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DOPAMINE HYPOTHESIS BIOLOGICAL EXPLANATION OF SZ - Coggle Diagram
DOPAMINE HYPOTHESIS BIOLOGICAL EXPLANATION OF SZ
INITIAL HYPOTHESIS
Griffith et al (1968) induced psychosis in non-schizophrenic volunteers with a drug that increased dopamine and they demonstrated paranoid delusions and cold detached emotional response
The initial hypothesis was too simple as drugs that reduced the levels of dopamine has little or no effect on those who mainly suffered from negative symptoms
It was found that there were several subtypes of dopamine receptor sites, D1-D5, which are found in the cerebral cortex and the limbic system
Individuals with schizophrenia had too much of the neurotransmitter dopamine
REVISED DOPAMINE HYPOTHESIS
The limbic system has a variety of subcortical structures that are engaged in many functions- emotions, memory formation and arousal
Nerve pathways leave from the limbic system to other subcortical structures and also to the cerebral cortex
The role of dopamine in the limbic system is the main focus
Mesolimbic pathway and mesocortical pathway are associated with schizophrenia
MESOLIMBIC PATHWAY
The pathway carries signals from the ventral tegmental area to the nucleus accumbens
Too much dopamine causes overstimulation- positive symptoms
Dopamine is a major neurotransmitter here
Anti-psychotic drugs reduce dopaminergic transmission and reduces dopamine activity
MESOCORTICAL PATHWAY
Pathway carries signals from the ventral tegmental area to the frontal lobe
Nerve pathway- emotional responses, motivation and cognition
Dopamine is a major neurotransmitter
Too little dopamine is evident in D1 receptors of the frontal lobe of individuals with negative symptoms of schizophrenia