Detail of "2709-56-0"

Reference

Assay of dopamine receptors with [a-3H]flupenthixol

Assay of dopamine receptors with [a-3H]flupenthixol. Huff, Rita M.; Molinoff, Perry B. (Sch. Med., Univ. Pennsylvania, Philadelphia, PA 19104, USA). J. Pharmacol. Exp. Ther., 232(1), 57-61 (English) 1985. CODEN: JPETAB. ISSN: 0022-3565. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Although Scatchard anal. of the binding of a-3H-labeled flupenthixol [2709-56-0] is consistent with the presence of a homogeneous population of receptors in rat striata, subpopulations of these sites can be distinguished by their differing affinities for spiroperidol [749-02-0], which has a dissocn. const. (Kd) for D-1 receptors of about 0.3 mM and a Kd for D-2 receptors of approx. 50 pM. The no. of D-1 receptors in rat striatum is approx. 4 times the no. of D-2 receptors. D-1 receptors can be studied by including 10 nM spiroperidol in assays carried out with [a-3H]flupenthixol, thus blocking the binding of [a-3H]flupenthixol to D-2 receptors. The affinity of these receptors for dopamine [51-61-6] is decreased by GTP [86-01-1], as has been obsd. in studies of other receptors whose effects are mediated through changes in adenylate cyclase activity. In the presence of spiroperidol, the Hill coeffs. detd. from dose-response curves of the inhibition of the binding of [a-3H]flupenthixol by antagonists or by agonists in the presence of GTP suggest that the binding reaction obeys simple Michaelis-Menten kinetics for a single class of binding sites.

Multiple dopamine receptors: relevance of in vitro binding data for subclassification of binding sites

Multiple dopamine receptors: relevance of in vitro binding data for subclassification of binding sites. Leysen, J. E. (Dep. Biochem. Pharmacol., Janssen Pharm., Beerse B-2340, Belg.). Neurol. Neurobiol., 8A(Catecholamines, Pt. A), 225-35 (English) 1984. CODEN: NEUND9. ISSN: 0736-4563. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) The striatal dopamine (DA) [51-61-6] D2 receptor binding properties of 11 DA agonists and 20 DA antagonists were investigated for their inhibition of 3H-labeled haloperidol (HAL) [52-86-8] and labeled N-propylnorapomorphine (NPA) [18426-20-5] binding in Tris-HCl buffers contg. physiol. salts or EDTA. Shifts in concn. producing 50% inhibition of 3H-labeled ligand binding (IC50) in both buffers were most pronounced for inhibition of [3H]HAL binding, esp. in the salt buffer. Thus, lisuride [18016-80-3], bromocriptine [25614-03-3], spiperone [749-02-0], pimozide [2062-78-4], fluphenazine [69-23-8], (+)-butaclamol [56245-67-1], piflutixol [54341-02-5], flupenthixol [2709-56-0], molindone [7416-34-4], and metoclopramide [364-62-5] were 5-10-fold more potent in the salt buffer than in the EDTA buffer. In inhibiting NPA binding, the compds. tended to be more potent in the EDTA buffer. Apparently buffer conditions randomly affect the inhibitory potencies of these agonists and antagonists. Correlations were high between the IC50 values of DA antagonists using [3H]HAL and [3H]NPA in the salt and EDTA buffers, resp. 6255-90-9 is the cas registry number. This chemical is also mentioned in this article., and previously obsd. inhibition of apomorphine-induced stereotypy. Thus, the overall binding abilities of the drugs were correlated with their in vivo DA antagonistic potencies, indicating that the drugs interacted with same receptor complex in the various binding assay conditions. GTP [86-01-1] effects on DA agonist binding were also examd. and related to assay condtions and DA receptor subtype. .