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Biochemical explanation
Caused by elevated levels of dopamine at key synaptic sites in subcortical regions of the brain
Excess DA leads to too many impulses being transmitted triggering positive symptoms of schizophrenia
Can be caused by numerous factors, including presynaptic neurons releasing too much DA
Post synaptic there may not be enough dopamine being broken down, leaving too much dopamine in surrounding cells
Reuptake processes may be impaired leaving too much dopamine in the synapse
Revised dopamine hypothesis
Davis et al (1991) pointed out that in the prefrontal cortex there are no D2 receptors so there may be a deficiency of dopamine in the region
Hyperdopaminergia
When there are overactive D2 receptors firing along the mesolimbic pathway from the ventral tegmental area to the nucleus accumbens, this leads to increased positive symptoms
hypodopaminergia
Caused by underactive D2 receptors in the mesocortical pathway from the ventral tegmental area to the prefrontal cortex, leading to negative symptoms
Evaluation points
Research support: Randrup and Munkvad
Alternative explanations
Biologically reductionist
Practical applications through drug treatments
Cause and effect
Can be compared to the diathesis stress model