3
However, the dopamine hypothesis has contradicting evidence. Dopamine is a
brain chemical that increases the sensitivity of brain cells. This promotes the
individual’s awareness of the world around them as dopamine is involved in attention
and alertness. Alpert (1980) reported that some patients with schizophrenia don’t
improve after taking dopamine antagonists which prevent dopamine being absorbed in
large quantities. This implies that the dopamine hypothesis may not be an accurate
explanation for the symptoms of schizophrenia as it would predict that lower dopamine
levels may result in an improvement in symptoms. This is a weakness because the
dopamine hypothesis could not be successfully applied to real world treatment of
schizophrenia, thus decreasing the credibility of this theory. On the other hand, this
might be because antipsychotic drugs cause up-regulation, where the number of
dopamine receptors increases in response to the blocked receptors. This increases
dopamine levels, which means that the symptoms may not be managed as the
dopamine levels are not corrected properly. This suggests there may not be any issues
with applying the dopamine hypothesis to real world treatment of schizophrenia, rather,
problems lie in the mode of action of antipsychotics which decrease dopamine levels
too much and lead to up-regulation of dopamine receptors.
In conclusion, the dopamine hypothesis proposes that hypersensitivity of D2 dopamine
receptors leads to patients overreacting to the presence of the neurotransmitters, which
leads to hallucinations as the brain is too active.
There is supporting evidence from brain imaging techniques that show brains of
patients with schizophrenia have a higher number of dopamine receptors than normal,
regardless, some patients don’t respond to dopamine inhibiting drugs, contrary to what
the hypothesis would predict.
Therefore, it may be necessary to consider other neurotransmitters that may influence
dopamine levels such as glutamate, and other neurotransmitters which may influence
whether patients may recover from symptoms of schizophrenia, such as serotonin.
Evaluate 1 bio explanation of SZ other than function of NTs (12)
One strength of the genetic explanation for schizophrenia is that it has
supporting evidence. People with a greater degree of genetic relatedness to someone
with schizophrenia have a higher risk of developing schizophrenia themselves.
However, the dopamine hypothesis has contradicting evidence. Dopamine is a
brain chemical that increases the sensitivity of brain cells. This promotes the
individual’s awareness of the world around them as dopamine is involved in attention
and alertness. Alpert (1980) reported that some patients with schizophrenia don’t
improve after taking dopamine antagonists which prevent dopamine being absorbed in
large quantities. This implies that the dopamine hypothesis may not be an accurate
explanation for the symptoms of schizophrenia as it would predict that lower dopamine
levels may result in an improvement in symptoms. This is a weakness because the
dopamine hypothesis could not be successfully applied to real world treatment of
schizophrenia, thus decreasing the credibility of this theory. On the other hand, this
might be because antipsychotic drugs cause up-regulation, where the number of
dopamine receptors increases in response to the blocked receptors. This increases
dopamine levels, which means that the symptoms may not be managed as the
dopamine levels are not corrected properly. This suggests there may not be any issues
with applying the dopamine hypothesis to real world treatment of schizophrenia, rather,
problems lie in the mode of action of antipsychotics which decrease dopamine levels
too much and lead to up-regulation of dopamine receptors.
In conclusion, the dopamine hypothesis proposes that hypersensitivity of D2 dopamine
receptors leads to patients overreacting to the presence of the neurotransmitters, which
leads to hallucinations as the brain is too active.
There is supporting evidence from brain imaging techniques that show brains of
patients with schizophrenia have a higher number of dopamine receptors than normal,
regardless, some patients don’t respond to dopamine inhibiting drugs, contrary to what
the hypothesis would predict.
Therefore, it may be necessary to consider other neurotransmitters that may influence
dopamine levels such as glutamate, and other neurotransmitters which may influence
whether patients may recover from symptoms of schizophrenia, such as serotonin.
Evaluate 1 bio explanation of SZ other than function of NTs (12)
One strength of the genetic explanation for schizophrenia is that it has
supporting evidence. People with a greater degree of genetic relatedness to someone
with schizophrenia have a higher risk of developing schizophrenia themselves.
