Studied by 0 people
Looks like no one added any tags here yet for you.
The link between dopamine and schizophrenia
dopamine is a neurotransmitter involved in initiating movement and plays a major role in reward motivated behaviour
Widely believed to work differently in the brain of a patient with schizophrenia and may result in the symptoms observed in suffers
Faulty dopaminergic systems probably linked to genetic factors
Where does dopamine originate in the brain
Ventral tagmentum
Original hypothesis (HIGH levels of dopamine)
hyperdopaminergic activity (HIGH dopamine)
In the mesolimbic pathway, which goes through subcortex areas of the brain (e.g. Broca’s area)
May be associated with positive symptoms of schizophrenia (e.g. auditory hallucinations), as well as disorganised speech- as high dopamine levels in Broca’s area can affect speech
The revise dopamine hypothesis (LOW)
hypodopaminergic activity (LOW levels of dopamine)
In the mesocortical pathway (connects ventral tagmentum to the pre-frontal cortex)
Negative symptoms (e.g. decision making, depressive symptoms)
Because the pre-frontal cortex (which controls thought, memory, decision making, movement) cannot function properly
AO3- research
P- support for abnormal dopamine functioning in schizophrenia
E- Curren et al: when amphetamines (which activate dopamine production-agonists) are given to non-sufferers it can produce schizophrenia-like symptoms and make symptoms worse in those already suffering from schizophrenia- as amphetamines I increase dopamine activity this suggests that excess dopamine activity may lead to schizophrenia
E- Kessler et al: used PET and MRI scans to compare people with schizophrenia with non-sufferers, finding that schizophrenics have elevated dopamine receptor levels in certain brain areas (such as the mesolimbic pathway, which is linked to positive symptoms) and differences in levels of dopamine in the cortexes can be found
L- supports dopamine hypothesis- neurobiological support
AO3- issues
P- evidence for the dopamine hypothesis is still inconclusive and there are issues with establishing causation
E- the differences in biochemistry could just as easily be an effect rather than a cause of the disorder
E- Lloyd: if dopamine is a causative factor, it may be an indirect factor mediated through environmental factors, because abnormal family circumstances can lead to high levels of dopamine, which in turn trigger schizophrenic symptoms. Furthermore other neurotransmitters, such as glutamate may also play a role in the development of schizophrenia.
L- we should be cautious in drawing firm conclusions about the direct role of dopamine in the development of schizophrenia
AO3-debates/issues
P- can be criticised for being biologically reductionist. Simplifies the complex development of schizophrenia to a single biological component, neurotransmitter dopamine.
E- could be the case that many other neurotransmitters are also involved in the development of the disorder. E.g. lots of current research has focused on the role of glutamate., as well as newer anti-psychotic drugs that implicate seretonin’s involvement too
E- reductionist approach can be problematic because a variety of factors that may be involved in the development of the disorder are being overlooked by isolating one single biological cause. However taking a reductionist approach can also be very beneficial- helped to inform the development of drug treatments. E.g. anti-psychotic drugs that affect dopamine levels are the principal treatment offered to patients with schizophrenia and have been shown to be effective at reducing severity of symptoms
L- illustrates usefulness of this explanation of schizophrenia, despite its reductionist nature
