Dopamine turnover and glutamate decarboxylase activity in the rat brain after acute and chronic treatment with raclopride, a dopamine D2-selective antagonist.
The effect of acute and chronic (94, 141 and/or 199 days) oral treatment of rats with the dopamine D2-selective antagonist raclopride (0, 5, 15, 45 and 135 mumol/kg) upon the turnover of dopamine in the striatum and limbic system and upon the activity of glutamate decarboxylase (GAD) in the s. nigra, striatum and frontal cortex has been investigated. A dose-dependent tolerance to the effect of raclopride on the turnover of dopamine was observed after chronic treatment, although the degree of tolerance was marginal at the 5 and 15 mumol/kg doses. Acute treatment with raclopride was without effect on the activity of GAD in the s. nigra, striatum or frontal cortex, whereas chronic (199 days) treatment with 45 mumol/kg of raclopride produced an increase in the activity of GAD in the s. nigra and striatum.
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000818:Animals; D004298:Dopamine / Q000378:metabolism*; D005968:Glutamate Decarboxylase / Q000378:metabolism*; D006897:Hydroxyindoleacetic Acid / Q000378:metabolism; D008032:Limbic System / Q000187:drug effects* / Q000378:metabolism; D020891:Raclopride; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000187:drug effects; D017448:Receptors, Dopamine D2; D012457:Salicylamides / Q000494:pharmacology*; D012701:Serotonin / Q000378:metabolism; D013687:Telencephalon / Q000187:drug effects* / Q000378:metabolism
D011954:Receptors, Dopamine; D017448:Receptors, Dopamine D2; D012457:Salicylamides; D015102:3,4-Dihydroxyphenylacetic Acid; D012701:Serotonin; D020891:Raclopride; D006897:Hydroxyindoleacetic Acid; D005968:Glutamate Decarboxylase; D004298:Dopamine