Modulation of dopamine D3 receptor binding by N-ethylmaleimide and neurotensin

• Published in: Brain research Vol. 643; no. 1-2; pp. 343 - 348
• Main Authors: YUN LIU, HILLEFORS-BERGLUND, M, VON EULER, G
• Format: Journal Article
• Language: English
• Published: London Elsevier 18.04.1994; Amsterdam; New York, NY
• Subjects: Animals; Binding, Competitive; Biological and medical sciences; Cell Membrane - metabolism; Central nervous system; Central neurotransmission. Neuromudulation. Pathways and receptors; Dopamine Agents - pharmacology; Dose-Response Relationship, Drug; Ethylmaleimide - pharmacology; Fundamental and applied biological sciences. Psychology; Kinetics; Limbic System - metabolism; Male; Neurotensin - pharmacology; Rats; Rats, Sprague-Dawley; Receptors, Dopamine - drug effects; Receptors, Dopamine - metabolism; Receptors, Dopamine D2; Receptors, Dopamine D3; Tetrahydronaphthalenes - metabolism; Vertebrates: nervous system and sense organs; Vertebrata; Mammalia; Rat; Rodentia; Central nervous system; Neurotensin; Neuropeptide; D3 Dopamine receptor; Brain (vertebrata); G protein
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/0006-8993(94)90045-0

GTP or G protein inactivation by N-ethylmaleimide reduced the Bmax value but not the KD value of 7-[3H]hydroxy-N,N-di-n-propyl-2-aminotetralin ([3H]7-OH-DPAT) binding in the rat subcortical limbic area. Neurotensin (10 nM) increased the KD and the Bmax values of [3H]7-OH-DPAT binding, and these effects persisted also following N-ethylmaleimide pretreatment. N-Propylnorapomorphine, quinpirole, raclopride, and remoxipride inhibited [3H]7-OH-DPAT binding with Ki values of 0.093, 1.97, 10.6, and 710 nM, respectively. These findings indicate that the D3 receptor is coupled to G proteins in the brain, and that neurotensin can modulate D3 agonist binding by a G protein-independent mechanism.