No link of serotonin 2C receptor editing to serotonin transporter genotype

Neuroreport. 2010 Dec 8;21(17):1080-4. doi: 10.1097/WNR.0b013e32834052f0.

Abstract

RNA editing is a post-transcriptional process, which has the potential to alter the function of encoded proteins. In particular, serotonin 2C receptor (5-HT2cR) mRNA editing can produce 24 protein isoforms of varying functionality. Rodent studies have shown that 5-HT2cR editing is dynamically modulated in response to environmental challenges. Basal extracellular serotonin, which is strongly influenced by serotonin transporter (SERT), was proposed as a potential trigger for this modulation; however, the data remain inconclusive. Here, 5-HT2cR editing is evaluated in SERT mutant versus wild-type rats, and in humans with different SERT genotypes. Our findings argue against the hypothesis that 5-HT2cR editing efficiency is regulated by extracellular serotonin levels.

Publication types

  • Comparative Study

MeSH terms

  • Animals
  • Disease Models, Animal
  • Extracellular Fluid / metabolism
  • Gene Knockout Techniques
  • Genetic Testing
  • Genotype
  • Humans
  • Polymorphism, Genetic
  • RNA Editing / genetics*
  • Rats
  • Receptor, Serotonin, 5-HT2C / deficiency
  • Receptor, Serotonin, 5-HT2C / genetics*
  • Serotonin / metabolism*
  • Serotonin Plasma Membrane Transport Proteins / genetics*
  • Serotonin Plasma Membrane Transport Proteins / physiology
  • Serotyping

Substances

  • Receptor, Serotonin, 5-HT2C
  • Serotonin Plasma Membrane Transport Proteins
  • Serotonin