Dopamine antagonism by thioridazine in schizophrenia.
One of the leading current theories of the etiology of schizophrenia is excessive activity of some brain dopaminergic tracts. One of the major objections to the theory is that thioridazine is clinically as effective a treatment of schizophrenia as other neuroleptic drugs but appears to have much less dopamine-blocking properties than these agents in man and laboratory animals. Serum prolactin levels are increased by dopamine receptor-blocking drugs. We have found that thioridazine is as effective as chlorpromazine, trifluperazine, and prolixin enanthate in increasing serum prolactin levels in unmediated schizophrenic patients, indicating it is an effective dopamine-blocking agent.
D000284:Administration, Oral; D002746:Chlorpromazine / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use; D018492:Dopamine Antagonists; D005260:Female; D005476:Fluphenazine / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D007279:Injections, Subcutaneous; D008297:Male; D011388:Prolactin / Q000097:blood; D011955:Receptors, Drug; D012559:Schizophrenia / Q000097:blood / Q000188:drug therapy*; D013881:Thioridazine / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D014268:Trifluoperazine / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use
D018492:Dopamine Antagonists; D011955:Receptors, Drug; D014268:Trifluoperazine; D011388:Prolactin; D013881:Thioridazine; D005476:Fluphenazine; D002746:Chlorpromazine