The Dopamine Hypothesis

• Dopamine is a neurotransmitter and one of the chemicals in the brain that causes neurons to fire. The original dopamine hypothesis stated that schizophrenia suffered from an excessive amount of dopamine. This causes the neurons that use dopamine to fire too often and transmit too many messages.  High dopamine activity leads to acute episodes, and positive symptoms such as delusions, hallucinations, confused thinking.
• This idea is supported by evidence from psychoactive drugs (cocaine and amphetamines) which produce behaviour similar to schizophrenic behaviour, and they stimulate the receptors for dopamine. Additionally Parkinson’s disease sufferers have low levels of dopamine and take a drug – L-dopa to increase these levels. As a side effect of these drugs, some patients suffer schizophrenic type symptoms (e.g. hallucinations) because of the increase in dopamine.
• However this initial explanation was seen to be too simple as antipsychotic medication that blocks the dopamine receptor sites with the effect of reducing dopamine at the synapse only reduces the positive symptoms of SZ and not the negative ones. Additionally newer research discovered that there were 5 different dopamine receptor sites (D1 to D5), and it was the D2 receptor sites that seemed to be the main subtype linked to schizophrenia – and this has a role in perception.
• D2 receptors are mainly found in the limbic system and therefore the dopamine hypothesis was revised to focus mainly on the D2 receptors in the limbic system – particularly the mesolimbic pathway. This limbic pathway carries signals from the ventral tegmental area to the nucleus accumbens. Too much dopamine here will over stimulate the neurons or cause them to fire too quickly causing the positive symptoms of schizophrenia.
• The revised hypothesis explains negative symptoms as a result of too little dopamine in the D1 receptors in the mesocortical pathway. This pathway carries signals from the ventral tegmental area to the frontal lobe is involved in motivation and cognition. Too little dopamine in this pathway will mean the neurons will fire less, which would explain the cognitive impairments that accompany SZ and the negative symptoms such as avolition and affective flattening.