title: Altered 5-HT(2A) receptor binding after recovery from bulimia-type anorexia nervosa: relationships to harm avoidance and drive for thinness.
abstract: Several lines of evidence suggest that a disturbance of serotonin neuronal pathways may contribute to the pathogenesis of anorexia nervosa (AN) and bulimia nervosa (BN). This study applied positron emission tomography (PET) to investigate the brain serotonin 2A (5-HT(2A)) receptor, which could contribute to disturbances of appetite and behavior in AN and BN. To avoid the confounding effects of malnutrition, we studied 10 women recovered from bulimia-type AN (REC AN-BN, > 1 year normal weight, regular menstrual cycles, no binging, or purging) compared with 16 healthy control women (CW) using PET imaging and a specific 5-HT(2A) receptor antagonist, [18F]altanserin. REC AN-BN women had significantly reduced [18F]altanserin binding potential relative to CW in the left subgenual cingulate, the left parietal cortex, and the right occipital cortex. [18F]altanserin binding potential was positively related to harm avoidance and negatively related to novelty seeking in cingulate and temporal regions only in REC AN-BN subjects. In addition, REC AN-BN had negative relationships between [18F]altanserin binding potential and drive for thinness in several cortical regions. In conclusion, this study extends research suggesting that altered 5-HT neuronal system activity persists after recovery from bulimia-type AN, particularly in subgenual cingulate regions. Altered 5-HT neurotransmission after recovery also supports the possibility that this may be a trait-related disturbance that contributes to the pathophysiology of eating disorders. It is possible that subgenual cingulate findings are not specific for AN-BN, but may be related to the high incidence of lifetime major depressive disorder diagnosis in these subjects.
authors.affiliation: Department of Psychiatry, School of Medicine, University of Pittsburgh, Western Psychiatric Institute and Clinic, Pittsburgh, PA 15213, USA.
authors.forename: Ursula F
authors.initials: UF
authors.lastname: Bailer
authors.forename: Julie C
authors.initials: JC
authors.lastname: Price
authors.forename: Carolyn C
authors.initials: CC
authors.lastname: Meltzer
authors.forename: Chester A
authors.initials: CA
authors.lastname: Mathis
authors.forename: Guido K
authors.initials: GK
authors.lastname: Frank
authors.forename: Lisa
authors.initials: L
authors.lastname: Weissfeld
authors.forename: Claire W
authors.initials: CW
authors.lastname: McConaha
authors.forename: Shannan E
authors.initials: SE
authors.lastname: Henry
authors.forename: Sarah
authors.initials: S
authors.lastname: Brooks-Achenbach
authors.forename: Nicole C
authors.initials: NC
authors.lastname: Barbarich
authors.forename: Walter H
authors.initials: WH
authors.lastname: Kaye
mesh_terms: D000328:Adult; D000367:Age Factors; D000856:Anorexia Nervosa / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D001921:Brain / Q000033:anatomy & histology / Q000000981:diagnostic imaging; D001931:Brain Mapping; D002032:Bulimia / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000503:physiopathology; D004328:Drive; D005260:Female; D005462:Fluorine Radioisotopes / Q000493:pharmacokinetics; D040261:Harm Reduction / Q000502:physiology*; D006801:Humans; D007650:Ketanserin / Q000031:analogs & derivatives* / Q000493:pharmacokinetics; D011485:Protein Binding / Q000187:drug effects; D044402:Receptor, Serotonin, 5-HT2A / Q000378:metabolism*; D058830:Serotonin 5-HT2 Receptor Antagonists; D013851:Thinness / Q000378:metabolism* / Q000503:physiopathology; D013997:Time Factors; D014055:Tomography, Emission-Computed / Q000379:methods
chemical_list: D005462:Fluorine Radioisotopes; D044402:Receptor, Serotonin, 5-HT2A; D058830:Serotonin 5-HT2 Receptor Antagonists; C071983:altanserin; D007650:Ketanserin