The Dopamine Hypothesis

The proximate organic cause of schizophrenia is an abnormally high level of activity in certain brain circuits sensitive to the neurotransmitter dopamine. The increased activity may result from any of several mechanisms including an overabundance of dopamine itself, an overabundance or oversensitivity of dopamine receptors, or the abnormal facilitation of dopamine transmission by other transmitters.

Evidence:

The effects of a number of medications known as classical/first generation antipsychotics (neuroleptics) e.g Thorazine or Haldol. These block receptors for dopamine. Some are more effective in producing this blockade and, as predicted, the stronger the blockade, the more therapeutic the drug is.

A study took schizophrenics who were in a relatively mild state and injected them with a small dose of a drug that temporarily increases dopamine activity. Within minutes they began tearing paper, annoucing they were receiving signals from Egyptians or becoming catatonic. These effects were short lived and so supports the hypothesis without any long term damage to the patients.

Related effects are seen in non-schizophrenics who take overdoses of amphetamines. These are stimulants whose effects include the enhancement of dopamine activity. When taken often enough, and in large doses, they produce a temporary amphetamine psychosis, that is similar to paranoid schizophrenia. As predicted, medications that block dopamine activity at the synapse also reduce the psychotic symptoms that follow chronic amphetamine abuse.

One possibility as to why dopamine does this is that it essentially leads to chronic overstimulation of the brain. For instance, when dopamine neurons are destroyed in animals, they ignore all sensory stimuli and so perhaps the opposite- a diminished ability to ignore- is produced when dopamine tracts are hyperactive. This may cause an inability to shut out the external sensory…