Schizophrenia: The Dopamine Hypothesis Flashcards
(19 cards)
Define ‘neurons’.
Brain cells that transmit and receive messages through communication with neurotransmitters.
Define ‘neurotransmitter’.
A chemical substance that transfers an electrical impulse by diffusion at the synapse.
How does neurotransmitter relate to mental disorders?
One theory states that mental disorders are caused through imbalance of neurotransmitters.
Briefly describe synaptic transmission, using 5 points.
The electrical impulse travels down the axon terminal and stimulates the vesicles full of neurotransmitters.
The vesicles then move down the pre-synaptic neuron to fuse with the pre-synaptic membrane.
The neurotransmitters are then released as chemical messengers and diffuse across the synaptic gap.
They attach to the corresponding receptor on the dendrite of the post-synaptic neuron and will then be absorbed.
Any neurotransmitters that are not absorbed will get reabsorbed by the pre-synaptic neuron in the process of reuptake through the transporters
What is the rationale behind a biological theory for schizophrenia?
If schizophrenia can be inherited genetically then bio-chemical abnormalities should be detectable.
What does the dopamine hypothesis basically mean/say
Chemical imbalance through excess dopamine in the brain causes schizophrenic symptoms.
What 3 ways can excess dopamine activity be explained?
- Through excess release by the axon
- Having too many dopamine receptors (D2 receptors- so more dopamine is absorbed)
- Over-sensitivity of the receptors on the post synaptic cell, so more dopamine binding, so over firing of neurons.
(Dopamine neurons are related to attention so any disturbance/overfiring etc would result in problems with attention and perception).
how can d2 receptors explain sz?
- Patients having more D2 receptors means more dopamine can bind to them which could lead to over-sensitivity that can occur through genetic inheritance
- Positive symptoms, such as paranoia, are therefore caused by over-activation of the D2 receptors
How can the mesocortical pathway explain sz
- the MESOCORTICAL pathway is essential for cognitive function.
- abnormalities/lack of dopamine in the mesocortical pathway can lead to NEGATIVE symptoms
- e.g. lack of organisation, cognitive deficits and lack of motivation.
How can the mesolimbic pathway explain sz?
- the MESOLIMBIC pathway is the reward and fear pathway that can contribute to POSITIVE symptoms.
- when there is an excess of dopamine in the mesolimbic pathway, there is intensified emotions.
How would drugs explain development of schizophrenia?
They change the neurochemicals within the brain and so may cause and imbalance.
How might amphetamines link to schizophrenia?
They give similar symptoms to those of excess dopamine through flooding the synapse with this neurotransmitter which can cause psychosis.
How might Parkinsons’s disease link to schizophrenia?
These people suffer from low levels of dopamine whereby they take drugs to increase activity that correlate to developing schizophrenic symptoms.
How might L-DOPA link to schizophrenia?
L-DOPA is a chemical that the brain uses to produce dopamine therefore taking drugs that use this chemical may cause an onset of schizophrenia.
Supporting evidence for dopamine hypothesis (L,F)
A strength of the dopamine hypothesis is that there is supporting evidence. Lindstroem et al (1999) supports. He used PET scans to compare L-DOPA uptake of people with and without schizophrenia and found that those with schizophrenia took it up quicker. This therefore suggests that people with schizophrenia have more D2 receptors
Additionally, Falkai (1988) supports. He found that there was an increased amount of dopamine activity in schizophrenia patients when conducting post-mortems. Therefore showing that higher levels of dopamine activity correlates with schizophrenic symptoms
Evaluate the supporting evidence
Lindstroem et al (1999) has high reliability. He used PET scans to trace the chemical L-DOPA which produce scientific and objective data. This can be replicated and compared easily.
A weakness is that data is correlational. This lowers validity as we can’t establish cause and effect- no research into the dopamine hypothesis has been able to establish whether schizophrenia is the consequence or cause of increased dopamine activity. Therefore it’s difficult to establish whether increased dopamine activity causes schizophrenia or is a result of it, reducing the validity/credibility of the explanation.
Are there any applications?
A strength is that there are positive applications. It states that dopamine activity could be an explanation of sz… this has led to targeted treatments of medication such as anti-psychotics that can be used to combat this.
Using the acronym ‘EACH’, evaluate 2 ‘criticisms’ points.
A weakness of the dopamine hypothesis is that it is reductionist. It narrows the cause of sz simply down to dopamine, and ignores the interaction of other bio-chemicals such as neurotransmitters such as glutamate. The dopamine hypothesis cannot explain why Faustman et al found low levels of glutamate in the cerebrospinal fluid of patients with sz- so dopamine may only be one part of the explanation for sz, and so considering dopamine by itself is reductionist and reduces the explanations credibility.
What is a better alternative explanation?
Stress diathesis model- this is a more holistic explanation that takes into account that there may be a biological predisposition but sz may only develop when there is environmental triggers that make it happen- such as low income, poor housing etc, explaining why sz is more common in poorer sections of communities- as environmental triggers are more abundant.
