In fact, through the use of certain drugs such as neuroleptics, drugs that helps to reduce nervous tension by depressing nerve functions, and the DA precursor L-Dopa, clinicians have developed a better understanding of the biology of psychosis (Brisch, 2014). Neuroleptics are DA receptor antagonists and, when prescribed, can cause parkinsonian symptoms (Brisch, 2014). These are known as extra pyramidal system (EPS) side effects. These side effects are caused by increased dopamine in the nigrostriatal pathway. The DA precursor L-Dopa is a DA receptor agonist and, when prescribed, can actually cause symptoms of psychosis (Meyer, 2019). This is also true for stimulants such as cocaine and amphetamine, which increase dopamine levels and have to potential to induce psychosis. Neuroleptics (typical antipsychotics) medications are high affinity D2 receptor antagonists (Meyer, 2019). These findings further conclude the DA receptor hypothesis for psychosis.
Due to the promising findings of the DA hypothesis, researchers have sought to find the direct cause of psychosis by looking at DA subtypes. DA receptors are G-protein-coupled receptors and can be divided into D1, D2, D3, and D4 receptors respectively (Brisch, 2014). Brain imaging studies show that individuals who suffer from narcolepsy, a sleep disorder, selectively inhibit D2 receptors in the striatum, and serotonin (5-HT) 2A receptors in the PFC, which results in increased dopamine activity (Brisch, 2014). It was also found that the D2 receptor is required to be at least eighty percent occupied in order to effectively treat the positive effects of psychosis (Brisch, 2014). Based on this finding, we now know that not all positive and negative symptoms of psychosis are caused by this receptor alone. This challenged the DA hypothesis and called for a new theory of causation.
