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The Journal of Neuroscience, December 15, 2002, 22(24):10529-10532

BRIEF COMMUNICATION
Modulation of Serotonin 2C Receptor Editing by Sustained Changes in Serotonergic Neurotransmission

Ilona Gurevich^{1, 2}, Michael T. Englander², Mella Adlersberg², Nathan B. Siegal², and Claudia Schmauss^{1, 2}

¹ Department of Psychiatry and ² Division of Neuroscience, Columbia University College of Physicians and Surgeons, New York, New York 10032

Serotonin 2C (5-HT_2C) receptor pre-mRNA is a substrate for RNA editing enzymes that convert five adenosines (named A, B, C', C, and D editing sites) to inosines. Editing of two of these sites (C' and C) is crucial for decreasing the efficiency of the receptor to activate G-protein. Nucleotide sequence analysis of mouse forebrain neocortical 5-HT_2C mRNA isoforms revealed that editing at these two sites is regulated in a serotonin-dependent manner. In serotonin-depleted mice, C'- and C-site editing is significantly decreased. This results in an increased expression of 5-HT_2C mRNA isoforms encoding receptors with higher sensitivity to serotonin. In contrast, a 4 d treatment with the 5-HT_2A/2C agonist (±)-1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane significantly increases the editing frequency at the C' site and leads to increased expression of 5-HT_2C mRNA isoforms encoding receptors that activate G-protein least efficiently. None of the drug treatments led to alterations in cytoplasmic 5-HT_2C mRNA levels. These data indicate that editing of 5-HT_2C pre-mRNA is a mechanism that retains basic response properties of 5-HT_2C receptors in the face of changing synaptic input to keep receptor activation within an optimal range for information processing.

Key words: serotonin; 5-HT_2C receptor; RNA editing; forebrain neocortex; 5-HT depletion; 5-HT_2A/2C agonist

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Copyright © 2002 Society for Neuroscience  0270-6474/02/222410529-04$05.00/0

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