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Regulation of Serotonin 2A Receptor Expression by an Antisense Oligodeoxynucleotide
Author(s) -
Scalzitti J. M.,
Berg K. A.,
Kratowicz S. A.,
Hensler J. G.
Publication year - 1998
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1998.71041457.x
Subject(s) - quipazine , receptor , agonist , stimulation , chemistry , microbiology and biotechnology , messenger rna , biology , 5 ht receptor , endocrinology , serotonin , biochemistry , gene
The regulation of 5‐HT 2A receptor expression by an antisense oligodeoxynucleotide, complementary to the coding region of rat 5‐HT 2A receptor mRNA, was examined in a cortically derived cell line and in rat brain. Treatment of A 1 A 1 variant cells, which express the 5‐HT 2A receptor coupled to the stimulation of phosphatidylinositol (PI) hydrolysis, with antisense oligodeoxynucleotide decreased the maximal stimulation of PI hydrolysis by the partial agonist quipazine and the number of 5‐HT 2A receptor sites as measured by the binding of 2‐[ 125 I]‐iodolysergic acid diethylamide. Treatment of cells with random, sense, or mismatch oligodeoxynucleotide did not alter the stimulation of PI hydrolysis by quipazine or 5‐HT 2A receptor number. Intracerebroventricular infusion of antisense, but not mismatch, oligodeoxynucleotide for 8 days resulted in a significant increase in cortical 5‐HT 2A receptor density and an increase in headshake behavior induced by the 5‐HT 2 receptor agonist 1‐(2,5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane. The density of cortical 5‐HT 2A receptors was not altered by administration of antisense oligodeoxynucleotide for 1, 2, or 4 days. We hypothesize that in brain this antisense oligodeoxynucleotide relieved some form of translational suppression, resulting in an increase in 5‐HT 2A receptor expression.