CARLSSON ET AL
CONTEMPORARY STUDY: 2000
This study was carried out by Arvid Carlsson, as a review of the Dopamine Hypothesis of
schizophrenia. It analyses a different possible route of schizophrenia, caused by glutamate,
as opposed to dopamine. This is a very significant study, because Carlsson pioneered the
dopamine hypothesis in the 60’s, and therefore his change of opinion would not have come
easily. The study also focusses on biological explanations for schizophrenia, and shows how
PET scans can be used to investigate neurological networks.
Glutamate:
Glutamate is an unusual chemical, it has lots of functions and it took a long time for
scientists to realise that it also worked as a neurotransmitter. Glutamate is present in high
quantities throughout the brain, in very high quantities it is toxic, but in the majority of
cases, it is stored INSIDE brain cells. Glutamate will only work as a neurotransmitter when it
is OUTSIDE the brain cells. Glutamate transporters are chemicals that “uptake” loose
molecules of glutamate, and locks them up inside cells.
The glutamate neurotransmitter controls memory and learning, by binding to glutamate
receptors – these receptors are found everywhere in the brain, which is why it is so
important for glutamate levels to be kept low through a healthy glutamate uptake.
THE STUDY
Aim: to present the current view of the relationship between schizophrenia and
dopaminergic dysfunction, as well as to explore a rival theory, that of glutamatergic
deficiency/hypoglutamatergia (not enough glutamate neurotransmitter).
IV: This is NOT an experiment, therefore there is no IV.
DV: As this is not empirical research, there is NO DV, however Carlsson et al do describe the
findings of a number of earlier studies.
Sample: Carlsson was not carrying out empirical research, therefore Carlsson et al do not
have a sample of their own, however they do refer to a large number of studies conducted
previously, each with their own samples of patients with schizophrenia.
Procedure: As this is not actually a study, there is no set procedure, however Carlsson et al
refer to a number of studies that have used positron emission tomography (PET).
PET is a brain imaging technique where a participant is injected with a radioactive tracer
that dissolves in the blood stream. The tracer is carried by the blood to the brain, where it
concentrates around particularly active brain structures. A PET scan detects the radioactivity
and converts it into a digital image of the brain – active areas are highlighted in red and
yellow.
Results:
1. Schizophrenic patients do have more dopamine activity than a healthy control group,
especially in the basal ganglia part of the brain, however Laruelle et al (1999) found
that patients in remission had normal dopamine activity. This is not surprising if they
are taking antipsychotics which reduce their dopamine, causing normal dopamine
activity for the person. These drugs however are causing hypodopaminergia, as the
people are used to more dopamine.
2. Neurotransmitters interact with one another, so it doesn’t make sense that ONLY
dopamine is linked to schizophrenia. Carlsson decided to focus on glutamate,
because:
a. Drugs like PCP and ketamine produce psychotic symptoms, but instead of
activating dopamine, they stimulate glutamate receptors called NMDA
CONTEMPORARY STUDY: 2000
This study was carried out by Arvid Carlsson, as a review of the Dopamine Hypothesis of
schizophrenia. It analyses a different possible route of schizophrenia, caused by glutamate,
as opposed to dopamine. This is a very significant study, because Carlsson pioneered the
dopamine hypothesis in the 60’s, and therefore his change of opinion would not have come
easily. The study also focusses on biological explanations for schizophrenia, and shows how
PET scans can be used to investigate neurological networks.
Glutamate:
Glutamate is an unusual chemical, it has lots of functions and it took a long time for
scientists to realise that it also worked as a neurotransmitter. Glutamate is present in high
quantities throughout the brain, in very high quantities it is toxic, but in the majority of
cases, it is stored INSIDE brain cells. Glutamate will only work as a neurotransmitter when it
is OUTSIDE the brain cells. Glutamate transporters are chemicals that “uptake” loose
molecules of glutamate, and locks them up inside cells.
The glutamate neurotransmitter controls memory and learning, by binding to glutamate
receptors – these receptors are found everywhere in the brain, which is why it is so
important for glutamate levels to be kept low through a healthy glutamate uptake.
THE STUDY
Aim: to present the current view of the relationship between schizophrenia and
dopaminergic dysfunction, as well as to explore a rival theory, that of glutamatergic
deficiency/hypoglutamatergia (not enough glutamate neurotransmitter).
IV: This is NOT an experiment, therefore there is no IV.
DV: As this is not empirical research, there is NO DV, however Carlsson et al do describe the
findings of a number of earlier studies.
Sample: Carlsson was not carrying out empirical research, therefore Carlsson et al do not
have a sample of their own, however they do refer to a large number of studies conducted
previously, each with their own samples of patients with schizophrenia.
Procedure: As this is not actually a study, there is no set procedure, however Carlsson et al
refer to a number of studies that have used positron emission tomography (PET).
PET is a brain imaging technique where a participant is injected with a radioactive tracer
that dissolves in the blood stream. The tracer is carried by the blood to the brain, where it
concentrates around particularly active brain structures. A PET scan detects the radioactivity
and converts it into a digital image of the brain – active areas are highlighted in red and
yellow.
Results:
1. Schizophrenic patients do have more dopamine activity than a healthy control group,
especially in the basal ganglia part of the brain, however Laruelle et al (1999) found
that patients in remission had normal dopamine activity. This is not surprising if they
are taking antipsychotics which reduce their dopamine, causing normal dopamine
activity for the person. These drugs however are causing hypodopaminergia, as the
people are used to more dopamine.
2. Neurotransmitters interact with one another, so it doesn’t make sense that ONLY
dopamine is linked to schizophrenia. Carlsson decided to focus on glutamate,
because:
a. Drugs like PCP and ketamine produce psychotic symptoms, but instead of
activating dopamine, they stimulate glutamate receptors called NMDA
