Concepts of Dopamine hypothesis

What are the key concepts of version 1?

Excess dopamine in certain regions is associated with positive symptoms of schizophrenia, in SCZ when dopamine is released into synapse it results in more binding to post synaptic receptor sites and more neuron’s firing so if increased activity in auditory cortex could cause too many neuron’s firing in that area and experience auditory hallucinations

How did version 1 originally emerge?

Carlsson and Lindqvist (1957) identified antipsychotic drugs reduced levels of dopamine uptake when administered to animals

What other evidence adds to version 1?

Comer (2003) found that dopamine neurons play a key role in guiding attention, so disturbances in this process may well lead to problems of attention, perception and thought found in people with schizophrenia

What are the key concepts of version 2?

Dopamine receptors show different brain distribution, SCZ is not just due to excess levels of dopamine but abnormal level of dopaminergic activity too high or too low

What causes positive and negative symptoms according to version 2?

Positive symptoms are due to striatal hyperdopaminergia and negative symptoms are due to prefrontal hypodopaminergia

Who developed version 2 what did they say?

Davis 1991, found research not compatible with version 1. Suggested abnormal levels of dopaminergic activity such as too much dopamine in mesolimbic pathway could cause positive symptoms and a deficit in prefrontal cortex could cause negative symptoms

What does version 3 say?

Links risk factors such as pregnancy, stress and drug use to increase presynaptic striatal dopaminergic function rather than D2 receptor activity

What evidence supports version 3

Howes and Kapur 2009 hypothesised that multiple hits interact to result in dopamine dis regulation linked to psychosis which can alter the appraisal of stimuli