G-protein coupled receptor for 5-hydroxytryptamine (serotonin) (PubMed:1426253). Also functions as a receptor for various ergot alkaloid derivatives and psychoactive substances (PubMed:1426253, PubMed:16940156). Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of downstream effectors. Beta-arrestin family members inhibit signaling via G proteins and mediate activation of alternative signaling pathways. Signaling activates a phosphatidylinositol-calcium second messenger system that modulates the activity of phosphatidylinositol 3-kinase and downstream signaling cascades and promotes the release of Ca(2+) ions from intracellular stores (By similarity). Plays a role in the regulation of dopamine and 5-hydroxytryptamine release, 5-hydroxytryptamine uptake and in the regulation of extracellular dopamine and 5-hydroxytryptamine levels, and thereby affects neural activity (PubMed:16940156, PubMed:18337424). May play a role in the perception of pain (PubMed:21273425). Plays a role in the regulation of behavior, including impulsive behavior (PubMed:21179162). Required for normal proliferation of embryonic cardiac myocytes and normal heart development (PubMed:10944220, PubMed:11413089). Protects cardiomyocytes against apoptosis (PubMed:12738797). Plays a role in the adaptation of pulmonary arteries to chronic hypoxia (PubMed:12244304). Plays a role in vasoconstriction (PubMed:12244304, PubMed:23346101). Required for normal osteoblast function and proliferation, and for maintaining normal bone density (PubMed:17846081). Required for normal proliferation of the interstitial cells of Cajal in the intestine (PubMed:19941613). Interacts (via C-terminus) with MPDZ. Ubiquitous. Detected in intestine, heart, skeletal muscle, testis, urinary bladder, stomach, liver, lung, brain and kidney. Detected in osteoblasts. Detected in the raphe nucleus in the brain, in dorsal root ganglion neurons, the brain stem, cerebellum and spinal cord. Detected in interstitial cells of Cajal in the small intestine. Ligands are bound in a hydrophobic pocket formed by the transmembrane helices. Partial embryonic and perinatal lethality, due to heart ventricle hypoplasia and impaired proliferative capacity of heart myocytes. Mutant mice that survive into adulthood have a decreased heart weight relative to body weight. They display dilated cardiomyopathy with a loss of ventricular mass, due to a reduction in the number and size of cardiomyocytes. The myocardium from mutant mice displays abnormal organization of the contractile elements, with an irregular array of sarcomeric myofibrils and abnormally wide Z bands. In addition, heart muscle mitochondria display structural and functional defects. Mutant mice do not respond to chronic exposure to low oxygen levels by remodeling of their lung arteries, unlike wild-type mice, and as a consequence, do not develop increased right ventricular systolic pressure in response to chronic hypoxia. Adult mutant female mice display reduced bone density that worsens with age. Osteopenia is due to reduced proliferation and delayed differentiation of osteoblasts and reduced calcium incorporation by osteoblasts (PubMed:17846081). In addition, mutant mice display a reduced number of proliferating interstitial cells of Cajal in the myenteric plexus in jejunum muscle, and a reduced number of interstitial cells of Cajal in the deep muscular plexus (PubMed:19941613). Mutant mice also show increased locomotor activity in a novel environment, compared to the wild-type. Unlike the wild-type, they do not respond to the drug 3,4-methylenedioxymethamphetamine with increased locomotion and increased 5-hydroxytryptamine and dopamine levels in the brain (PubMed:18337424). Belongs to the G-protein coupled receptor 1 family. Extended C-terminus.