چگالی کم و علاقه بالای اتصال پلاکت [3H] پاروکستین در زنان مبتلا به بولیمیا
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|32505||2006||5 صفحه PDF||سفارش دهید||2930 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Psychiatry Research, Volume 142, Issues 2–3, 15 June 2006, Pages 219–223
Impaired serotonin transmission has been suggested to be implicated in the pathophysiology of bulimia nervosa. As an indirect measure of brain serotonergic activity, the binding of tritiated ligands to platelet serotonin transporters has been studied in bulimia nervosa as well as in other putatively serotonin-related psychiatric disorders. In this study, the density and affinity of platelet serotonin transporters were assessed in 20 women meeting the DSM-IV criteria for bulimia nervosa and in 14 controls without previous or ongoing eating disorder using [3H]paroxetine as a ligand. In comparison to controls, women with bulimia nervosa had a significantly reduced number of platelet binding sites (Bmax = 721 ± 313 vs. 1145 ± 293 fmol/mg protein) and an increase in the affinity for the ligand demonstrated by a lower dissociaton constant (Kd = 33 ± 10 vs. 44 ± 10 pM). A significant correlation between Bmax and Kd values was found in patients but not in controls. Our results support the notion that bulimia nervosa is associated with a reduction in platelet serotonin transporter density. In addition, our study is the first to report that this reduced transporter density in women with bulimia nervosa is accompanied by an increase in the affinity of the transporter for the ligand.
Bulimia nervosa is characterised by recurrent episodes of binge eating and compensatory behaviour to prevent weight gain, e.g. self-induced vomiting. The disorder is much more common in women than in men (Halmi, 2002 and Mehler, 2003). An involvement of serotonin in this condition gains support mainly from the fact that treatment with serotonin reuptake inhibitors leads to a symptom reduction (Kaye et al., 1998, McElroy et al., 2000 and Arnold et al., 2002) but also from reports suggesting that subjects with bulimia display decreased concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid in cerebrospinal fluid (Jimerson et al., 1992) and blunted prolactin responses to a variety of serotonergic agents (for references, see Brewerton, 1995). The serotonin transporter expressed in platelets is identical to that found in brain (Lesch et al., 1993 and Ozaki et al., 1994). The binding of tritiated serotonin reuptake inhibitors to platelets has been studied in patients suffering from putative serotonin-related psychiatric disorders as an indirect measure of brain serotonergic activity. In contrast to the notorious difficulty in finding biological markers that are consistently aberrant in groups of psychiatric patients, a majority of these studies have in fact revealed a reduced density of platelet serotonin transporter binding sites in patients with, for example, depression (Briley et al., 1980, Nemeroff et al., 1994 and Alvarez et al., 1999), obsessive–compulsive disorder (Marazziti et al., 1996 and Sallee et al., 1996), premenstrual dysphoria (Rojansky et al., 1991 and Melke et al., 2003), and panic disorder (Marazziti et al., 1999 and Neuger et al., 2000). The purpose of this study was to determine if it is possible to replicate that women with bulimia nervosa differ from controls with respect to the number and affinity of platelet serotonin transporters using the tritiated selective serotonin reuptake inhibitor paroxetine as ligand.