The Dopamine Hypothesis of Schizophrenia – Advances in Neurobiology and Clinical Application

Posted on January 27, 2018
Time to read: 6 minutes

The dopamine hypothesis stems from early research carried out in the 1960’s and 1970’s when studies involved the use of amphetamine (increases dopamine levels) which increased psychotic symptoms while reserpine which depletes dopamine levels reduced psychotic symptoms.

The original dopamine hypothesis was put forward by Van Rossum in 1967 that stated that there was hyperactivity of dopamine transmission, which resulted in symptoms of schizophrenia and drugs that blocked dopamine reduced psychotic symptoms. [1]

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  • Romesh Senewiratne-Alagaratnam

    The blockade of dopamine receptors by ‘antipsychotic’ drugs is an important cause of the ‘negative symptoms’ of ‘schizophrenia’. These drugs are known to cause anhedonia and emotional flatness. The label of an ‘incurable brain disease’ and the consequences of stigmatisation also contribute to loss of motivation, depression and suicide.

    • Psychscenehub

      Thanks for your comment. Primary negative symptoms are a symptom of schizophrenia while secondary negative symptoms are likely due to D2 blockade by antipsychotics as you have stated. Good points about stigma as well.

  • Gellie

    Dopamine blockers only block dopamine, the neurotransmitter of the reward system. Dopamine blockers don’t reduce percentage of brain use; rather, they increase percentage of brain use, as shown in the recent ad about Parkensen’s disease, which itself is the failure of the dopamine producers to produce enough, if any, dopamine. The torment causes by dopamine blockers may be distracting, but this torment increases percentage brain use by causing what is called “nervous breakdown”. There is an evolved survival mechanism to increase percentage of brain use in crisis situations. When this gets out of hand it is called a “nervous breakdown”.