Serotonin
(Synonyms: 5-羟基色胺,5-Hydroxytryptamine; 5-HT) 目录号 : GC63188
Serotonin HCl (5-HT) is a monoamine neurotransmitter and Endogenous 5-HT receptor agonist.
Cas No.:50-67-9
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
For macrophage culture, peritoneal cavity cells are collected from WT and IL-13-/- mice with or without dextran sodium sulfate (DSS) treatment and cultured. Cells are plated at a concentration of 3.0×106 cells per millilitre, and treated with either lipopolysaccharides (LPS); (100 ng/mL) or Serotonin (10-10 M) for 24 hours. The culture supernatant are collected and stored in -80°C until determination of cytokine levels using protein array system[2].
Dextran sodium sulfate (DSS) colitis is induced by orally administering 5% DSS in drinking water for 5 days. In a separate experiment, IL-13-/- mice are injected subcutaneously with 100 mg/kg of Serotonin (5-HTP) twice daily for 8 days beginning 3 days prior to induction of DSS colitis; whereas, the control IL-13-/- mice receive saline as vehicle. Animals are anaesthetized prior to euthanization via cervical dislocation at the conclusion of each experiment or if they reach a predetermined end point (ie, loss of ≥20% body weight and/or significant deterioration of body condition)[2].
[1]. Tsao D, et al. Serotonin-induced hypersensitivity via inhibition of catechol O-methyltransferase activity. Mol Pain. 2012 Apr 13;8:25.
[2]. Shajib MS, et al. Interleukin 13 and serotonin: linking the immune and endocrine systems in murine models of intestinal inflammation. PLoS One. 2013 Aug 28;8(8):e72774.
Serotonin HCl (5-HT) is a monoamine neurotransmitter and Endogenous 5-HT receptor agonist.
Serotonin stimulates acid–base transport by the anterior stomach region of the midgut in vitro. The function of this stimulation is assumed to be maintenance of optimal conditions for digestion and absorption of nutrients rather than regulation of hemolymph acid–base homeostasis. [1]
The role of serotonin in the regulation of larval Aedes aegypti hemolymph composition is investigated in vivo using two reuptake inhibitors (SSRIs), alaproclate HCl and 6-nitroquipazine maleate, and the receptor antagonist methiothepin mesylate. [1]
[1] Onken, H, et al. J Insect Sci, 2008, 8, 1-20.
| Cas No. | 50-67-9 | SDF | |
| 别名 | 5-羟基色胺,5-Hydroxytryptamine; 5-HT | ||
| 分子式 | C10H12N2O | 分子量 | 176.22 |
| 溶解度 | DMSO : 100 mg/mL (567.47 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 5.6747 mL | 28.3736 mL | 56.7472 mL |
| 5 mM | 1.1349 mL | 5.6747 mL | 11.3494 mL |
| 10 mM | 0.5675 mL | 2.8374 mL | 5.6747 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Serotonin, hematopoiesis and stem cells
Pharmacol Res 2019 Feb;140:67-74.PMID:30107202DOI:10.1016/j.phrs.2018.08.005.
A large number of studies have focused on the role of Serotonin as a neurotransmitter in the central nervous system, although only a small percentage of the body's Serotonin (∼5%) can be found in the mature brain of mammals. In the gut, the enterochromaffin cells are scattered in the enteric epithelium from the stomach through the colon and produce over 95% of the body's Serotonin. Since the generation of tryptophan hydroxylase (Tph1 and Tph2) knockout mice, unsuspected roles have been identified for Serotonin synthesized outside the brain. Moreover, the murine model deficient in peripheral Serotonin (Tph1-/-) is a unique experimental tool for exploring the molecular and cellular mechanisms involving Serotonin's local effects through microserotonergic systems. In this review, we focus on peripheral Serotonin and its role on progenitor or stem cells as well as on hematopoietic progenitors. We discuss the possible role of Serotonin in hematopoietic diseases, and whether targeting the serotonergic system could be of therapeutic value for the regulation of normal and pathological hematopoiesis.
[The pharmacological basis of the Serotonin system: Application to antidepressant response]
Encephale 2016 Jun;42(3):255-63.PMID:27112704DOI:10.1016/j.encep.2016.03.012.
If Serotonin (5-hydroxytryptamin [5-HT]) is well known for its role in mood regulation, it also impacts numerous physiological functions at periphery. Serotonin is synthetized at the periphery into the gut by intestinal enterochromaffin cells and in the central nervous system (CNS) in the raphe nucleus from the essential amino acid tryptophan. Physiological effects of 5-HT are mediated by about 15 serotoninergic receptors grouped into seven broad families (5-HT1, 5-HT2, 5-HT3, 5-HT4, 5-HT5, 5-HT6, 5-HT7 receptor families). Except 5-HT3 receptor, a ligand-gated ion channels, all the others are G protein-coupled receptors. Serotonin's homeostasis involves serotoninergic autoreceptor such as 5-HT1A, 5-HT1B, 5-HT1D, the enzymatic degradation of Serotonin by monoamine oxidase A (MAO-A), and a transporter (serotoninergic transporter [SERT]). In the CNS, the SERT is a key target for various antidepressant drugs such as Selective Serotonin Reuptake Inhibitors (SSRI), Serotonin Norepinephrin Reuptake Inhibitors (SNRI) and tricyclics family. However, antidepressant activity of SERT inhibitors is not directly mediated by the SERT inhibition, but a consequence of postsynaptic 5-HT receptor activation following the increase in 5-HT levels in the synaptic cleft. In pharmacology, SSRIs are defined as indirect agonist of postsynaptic receptor. Among all the 5-HT receptors, 5-HT1A, 5-HT1B, 5-HT1D, 5-HT2B and 5-HT4 receptors activation would mediate antidepressant effects. In the meanwhile, 5-HT2A, 5-HT2C, 5-HT3, 5-HT6 and 5-HT7 receptors activation would induce opposite effects. The best serotoninergic antidepressant would directly activate 5-HT1A, 5-HT1B, 5-HT1D, 5-HT2B and 5-HT4 and would block 5-HT2A, 5-HT2C, 5-HT3, 5-HT6 and 5-HT7 receptor. If the chemical synthesis of such a compound may be compromised, SERT inhibition associated with the blockade of some but not all 5-HT receptor could shorten onset of action and/or improve antidepressant efficacy on the overall symptomatology of depression.
Impact of specific Serotonin receptor modulation on behavioral flexibility
Pharmacol Biochem Behav 2021 Oct;209:173243.PMID:34314738DOI:10.1016/j.pbb.2021.173243.
Serotonin (5-HT) is known to play a critical role in regulation of essential neural processes, whereas more recent research highlights Serotonin's modulatory effects on cognition and executive functioning. Current examinations have identified specific Serotonin receptors for their direct impact on behavioral flexibility. Providing definitive evidence for the impact of specific receptor targets on behavioral flexibility is difficult, due to the range of behavioral tests used. Due to limited studies and the sheer amount of different Serotonin receptor targets, beginning to bring these studies together is important for the field. Our current review of the literature aims to differentiate how modulation of specific 5-HT receptors affects behavioral flexibility. Although more studies have examined 5-HT2A, 5-HT2C, and 5-HT6 receptors, it is unclear why this is the case. Above all, there are some paradoxical results pertaining to these receptor targets. There is a clear distinction between 5-HT2A and 5-HT2C, which conveys that these two receptor subtypes have inverse effects when compared to each other. In addition, some findings support one another, such as upregulation of 5-HT6 receptors impairs flexibility, while blockade alleviates this impairment in both drug-induced and disease model rodent studies. Further understanding how modulatory effects of specific 5-HT receptors impact behavioral flexibility is imperative to advance the development of new therapeutics for neuropsychiatric disorders afflicted by behavioral inflexibility.
Serotonin and orthodontic tooth movement
Biochimie 2019 Jun;161:73-79.PMID:30953672DOI:10.1016/j.biochi.2019.04.002.
Peripheral Serotonin continuously reveals its unexpected involvements in many organ functions. In bone tissue, there is an increasing evidence for a local serotonergic system affecting the cellular and molecular actors involved in bone turnover. During orthodontic treatment, tooth movement relies on bone remodeling, itself a result of the inflammatory process triggered by application of orthodontic forces to the teeth. Nowadays, many adults proceed to an orthodontic treatment, it therefore seems important to consider physiological growth-related factors and external factors as medications that may influence adverse effects and efficacy of orthodontic treatment techniques. In this review, we focus on peripheral Serotonin mechanism of regulation of bone remodeling during orthodontic movement. We discuss the differential effect of Serotonin on alveolar bone inflammation that may open new strategies in orthodontics.
Serotonin as a Mitogen in the Gastrointestinal Tract: Revisiting a Familiar Molecule in a New Role
Cell Mol Gastroenterol Hepatol 2021;12(3):1093-1104.PMID:34022423DOI:10.1016/j.jcmgh.2021.05.008.
Serotonin signaling is ubiquitous in the gastrointestinal (GI) system, where it acts as a neurotransmitter in the enteric nervous system (ENS) and influences intestinal motility and inflammation. Since its discovery, Serotonin has been linked to cellular proliferation in several types of tissues, including vascular smooth muscle, neurons, and hepatocytes. Activation of Serotonin receptors on distinct cell types has been shown to induce well-known intracellular proliferation pathways. In the GI tract, potentiation of Serotonin signaling results in enhanced intestinal epithelial proliferation, and decreased injury from intestinal inflammation. Furthermore, activation of the type 4 Serotonin receptor on enteric neurons leads to neurogenesis and neuroprotection in the setting of intestinal injury. It is not surprising that the mitogenic properties of Serotonin are pronounced within the GI tract, where enterochromaffin cells in the intestinal epithelium produce 90% of the body's Serotonin; however, these proliferative effects are attributed to increased Serotonin signaling within the ENS compartment as opposed to the intestinal mucosa, which are functionally and chemically separate by virtue of the distinct tryptophan hydroxylase enzyme isoforms involved in Serotonin synthesis. The exact mechanism by which serotonergic neurons in the ENS lead to intestinal proliferation are not known, but the activation of muscarinic receptors on intestinal crypt cells indicate that cholinergic signaling is essential to this signaling pathway. Further understanding of Serotonin's role in mucosal and enteric nervous system mitogenesis may aid in harnessing Serotonin signaling for therapeutic benefit in many GI diseases, including inflammatory bowel disease, malabsorptive conditions, and cancer.