Antipsychotic drugs are central to the treatment of schizophrenia and psychosis. The search for a selective mechanism shared by all antipsychotics has focused mainly on the antipsychotic effects mediated by dopamine D₂ receptor blockade. However, the risk of Parkinsonism is high when antipsychotics occupy dopamine D₂ receptors above 80%. Antipsychotics which are atypical have a low tendency to induce these extrapyramidal side effects in humans and require high doses to elicit catalepsy in animals. Blockade of serotonin receptors has been suggested as a basis for atypical antipsychotic drug action. The current evidence on dopamine/serotonin interactions, however, is inconclusive. Thus, speculation of other such receptor sites contributing to the absence or low Parkinsonism observed with atypical antipsychotics has here been the impetus for a novel receptor search. Using a strategy based on the strong homology between dopamine and serotonin receptors, a serotonin-7B receptor pseudogene was previously isolated. In an effort to identify the functional serotonin-7B receptor gene through homologous hybridization screening techniques, a serotonin-7B receptor pseudogene polymorphism was detected from human fetal brain cDNA. In comparison to the pseudogene, its polymorphism contains four nucleotide substitutions and one deletion creating four amino acid changes. The intronless coding sequence of 1325 base pairs produces a truncated protein of 84 amino acids, the function of which is not known. The continuing search for the functional serotonin-7B receptor gene may elucidate these and other issues pertaining to antipsychotic drug action.