Remoxipride and raclopride differentially alter the activity of incertohypothalamic dopaminergic neurons.
The effects of two dopaminergic (DA) antagonists, raclopride (S-(-)-3,5-dichloro-N-[(1-ethyl-2-pyrrolidinyl)methyl]-2-hydroxy- 6-methoxybenzamide(+)-tartrate) and remoxipride (S(-)-3-bromo-N-[(1-ethyl-2-pyrrolidinyl)methyl]-2, 6-dimethoxybenzamide hydrochloride monohydrate), were compared on the DA receptor-mediated regulation of incertohypothalamic and nigrostriatal DA neurons. Both drugs produced dose- and time-related increases in concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) in the striatum, which contains the terminals of the nigrostriatal DA neurons. On the other hand, raclopride but not remoxipride increased concentrations of DOPAC in the medial zona incerta and dorsomedial hypothalamic nucleus, regions that contains cell bodies and terminals, respectively, of incertohypothalamic DA neurons. These results suggest that raclopride blocks a population of DA receptors that regulates the activity of incertohypothalamic DA neurons, whereas remoxipride does not.
Eaton
M J
MJ
Michigan State University, Department of Pharmacology and Toxicology, East Lansing 48824.
Tian
Y
Y
Lookingland
K J
KJ
Moore
K E
KE
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000818:Animals; D015306:Biogenic Monoamines / Q000378:metabolism; D004298:Dopamine / Q000502:physiology*; D065127:Dopamine D2 Receptor Antagonists; D004305:Dose-Response Relationship, Drug; D007031:Hypothalamus / Q000166:cytology / Q000187:drug effects*; D008297:Male; D009474:Neurons / Q000187:drug effects*; D020891:Raclopride; D051381:Rats; D017330:Remoxipride / Q000494:pharmacology*; D012457:Salicylamides / Q000494:pharmacology*
D015306:Biogenic Monoamines; D065127:Dopamine D2 Receptor Antagonists; D012457:Salicylamides; D017330:Remoxipride; D015102:3,4-Dihydroxyphenylacetic Acid; D020891:Raclopride; D004298:Dopamine