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Summary Schizophrenia Explanations: Dopamine Hypothesis
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Detailed revision notes for WJEC Psychology Unit 3. Dopamine hypothesis explanation of schizophrenia including research references and evaluation points.
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By: laurennbreakwell • 2 year ago
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Biological ExplanationsDopamine Hypothesis
What is dopamine?
- The nervous system consists of 2 main parts, the central nervous system and the peripheral
nervous system.
- Messages are carried around the nervous system by neurotransmitters.
- Dopamine is a neurotransmitter which is associated with pleasure, motivation and movement.
- Dopamine begins by being synthesized by the presynaptic neuron, which then releases it into the
synaptic gap. Dopamine molecules can then bind to receptors on the other neuron which transmit
the signal. Once it has relayed the message, it is rapidly reabsorbed and degrades.
- Dopamine is made up by combining the amino acid tyrosine with the enzyme tyrosine
hydroxylase.
- Dopamine is found in the neurons of both the central and peripheral nervous system and there are
5 dopamine receptor subtypes. Dopamine interacts with specific membrane receptors to produce
its effects and these effects are terminated by re-uptake.
- Research has shown that humans have about 3 times as much dopamine as other primates and
Emily Deans wrote in 2011 that ‘dopamine is what made humans so successful’
Roles of Dopamine
- Dopamine plays a critical role in the way our brain controls our movements, so a shortage of
dopamine or the death of dopamine neurons is a cause of Parkinson’s disease.
- Dopamine is commonly associated with providing feelings of enjoyment and reinforcement to
motivate us to do certain activities.
- Dopamine has been strongly associated with psychosis and schizophrenia, particularly those in the
mesolimbic pathway.
- The mesolimbic pathway is connected to the limbic system, which controls reward and emotion.
The Dopamine Hypothesis
- The original hypothesis states that the brain of schizophrenic patients produces more dopamine
than the brain of an ordinary person.
- This followed observations of patients who overdosed on stimulants like cocaine and
amphetamine, exhibiting symptoms similar to those in a schizophrenic psychosis.
- Additionally, in the early 1950’s anti-psychotic effects of chlorpromazine and reserpine were
documented and there is reference to a side effect of Parkinson’s disease. Later on, the brains of
recently deceased Parkinson’s patients were found with depleted dopamine.
- Further, people suffering from Parkinson’s disease can take L-Dopa to increase their dopamine
levels and manage symptoms, but can develop schizophrenic symptoms if they take too much.
- Thus, a link was drawn between the anti-psychotic drugs and dopamine, as there was a suggestion
that they reduced dopamine levels which led to a reduction in schizophrenic symptoms.
- JJ Griffith et al (1968): induced psychosis in non-schizophrenic volunteers by administering
dextro-amphetamine, a stimulant which increases dopamine levels. The volunteers exhibited a
sudden onset of paranoid delusions as well as flat affect.
- Nonetheless, the study was deemed too simplistic as drugs which reduce dopamine levels have
little to no effect on those suffering from negative symptoms of schizophrenia.
- It is now thought that schizophrenics have an abnormally high number of D2 receptors and that
anti-psychotic drugs block these.
Dopamine Receptor Sites
- The discovery of the D1-D5 receptor sites complicated the explanation of dopamine and
schizophrenia.
- There is not just an excess of dopamine in the brains of schizophrenics, but more receptors,
which lead to an over production of messages and overstimulation of neurons.
- Toda and Abi-Dargham (2007): Hyperactivity of dopamine D2 receptor neurotransmission in
subcortical and limbic brain regions contributes to the positive symptoms of schizophrenia,
whereas hypo-functionality of the D1 receptor neurotransmission in the pfc is linked with the
cognitive and negative symptoms.
- Studies have shown an increased density of the dopamine D2 receptor in post-mortem brain tissue
of schizophrenia sufferers.
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