title: A European multicenter association study of HTR2A receptor polymorphism in bipolar affective disorder.
abstract: The available data on the role of 5-HT in a variety of behaviors support the hypothesis that a dysfunction in brain serotoninergic system activity contributes to vulnerability to major depression. The diversity in the electrophysiological actions of 5-HT in the central nervous system can now be categorized according to receptor subtypes and their respective effector mechanisms. In particular, the implication of central postsynaptic 5-HT2A receptor in affective disorders has been supported by findings consistent with the hypothesis of 5-HT2A receptor up-regulation in depression. For these reasons, the 5-HT2A receptor (HTR2A) gene can be considered as a candidate gene in bipolar affective disorder (BPAD). We tested the possible genetic contribution of the polymorphic DNA variation T102C in exon 1 of HTR2A (chromosome 13q14-21) gene in a large European multicentric case-control sample. Allele and genotype frequencies, as well as homo-heterozygote distributions were compared between the two groups of 309 bipolar affective disorder patients and 309 matched controls. No significant differences were observed in the allelic and genotypic (also for homo-heterozygote) distribution between BPAD and controls. These results indicate that, in our sample, the 5-HT2A receptor polymorphism studied is unlikely to play a major role in the genetic susceptibility to BPAD. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:136-140, 2000.
authors.affiliation: Department of Psychiatry, University Clinics of Brussels, Erasme Hospital, Free University of Brussels, Brussels, Belgium. imassat@ulb.ac.be
authors.forename: I
authors.initials: I
authors.lastname: Massat
authors.forename: D
authors.initials: D
authors.lastname: Souery
authors.forename: O
authors.initials: O
authors.lastname: Lipp
authors.forename: S
authors.initials: S
authors.lastname: Blairy
authors.forename: G
authors.initials: G
authors.lastname: Papadimitriou
authors.forename: D
authors.initials: D
authors.lastname: Dikeos
authors.forename: M
authors.initials: M
authors.lastname: Ackenheil
authors.forename: S
authors.initials: S
authors.lastname: Fuchshuber
authors.forename: C
authors.initials: C
authors.lastname: Hilger
authors.forename: R
authors.initials: R
authors.lastname: Kaneva
authors.forename: V
authors.initials: V
authors.lastname: Milanova
authors.forename: G
authors.initials: G
authors.lastname: Verheyen
authors.forename: P
authors.initials: P
authors.lastname: Raeymaekers
authors.forename: L
authors.initials: L
authors.lastname: Staner
authors.forename: L
authors.initials: L
authors.lastname: Oruc
authors.forename: M
authors.initials: M
authors.lastname: Jakovljevic
authors.forename: A
authors.initials: A
authors.lastname: Serretti
authors.forename: F
authors.initials: F
authors.lastname: Macciardi
authors.forename: C
authors.initials: C
authors.lastname: Van Broeckhoven
authors.forename: J
authors.initials: J
authors.lastname: Mendlewicz
mesh_terms: D000328:Adult; D000483:Alleles; D001714:Bipolar Disorder / Q000235:genetics*; D005060:Europe; D005260:Female; D005838:Genotype; D006801:Humans; D015810:Linkage Disequilibrium; D019656:Loss of Heterozygosity / Q000235:genetics; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic / Q000235:genetics*; D044402:Receptor, Serotonin, 5-HT2A; D011985:Receptors, Serotonin / Q000235:genetics*
chemical_list: D044402:Receptor, Serotonin, 5-HT2A; D011985:Receptors, Serotonin