Journal
INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY
Volume 5, Issue 1, Pages 37-46Publisher
OXFORD UNIV PRESS
DOI: 10.1017/S1461145701002759
Keywords
antidepressants; bupropion; clonidine; imidazoline receptors; platelets
Funding
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH057601, R01MH049248] Funding Source: NIH RePORTER
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An elevation of I-1 (imidazoline-I)-binding sites on platelets may be a state marker for depression. Herein, platelet 1, sites were compared in two groups of unipolar depressed patients given different regimens of bupropion treatment: Regimen 1 (n = 13 titrated up to 300 mg/d by week 4 and held constant until week 6); Regimen 2 (n = 15 titrated up to 300 mg/d by week 2, to 450 mg/d by week 6, and held constant until week 8). Platelet I-1 sites were quantified by p-[I-125]iodoclonidine binding (0.5-15 nM) and displaced by moxonidine under a saturating concentration of norepinephrine to mask alpha(2)-adrenoceptors. I-1 B-max values were confirmed to be high at pretreatment in depressed patients (n = 28) compared to healthy control subjects (n; = 18; p = 0.02). Highest B-max values at pretreatment were found in patients who responded worst to treatment. More than two-thirds of patients recovered from depression (69 anti 80% in Regimens 1 and 2, respectively) after treatment. Dose and/or time of exposure to bupropion were relevant variables since (1) only Regimen 2 led to platelet I-1 down-regulation and (2) the extent of down-regulation correlated with plasma concentrations of bupropion. The data suggest a dissociation exists between I-1 down-regulation and therapeutic response, or else platelet I-1 down-regulation tags behind clinical antidepressant response before becoming measurable.
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