Abstract
Treatment of primary cultured cortical cells with erythro-9-(2-hydroxy-3-nonyl) adenine hydrochloride (EHNA), an inhibitor of adenosine deaminase (ADAR), for 6 d significantly and concentration-dependently reduced the editing efficacy at sites C and D but not at site A or B of 5-HT2CR mRNA. The treatment failed to affect the editing of ADAR-2 pre-mRNA and a subunit of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)-type glutamate receptor (GluR2) mRNA. These findings suggest that EHNA is useful for clarifying the functional roles of 5-HT2CR mRNA editing at sites C and D.
