| 15559 | Q02152 | 5HT2B_MOUSE | 5-hydroxytryptamine receptor 2B (5-HT-2B) (5-HT2B) (5-HT-2F) (NP75 protein) (Serotonin receptor 2B) | DISRUPTION PHENOTYPE | 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). {ECO:0000269|PubMed:10944220, ECO:0000269|PubMed:11413089, ECO:0000269|PubMed:12244304, ECO:0000269|PubMed:12738797, ECO:0000269|PubMed:17846081, ECO:0000269|PubMed:18337424, ECO:0000269|PubMed:19941613}. |