Fig. 2From: Increased alternate splicing of Htr2c in a mouse model for Prader-Willi syndrome leads disruption of 5HT2C receptor mediated appetiteIncreased levels of truncated Htr2c in PWS-IC hypothalamus. Gene expression and splice variant ratio was assessed using quantitative PCR (qPCR) in macro-dissected hypothalamus. a Expression of Snord115 was absent in PWS-IC hypothalamus. This deficiency promotes alternate splicing of Htr2c, with levels of the truncated, non-functional, receptor isoform increased in PWS-IC mice relative to WT. The level of another regionally relevant serotonin receptor, Htr1b was unaltered in PWS-IC mice. b The consequence of increased levels of truncated Htr2c expression in PWS-IC hypothalamus, is a significant shift in the ratio of full-length:truncated, with a decreased proportion of functional (full-length) variants. Data presented as Mean ± SEM. Student’s t-test, *p < 0.05, **p < 0.01, **p < 0.001 compared to WT controlsBack to article page