Platelet Serotonin Transporter in Depressed Children and Adolescents: 3H‐Paroxetine Platelet Binding Before and After Sertraline

Sallee, Floyd R.; Hilal, Raouf; Dougherty, Doug; Beach, Kevin; Nesbitt, Lori A.

doi:10.1097/00004583-199807000-00018

Cited by 31 publications

(15 citation statements)

References 39 publications

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“…In particular, the B max of [ 3 H]-Par binding, at t 0 was similar in 27 depressed patients and control subjects, albeit significantly lower in those patients at the first episode, and decreased after three months of treatment with fluoxetine or clomipramine 27. The same result was obtained in a sample of 24 depressed children and adolescents after six weeks and also after six months of sertraline 26. On the contrary, sertraline given for six months to a small sample (n = 10) of adult depressed patients seemed to provoke an increased B max of [ 3 H]-Par binding, while paroxetine led to the opposite findings in another 10 patients 28.…”

Section: Discussionsupporting

confidence: 66%

Trazodone effects on [3H]-paroxetine and α2-adrenoreceptors in platelets of patients with major depression

Marazziti

Consoli²,

Golia³

et al. 2010

NDT

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Trazodone is an antidepressant which behaves as a selective 5-HT2 antagonist and 5-HT reuptake inhibitor. The lack of information on its effects in vivo prompted us to evaluate α2-adrenoceptors by means of the specific binding of [3H]-rauwolscine, and the 5-HT transporter (SERT) by means of the binding of [3H]-paroxetine ([3H]-Par), in platelets of depressed patients, before and after one month of treatment with trazodone (75–300 mg/day). Twenty-five outpatients of both sexes with a diagnosis of major depression, as assessed by the Structured Clinical Interview for DSM IV, were included in the study. Depressive symptoms were evaluated by means of the Hamilton Rating Scale for Depression: the total score (mean ± SD) was 20 ± 6 at baseline (t0) and 7 ± 4 after one month of treatment (t1). Platelet membranes, [3H]- rauwolscine and [3H]-Par bindings were carried out according to standardized protocols. The results showed that the Bmax values of [3H]-Par were statistically lower at t1 than at t0 (733 ± 30 vs 1471 ± 99, P < 0.001), while the Kd and the [3H]-rauwolscine binding parameters remained unchanged. The findings of this study suggest that in vivo trazodone modifies the number of the SERT proteins and that, perhaps, most of its antidepressant properties are related to this activity.

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Section: Discussionsupporting

confidence: 66%

Trazodone effects on [3H]-paroxetine and α2-adrenoreceptors in platelets of patients with major depression

Marazziti

Consoli²,

Golia³

et al. 2010

NDT

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“…Our finding of no association of 5-HTTLPR genotype with sex agrees with results of other studies. 92,[106][107][108] Paradoxically, estradiol therapy increases the expression of the 5-HTT gene and the number of 5-HTT binding sites in several brain regions. [109][110][111] However, in a postmortem human brain study, Hernandez and Sokolov 112 found no association between 5-HTT messenger RNA levels and sex.…”

Section: Commentmentioning

confidence: 99%

A Serotonin Transporter Gene Promoter Polymorphism (5-HTTLPR) and Prefrontal Cortical Binding in Major Depression and Suicide

Mann¹,

Huang²,

Underwood³

et al. 2000

Arch Gen Psychiatry

558

303

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A diffuse reduction of 5-HTT binding in the PFC of individuals with major depression may reflect a widespread impairment of serotonergic function consistent with the range of psychopathologic features in major depression. The localized reduction in 5-HTT binding in the ventral PFC of suicides may reflect reduced serotonin input to that brain region, underlying the predisposition to act on suicidal thoughts. The 5-HTTLPR genotype was not related to the level of 5-HTT binding and does not explain why 5-HTT binding is lower in major depression or suicide. Arch Gen Psychiatry. 2000;57:729-738

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“…4,8,9 This was the a priori hypothesis of our study. SSRIs inhibit serotonin uptake into platelets, 11,26,27 block intracellular calcium mobilization, 28 and are associated with an increase in bleeding time. 13,29 These are the proposed mechanisms for the reduced platelet activity 10,11 and the increased bleeding risk observed with SSRI therapy.…”

Section: Depression Ssris and Platelet Functionmentioning

confidence: 99%

Selective Serotonin Reuptake Inhibitors and Myocardial Infarction

Sauer

Berlin²,

Kimmel³

2001

Circulation

269

106

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Background-Depression is an independent risk factor for myocardial infarction (MI). Selective serotonin reuptake inhibitors (SSRIs) may reduce this risk through attenuation of serotonin-mediated platelet activation in addition to treatment of depression itself. Methods and Results-A case-control study of first MI in smokers 30 to 65 years of age was conducted among all 68 hospitals in an 8-county area during a 28-month period. Cases were patients hospitalized with a first MI. Approximately 4 community control subjects per case were randomly selected from the same geographic area using random digit dialing. Detailed information regarding use of antidepressant medication as well as other clinical and demographic data were obtained by telephone interview. A total of 653 cases of first MI and 2990 control subjects participated. After adjustment, using multivariable logistic regression, for age, sex, race, education, exercise, quantity smoked per day, body mass index, aspirin use, family history of MI, number of physician encounters, and history of coronary disease, diabetes, hypertension, or hypercholesterolemia, the odds ratio for MI among current SSRI users compared with nonusers was 0.35 (95% CI 0.18, 0.68; PϽ0.01). Non-SSRI antidepressant users had a nonsignificant reduction in MI risk with wide confidence intervals (adjusted odds ratio 0.48, CI 0.17, 1.32; Pϭ0.15). However, analysis of this group was limited by the small number of exposed subjects. Conclusions-The use of SSRIs may confer a protective effect against MI. This could be attributable to the inhibitory effect SSRIs have on serotonin-mediated platelet activation or possibly amelioration of other factors associated with increased risk for MI in depression.

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Platelet Serotonin Transporter in Depressed Children and Adolescents: 3H‐Paroxetine Platelet Binding Before and After Sertraline

Cited by 31 publications

References 39 publications

Trazodone effects on [3H]-paroxetine and α2-adrenoreceptors in platelets of patients with major depression

Trazodone effects on [3H]-paroxetine and α2-adrenoreceptors in platelets of patients with major depression

A Serotonin Transporter Gene Promoter Polymorphism (5-HTTLPR) and Prefrontal Cortical Binding in Major Depression and Suicide

Selective Serotonin Reuptake Inhibitors and Myocardial Infarction

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Platelet Serotonin Transporter in Depressed Children and Adolescents: 3H‐Paroxetine Platelet Binding Before and After Sertraline

Cited by 31 publications

References 39 publications

Trazodone effects on [3H]-paroxetine and &alpha;2-adrenoreceptors in platelets of patients with major depression

Trazodone effects on [3H]-paroxetine and &alpha;2-adrenoreceptors in platelets of patients with major depression

A Serotonin Transporter Gene Promoter Polymorphism (5-HTTLPR) and Prefrontal Cortical Binding in Major Depression and Suicide

Selective Serotonin Reuptake Inhibitors and Myocardial Infarction

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Trazodone effects on [3H]-paroxetine and α2-adrenoreceptors in platelets of patients with major depression

Trazodone effects on [3H]-paroxetine and α2-adrenoreceptors in platelets of patients with major depression