<unk>  may occur due to upregulation of<unk>  2 receptors (D2). The D2 receptor is the primary target of almost all antipsychotics, which oppose the action of the neurotransmitter<unk>  at this receptor. The antagonizing or "blockade" of D2 by antipsychotics may cause neurons, a type of cell within the brain, to undergo compensatory changes to make up for the loss of activity at D2 receptors. The D2 signaling pathway within neurons is complex, and involves multiple enzymes and other secondary messengers. It may be the case that, in response to antipsychotics, neurons increase the production of D2 receptors (upregulation), thereby sensitizing the neuron to<unk> . However, this is likely an oversimplification, as—despite differences in sensitivity to<unk>  of around 3-fold in people that have taken antipsychotics chronically, there is a disproportionately low increase in the amount of D2 receptors in the brain in these people (around 1.4-fold in the striatum of the brain in people with schizophrenia). Other hypotheses include increases in the "active" D2 receptors (termed D2High) relative to the "inactive" conformation (D2Low). The end result is<unk><unk> . It is thought that the psychotic symptoms within schizophrenia are primarily due to overactive<unk>  activity in the mesolimbic area of the brain. Therefore,<unk><unk>  may reduce the effect of antipsychotics and increase the brain's response to endogenous<unk> , leading to worsening psychosis. Tardive dyskinesia, a type of rare movement disorder that can be caused by antipsychotics, may also be caused by<unk>  receptor sensitization. This may explain why, for people with tardive dyskinesia, increasing the dose of the antipsychotic may temporarily improve symptoms.
Dopamine supersensitivity psychosis
Substance-induced psychosis
Unitary psychosis
Pseudoneurotic schizophrenia
Stimulant psychosis
Myxedema psychosis
Tardive psychosis
Disorganized schizophrenia