Dopamine hypothesis
The explanation that in schizophrenia the signal carried by the brain chemical dopamine is too strong. It was built backwards from how effective drugs act, not from the illness itself.
In 1963 Arvid Carlsson and Margit Lindqvist found that in the brains of mice given chlorpromazine and similar drugs, substances related to dopamine were made faster than usual, and proposed that the drugs block the receptors that receive the signal[1][2]. In 1976 it was shown that the smaller the effective dose of an antischizophrenic drug, the more strongly it binds to dopamine receptors[3].
But a drug that weakens the signal and eases symptoms does not prove that too strong a signal is the root of the illness. Carlsson himself wrote in 1988 that the hypothesis still rested almost entirely on evidence about drugs, and that disturbed dopamine function in schizophrenia had not yet been demonstrated beyond doubt[4].
Related terms
- ChlorpromazineA drug that eases the hallucinations and delusions of schizophrenia. Synthesised in France in 1951 and tried as an aid to anaesthesia, it entered psychiatry in 1952.
- SchizophreniaAn illness in which the connections between mental functions such as thought and feeling break down. The word was coined in 1908 by the Swiss psychiatrist Eugen Bleuler.
Sources
- T. A. Ban, “Fifty years chlorpromazine: a historical perspective,” Neuropsychiatric Disease and Treatment 3(4), 495–500 (2007).
- A. Carlsson, M. Lindqvist, “Effect of Chlorpromazine or Haloperidol on Formation of 3-Methoxytyramine and Normetanephrine in Mouse Brain,” Acta Pharmacologica et Toxicologica 20, 140–144 (1963).
- I. Creese, D. R. Burt, S. H. Snyder, “Dopamine Receptor Binding Predicts Clinical and Pharmacological Potencies of Antischizophrenic Drugs,” Science 192(4238), 481–483 (1976).
- A. Carlsson, “The current status of the dopamine hypothesis of schizophrenia,” Neuropsychopharmacology 1(3), 179–186 (1988).