Detail of "487-93-4"

Reference

Long lasting effects of intrauterine growth retardation on basal and 5-HT-stimulated sodium-potassium ATPase in the brain of developing rats

Long lasting effects of intrauterine growth retardation on basal and 5-HT-stimulated sodium-potassium ATPase in the brain of developing rats. Chanez, Claude; Flexor, Marie Ange; Hamon, Michel (Cent. Rech. Biol. Dev. Foetal Neonatal, Hop. Port-Royal, Paris 75674, Fr.). Neurochem. Int., 7(2), 319-29 (English) 1985. CODEN: NEUIDS. ISSN: 0197-0186. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) Section cross-reference(s): 14 Intrauterine growth retardation induced by ligation of the uterine vessels in pregnant rats on the 5th day before delivery was assocd. with brain and body wts. of hypotrophic offspring lower than those of pair-aged control rats, even after 6 wk of postnatal rearing under normal conditions. In vitro measurements in homogenates indicated that Na+/K+ ATPase [9000-83-3] in the forebrain, cerebellum, and hippocampus was less active in hypotrophic rats than in pair-aged controls for at least the 1st month after birth. However, 5-HT [50-67-9] and related agonists (RU-24969 [66611-26-5], bufotenine [487-93-4], and to a lesser extent, tryptamine [61-54-1]) stimulated Na+/K+-ATPase activity more efficiently in tissues from hypotrophic rats than in those from control animals. Opposite changes were noted in the brain stem: basal Na+/K+-ATPase activity was higher in hypotrophic rats during the 2nd half of the 1st postnatal month but the stimulatory effect of 5-HT was lower than in pair-aged control animals. Since potent 5-HT antagonists, such as cinanserin, methiothepin, and methylsergide, prevented the 5-HT-induced activation of Na+/K+-ATPase in brain homogenates, these results are discussed in relation to the possible existence of a specific 5-HT receptor controlling Na+/K+-ATPase activity in the rat brain.

Postsynaptic serotonin-sensitive adenylate cyclase in the central nervous system

Postsynaptic serotonin-sensitive adenylate cyclase in the central nervous system. II. Comparison with dopamine- and isoproterenol-sensitive adenylate cyclases in rat brain. Enjalbert, Alain; Hamon, Michel; Bourgoin, Sylvie; Bockaert, Joel (Lab. Physiol. Cell., Coll. France, Paris, Fr.). Mol. Pharmacol., 14(1), 11-23 (English) 1978. CODEN: MOPMA3. DOCUMENT TYPE: Journal CA Section: 2 (Hormone Pharmacology) Section cross-reference(s): 1 The maximal effects of dopamine (I) [51-61-6] and serotonin creatinine sulfate (II creatinine sulfate) [971-74-4] on the adenylate cyclase [9012-42-4] activity in striatum and hypothalamus homogenates from newborn rats were not strictly additive. In fact, in striatum II inhibited the I sensitive adenylate cyclase noncompetitively. Conversely, the maximal effects of II and l-isoproterenol [51-31-0] on adenylate cyclase activity in homogenates of the cerebral cortex were strictly additive. Classical serotoninergic agonists LSD [50-37-3], bufotenine [487-93-4], 5-methoxy-N,N-dimethyltryptamine [1019-45-0] activated the adenylate cyclase in collicular homogenates. All but LSD were ineffective on the b-adrenergic-sensitive adenylate cyclase in C6 glioma cells. The antagonists tested were not specific for the serotoninergic or the dopaminergic receptors. Neuroleptics (clozapine [5786-21-0], thioridazine-HCl [130-61-0], chlorpromazine [50-53-3], fluphenazine [69-23-8], and haloperidol [52-86-8]) and classical serotoninergic antagonists (methiothepin maleate [19728-88-2], cyproheptadine-HCl [969-33-5], cinanserin [1166-34-3], mianserin [24219-97-4], and methergoline [17692-51-2]) interacted with both dopaminergic and serotoninergic receptors but not with b-adrenergic receptors. All these antagonists were more potent toward the I- than the II-sensitive adenylate cyclase. The drugs inhibited the I-sensitive adenylate cyclase in a competitive manner. Methergoline was the only drug that competitively inhibited the II-sensitive adenylate cyclase. The other classical serotoninergic antagonists, as well as the neuroleptics, inhibited the serotonin-sensitive enzyme by decreasing both its apparent affinity for II and its maximal activity. The serotoninergic and dopaminergic receptors may exist in agonist and antagonist forms. The structures of their antagonist forms may be closely related.