Enhancement of dopamine metabolism in rat brain frontal cortex: a common effect of chronically administered antipsychotic drugs.
Administration of 4 antipsychotic drugs, haloperidol, chlorpromazine, thioridazine and clozapine, for 21 days elicited increased dopamine metabolism in frontal cortex of rat brain. Only clozapine failed to decrease the apparent firing rate of dopamine neurons in the striatum, as indexed by [homovanillic acid]/[dopamine]. These data support the hypotheses that frontal cortex dopamine neurons may be a common site for antipsychotic action while decreased release of dopamine in the striatum may be associated with the development of extrapyramidal side effects.
Mefford
I N
IN
Department of Psychiatry and Behavioral Sciences, Stanford University Medical Center, CA 94305.
Roth
K A
KA
Agren
H
H
Barchas
J D
JD
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000818:Animals; D014150:Antipsychotic Agents / Q000008:administration & dosage*; D002746:Chlorpromazine / Q000494:pharmacology; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism*; D005625:Frontal Lobe / Q000187:drug effects / Q000378:metabolism*; D006220:Haloperidol / Q000494:pharmacology; D006719:Homovanillic Acid / Q000378:metabolism; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013881:Thioridazine / Q000494:pharmacology; D013997:Time Factors
D014150:Antipsychotic Agents; D015102:3,4-Dihydroxyphenylacetic Acid; D006220:Haloperidol; D013881:Thioridazine; D002746:Chlorpromazine; D004298:Dopamine; D006719:Homovanillic Acid