Assess the neurotransmitter/biological explanation for Schizophrenia. (20 Marks)
Studies show that the neurotransmitter dopamine which is an antagonist responsible for feelings of
pleasure and motivation has a direct effect on schizophrenia. The dopamine hypothesis explains. In the
1950’s the drug L-dopa which was administered to patients with Parkinson’s disease which typically is
caused by little dopamine. The drug help to increase the levels of dopamine (hyperdopaminergia) which
causes the patients to experience psychosis-like symptoms. In addition, they have concluded two causes
of schizophrenia. One would be is the low levels of beta hydroxylase, the enzyme responsible for the
break-up of dopamine which may have caused a build-up in the synapse. Second, would be the
hyperdopaminergic activity or an increase of D2 receptors in the synaptic cell. Furthermore, Davis et al
(1991) argue that positive symptoms of schizophrenia like delusions may results from this, while negative
symptoms such as social withdrawal can be due to hypodopaminergia or a lack of dopaminergic activity in
the mesocortical pathway.
One strength of the dopamine hypothesis is it has supporting research with rats treated with
amphetamines. For example, Tenn et al (2003) found that rats who were administered with the drug has
shown schizophrenia symptoms over three weeks, such as social withdrawal and since rats are known as
social animals. To reverse these effects, they have administered dopamine antagonists to block D1
receptors. This is important as it proves that increased dopamine levels may cause schizophrenia.
However, Depatie and Lal (2001) an increase intake of apomorphine, a dopamine agonist that stimulates
D2 receptors does not lead to symptoms of schizophrenia. This is important as it shows that
hyperdopaminergia may not be an effect of schizophrenia.
Furthermore, by the 2000s researchers also focused on other neurotransmitters such as GABA,
glutamate, and serotonin. The dopamine hypothesis was put into question when the drug clozapine was
introduced which had binded to the D1 and D4 receptors and as well as the serotonin receptors which
reduced both positive and negative symptoms of schizophrenia. It led to some conclusions that serotonin
can be linked to the negative symptoms of schizophrenia such as social withdrawal.
On the other hand, another strength is there is a support for the role of D2 receptors. For example,
Snyder (1985) found that chlorpromazine acts as an antagonist on dopamine receptors such as the D1
and D2 as well as antipsychotic effect. Furthermore, the antagonist drug haloperidol which has narrower
range of biochemical effects is more effective in reducing sz symptoms. This is important as it highlights
that sz can be linked due to the antagonistic effect of chlorpromazine on the receptors, which leads to one
of the symptoms of sz which is psychosis.
Furthermore, Howes and Kapur (2009) explains the dopamine dysregulation in the striatum a part of the
brain that is active for reward and movements as the common pathway for psychosis.
Therefore, a weakness of this explanation is it cannot explain non-biological factors such as why
second-generation immigrants are most likely to be diagnosed with sz. For example, Veiling et al, (2008)
study on Moroccan and Turkish immigrants. They have found that there is a difference between two
groups and that Moroccan immigrants are more likely to be sz, and this could be because of the
discrimination faced by the group. This is important as it shows that neurotransmitters such as dopamine
may not be the only explanation of sz but also environmental factors can make people more prone to
psychosis.
In conclusion, the biological explanation has its strengths for having evidence for the dopamine
hypothesis. However, it still has its weaknesses for not being able to explain non-biological factors and
that evidence shows that D2 receptors do not lead to sz symptoms.
Studies show that the neurotransmitter dopamine which is an antagonist responsible for feelings of
pleasure and motivation has a direct effect on schizophrenia. The dopamine hypothesis explains. In the
1950’s the drug L-dopa which was administered to patients with Parkinson’s disease which typically is
caused by little dopamine. The drug help to increase the levels of dopamine (hyperdopaminergia) which
causes the patients to experience psychosis-like symptoms. In addition, they have concluded two causes
of schizophrenia. One would be is the low levels of beta hydroxylase, the enzyme responsible for the
break-up of dopamine which may have caused a build-up in the synapse. Second, would be the
hyperdopaminergic activity or an increase of D2 receptors in the synaptic cell. Furthermore, Davis et al
(1991) argue that positive symptoms of schizophrenia like delusions may results from this, while negative
symptoms such as social withdrawal can be due to hypodopaminergia or a lack of dopaminergic activity in
the mesocortical pathway.
One strength of the dopamine hypothesis is it has supporting research with rats treated with
amphetamines. For example, Tenn et al (2003) found that rats who were administered with the drug has
shown schizophrenia symptoms over three weeks, such as social withdrawal and since rats are known as
social animals. To reverse these effects, they have administered dopamine antagonists to block D1
receptors. This is important as it proves that increased dopamine levels may cause schizophrenia.
However, Depatie and Lal (2001) an increase intake of apomorphine, a dopamine agonist that stimulates
D2 receptors does not lead to symptoms of schizophrenia. This is important as it shows that
hyperdopaminergia may not be an effect of schizophrenia.
Furthermore, by the 2000s researchers also focused on other neurotransmitters such as GABA,
glutamate, and serotonin. The dopamine hypothesis was put into question when the drug clozapine was
introduced which had binded to the D1 and D4 receptors and as well as the serotonin receptors which
reduced both positive and negative symptoms of schizophrenia. It led to some conclusions that serotonin
can be linked to the negative symptoms of schizophrenia such as social withdrawal.
On the other hand, another strength is there is a support for the role of D2 receptors. For example,
Snyder (1985) found that chlorpromazine acts as an antagonist on dopamine receptors such as the D1
and D2 as well as antipsychotic effect. Furthermore, the antagonist drug haloperidol which has narrower
range of biochemical effects is more effective in reducing sz symptoms. This is important as it highlights
that sz can be linked due to the antagonistic effect of chlorpromazine on the receptors, which leads to one
of the symptoms of sz which is psychosis.
Furthermore, Howes and Kapur (2009) explains the dopamine dysregulation in the striatum a part of the
brain that is active for reward and movements as the common pathway for psychosis.
Therefore, a weakness of this explanation is it cannot explain non-biological factors such as why
second-generation immigrants are most likely to be diagnosed with sz. For example, Veiling et al, (2008)
study on Moroccan and Turkish immigrants. They have found that there is a difference between two
groups and that Moroccan immigrants are more likely to be sz, and this could be because of the
discrimination faced by the group. This is important as it shows that neurotransmitters such as dopamine
may not be the only explanation of sz but also environmental factors can make people more prone to
psychosis.
In conclusion, the biological explanation has its strengths for having evidence for the dopamine
hypothesis. However, it still has its weaknesses for not being able to explain non-biological factors and
that evidence shows that D2 receptors do not lead to sz symptoms.
