dopamine hypothesis

the dopamine hypothesis

suggests that an excess of the neurotransmitter dopamine in certain regions of the brain is associated with the positive symptoms of schizophrenia

how the dopamine hypothesis works

messages from neurons that transmit dopamine fire too easily or too often, leading to hallucinations and delusions that are the characteristic positive symptoms of schizophrenia

schizophrenics are thought to have abnormally high numbers of D2 receptors on receiving neurons, resulting in more dopamine binding and therefore more neurons firing. they key role played by dopamine was highlighted in 2 sources of evidence

drugs that increase dopaminergic activity

amphetamine is a dopamine antagonist i.e. it stimulates nerve cells containing dopamine, causing the synapse to be flooded with this neurotransmitter

‘normal’ individuals who are exposed to large doses of dopamine-releasing drugs like amphetamines can develop characteristic hallucinations and delusions of a schizophrenic episode

this generally disappears with abstinence from the drug

Grilly

some people who differ Parkinson’s disease, a neurodegenerative disease categorised by low levels of dopamine, who take the drug L-Dopa to raise their dopamine levels have been found to develop schizophrenia type symptoms

drugs that decrease dopaminergic

all antipsychotic drugs block the activity of dopamine in the brain. by reducing the activity in neural pathways of the brain that use dopamine as the neurotransmitter, these drugs eliminate symptoms such as hallucinations and delusions. the fact that these drugs alleviated many of the symptoms of schizophrenia strengthened the case for the important role of dopamine in this disorder

Davis and Kahn

proposed that the positive symptoms of schizophrenia are caused by an excess of dopamine in subcortical areas of the brain, particularly in the mesolimbic pathway

revised dopamine hypothesis

the negative and cognitive symptoms of schizophrenia are thought to arise from a deficit of dopamine in areas of the prefrontal cortex (the mesocortical pathway). evidence for this revised hypothesis comes from various sources

neural imaging - Patel et al.

used PET scans o assess dopamine levels in schizophrenic and normal individuals and found lower levels of dopamine in the dorsolateral prefrontal cortex of schizophrenic patients compared to their normal controls

animal studies - Wang and Deutch

induced dopamine depletion in the prefrontal cortex in rats

this resulted in cognitive impairment e.g. memory deficits that the researchers were able to reverse using olanzapine, an atypical antipsychotic drug thought to have beneficial effects on negative symptoms in humans

strengths of the dopamine hypothesis

antipsychotic drugs affect dopamine levels and successfully treat the symptoms of schizophrenia

limitations of the dopamine hypothesis

Moncrieff claims that evidence for the dopamine hypothesis of schizophrenia is far from conclusive

Noll claims there is strong evidence against both the original dopamine hypothesis and the revised dopamine hypothesis. he argues that antipsychotic drugs don’t alleviate hallucinations and delusions in about 1/3 of people experiencing these problems