activity depending on the
Normally there is a balance between the
accelerator or brake.
‘accelerator’ and the ‘brake’ and a
M100907 - drug use.
disruption can lead to symptoms
associated with schizophrenia.
Aims:
Presented evidence for and against the dopamine hypothesis of schizophrenia.
Aimed to include a consideration of the role of other neurotransmitters like glutamate,
serotonin and GABA.
They wanted to explore new antipsychotics, especially for people who are ‘treatment-
resistant’ or who experience extreme side effects.
The Dopamine Hypothesis Revisited:
PET studies show that the drug
Glutamate-dopamine Interaction:
amphetamine enhances schizophrenic-
Hypoglutamatergia in the cerebral cortex
like symptoms in people with
may lead to negative symptoms of
schizophrenia more than controls.
schizophrenia.
The explanation is insufficient as it does
But in the subcortical basal ganglia could
not apply to all people with
be responsible for positive symptoms.
schizophrenia.
Proposal that dopamine and glutamate
Beyond Dopamine:
pathways interact and affect the
Unlikely that dopamine is the only
striatum.
neurotransmitter in the brain associated
The Thalamic Filter:
with schizophrenia.
Area of the brain involved in the
Glutamate induces schizophrenic-like
suggested ‘psychotogenic pathway’ -
symptoms and is a powerful antagonist of
brain system which governs a psychotic
NDMA receptors - a type of glutamate
response.
receptor.
Thalamus may be turned on or off
Decrease glutamate increases dopamine.
depending on which way the pathway is
Glutamatergic Control of Dopamine
activated.
Release:
Comparing 2 models:
Affects the release of GABA producing
Hyperdopaminergic model - traditional
the opposite effect.
view of the role of dopamine when
Acts like a ‘brake’ and reduces dopamine
increased produces psychotic symptoms.
activity.
Hypoglutamatergic model - glutamate
Low glutamate may increase/decrease
can produce an increase/decrease in
dopamine.
dopamine activity depending on the
Normally there is a balance between the
accelerator or brake.
‘accelerator’ and the ‘brake’ and a
M100907 - drug use.
disruption can lead to symptoms
associated with schizophrenia.
