Disease relevance of alpha-Methylserotonin

• Peripherally administered, the 5-HT2 receptor agonist, alpha-methyl-5-hydroxytryptamine (alpha-methyl-5-HT), significantly suppressed the food intake of food-deprived rats. alpha-Methyl-5-HT also inhibited 2-deoxy-D-glucose-induced hyperphagia in rats [1].

Psychiatry related information on alpha-Methylserotonin

• The serotonergic agonists quipazine, CGS-12066A, and alpha-methylserotonin alter motor activity and induce hindlimb stepping in the intact and spinal rat fetus [2].
• With 5-HT agonists, 8-OH-DPAT (5-HT1A) suppressed the two oral stereotypies and increased standing (all 1.0 mg/kg) and preening (0.2 mg/kg), alpha-methylserotonin (5-HT2) suppressed the oral stereotypies and increased sitting (all 1.0 mg/kg), and m-CPBG (5-HT3) suppressed drinker-directed activity (1.0 mg/kg) [3].

High impact information on alpha-Methylserotonin

• 2. 5-HT, the 5-HT1B-selective agonist 5-nonyloxytryptamine (5-NOT) and the 5-HT2B-selective agonist alpha-methyl-5-hydroxytryptamine (alpha-methyl-5-HT) added basolaterally stimulated Isc in a dose-dependent manner with EC50 values of 0.4, 20 and 0.3 microM, respectively [4].
• Alpha-methyltryptophan (AMTP), a synthetic amino acid, is metabolized by the rat in vivo to alpha-methylserotonin (AM5HT), which appears in the pineal gland just as it does in the brain [5].
• 5-HT1 and 5-HT2 binding profiles of the serotonergic agents alpha-methylserotonin and 2-methylserotonin [6].
• Agonists selective for the 5-HT1A/1B/1D or 5-HT3 receptor subtypes induced minimal or undetectable pulmonary responses, whereas infusion of alpha-methyl-5-hydroxytryptamine, a 5-HT2 receptor-selective agonist, led to dose-related decreases in Cdyn and GL [7].
• DOI and alpha-methylserotonin: comparative vascular and nonvascular smooth muscle effects and central 5-hydroxytryptamine2 receptor affinities [8].

Biological context of alpha-Methylserotonin

• The broad 5-HT(2) receptor agonist, alpha-methyl-5-hydroxytryptamine (alpha-Me-5-HT) enhances synaptic transmission, in a concentration-dependent manner, but it is not as potent as 5-HT [9].
• The branchial vasoconstriction produced by serotonin injection was completely blocked by the 5-HT1/5-HT2 receptor antagonist methysergide and the branchial vasoconstriction produced by WIDTH="9" HEIGHT="12" ALIGN="BOTTOM" NATURALSIZEFLAG= alpha-methylserotonin injection was completely blocked by the specific 5-HT2 receptor antagonist LY53857 [10].
• Characterization of the biphasic blood pressure response to alpha-methyl-5-hydroxytryptamine in anaesthetized rats [11].
• METHOD: Female Wistar rats on the 7th day postpartum were microinjected with the selective 5-HT(2A/2C) receptor agonist, alpha-methyl-5-hydroxytryptamine maleate (0.2 to 1.0 microg/0.2 microl) into the central amygdaloid nucleus and median preoptic nucleus [12].

Anatomical context of alpha-Methylserotonin

• This might suggest that binding to the agonist low-affinity state of the 5-HT2 receptor is more relevant to vascular agonist activity. alpha-Methylserotonin was slightly more potent than serotonin in contracting the rat aorta but not the jugular vein, whereas DOI was more potent in the jugular vein than in the aorta [8].
• Autoradiograms obtained at 6 h after injection revealed only the caudal part of the MFB but all raphe nuclei were labelled, indicating that the tracer was in the process of being transported, probably as an alpha-methyl-5-hydroxytryptamine, via the MFB [13].
• Presynaptic displacement of serotonin by alpha-methyl-5-hydroxytryptamine in the nucleus tractus solitarius of the rat [14].
• Endothelium-dependent relaxation to alpha-methyl-5-hydroxytryptamine in isolated horse coronary arteries [15].
• (iii) alpha-Methyl-5-hydroxytryptamine (alpha-Me-5-HT) and 5-carboxamidotryptamine (5-CT), relatively selective 5-HT1C/5-HT2 and 5-HT1-like receptor agonists, respectively, elicited contractions in the HUA, and the responses were reduced at low PO2 but unaffected by removal of the endothelium [16].

Associations of alpha-Methylserotonin with other chemical compounds

• Contractions induced by 8-hydroxy-2-(di-n-propylamino)-tetralin or alpha-methylserotonin maleate were attenuated by pretreatment with S(-)propranolol (2.6 microM), a relatively selective 5-HT1A and 5-HT1B receptor antagonist, and ketanserin (0.3 microM), a selective 5-HT2 receptor antagonist, respectively [17].
• The antiaversive effect produced by alpha-methyl-5-hydroxytryptamine was attenuated by the systemic administration of ketanserin, a preferential 5-HT2 receptor antagonist [18].

Gene context of alpha-Methylserotonin

• In contrast, application of high concentrations of alpha-methyl-5-hydroxytryptamine, a serotonin analog which activates 5-HT1C and 5-HT2 receptor subtypes, depolarized motoneurons [19].
• The effect of 5-HT was mimicked by the 5-HT2 receptor agonist, alpha-methyl-5-hydroxytryptamine (alpha-methyl-5-HT), but not by the 5-HT1A receptor agonist, (+/-) 8-hydroxydipropylaminotetralin hydrobromide (8-OH-DPAT), or the 5-HT1B agonist, CGS 12066A [20].
• The 5-HT1A receptor agonist 8-OH-DPAT ((+/-)-8-hydroxy-dipropylaminotetralin hydrobromide), the 5-HT1 receptor agonist 5-CT (5-carboxyamidotryptamine maleate) and the 5-HT2 receptor agonist alpha-CH3-5-HT (alpha-methylserotonin maleate) all reproduced the actions of 5-HT at both the cellular and the network levels [21].
• Scratching induced by 5-HT and alpha-methylserotonin was inhibited by peroral pretreatment with 5-HT1/2 receptor antagonists methysergide and cyproheptadine [22].

Analytical, diagnostic and therapeutic context of alpha-Methylserotonin

• Subcutaneous injection of 5-HT (50 microg) and alpha-methylserotonin (alpha-m-5-HT, 5-HT2A receptor agonist, 50 microg) into the unilateral hindpaw evoked significant decreases in paw withdrawal latency (PWL) [23].

References