- Peptide (C)KMSEQSTISEHILQK, corresponding to amino acid residues 6-20 of rat 5-Hydroxytryptamine receptor 2B (Accession P30994). Extracellular, N-terminus.
- Expression of 5-Hydroxytryptamine receptor 2B in mouse cerebellumImmunohistochemical staining of mouse cerebellum using Anti-5HT2B Receptor (HTR2B) (extracellular)-ATTO Fluor-488 Antibody (#ASR-035-AG), (1:80). A. 5-HT2B staining (green) appears in neurons of the Purkinje layer (vertical arrows) and in the molecular layer (horizontal arrow). B. Nuclear staining using DAPI as the counterstaining (blue). C. Merged image of panels A and B.
5-HT is involved in a variety of physiological and biological processes. In the brain, 5-HT has been found to affect sleep, mood, appetite, anxiety, aggression, perception, pain, and cognition1. Signaling of 5-HT is mediated by receptors that are located on the cell membrane of neurons and most other cells in the body. The 5-HT2 family consists of three G-protein coupled receptors (GPCRs): 5-HT2A, 5-HT2B, and 5-HT2C2. Like other members, they are transmembrane proteins consisting of seven membrane-spanning α-helical segments with an extracellular N-terminus and an intracellular C-terminus. The binding of 5-HT to one of its receptors is thought to elicit a conformational change that activates associated heterotrimeric G proteins and recruits other downstream signaling/scaffolding molecules, such as GPCR kinases and β-arrestins.
5-HT2B receptors have been found to be present in both rodent and human tissues, particularly in the cardiovascular system, gastrointestinal tract, bone, and central nervous system2. Only low expression levels are found in the brain and blood. The highest expression levels are found in the stomach fundus3.
Over-expression of 5-HT2B receptors in hearts of transgenic mice results in cardiac hypertrophy and decreased ventricular function due to enhanced extracellular matrix (ECM) and remodeling. Likewise, genetic deletion of 5-HT2B receptors was shown to lead to ventricular dilation and incomplete cardiac development5.