Trial reportJournal of psychiatric research2008
Platelet imidazoline receptors as state marker of depressive symptomatology.
Trial report in Journal of psychiatric research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 20 citations in OpenAlex.
- Moving beyond 5-HTPsychopharmacology · 2026Article
- The Influence of Serotonergic Signaling on Quality of Life, Depression, Insomnia, and Hypoxia in Obstructive Sleep Apnea Patients: Cross-Sectional Study.Journal of clinical medicine · 2025Article
- Antidepressant-like action of agmatine in the acute and sub-acute mouse models of depression: a receptor mechanism study.Metabolic brain disease · 2018Article
- A Biomarker to Differentiate between Primary and Cocaine-Induced Major Depression in Cocaine Use Disorder: The Role of Platelet IRAS/Nischarin (IFrontiers in psychiatry · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
objectivePrevious studies have shown that imidazoline receptors (IR-1) are increased in platelets and frontal cortex of depressed patients, and this up-regulation is normalized (down-regulated) after antidepressant drug treatments. It has been hypothesized that IR-1 up-regulation during the depressive episode may be a state marker for depressive symptomatology. The goal of the present study was to address the state versus trait question.
methodTwelve healthy subjects (six males and six females) met stringent inclusion and exclusion criteria for physical and mental health. They received desipramine for 6 weeks in order to simulate the length of time and dosing used previously to obtain an IR-1 down-regulation and a therapeutic response in depressed patients. Outcome and safety measures included clinical, psychological, and cardiovascular assessments obtained throughout the study. Plasma concentrations of desipramine were measured throughout the 6 weeks of treatment and again after 2 weeks following tapered discontinuation of desipramine. Platelet receptors were assessed by Western blotting and radioligand binding assays.
resultsHealthy subjects taking desipramine experienced mild dysphoric effects but there were no adverse events. The binding of 8 nM p-[(125)I]clonidine to IR-1 and alpha(2)-adrenoceptors in healthy subjects did not change during desipramine treatment. The immunodensity of the 33 kDa band associated with IR-1 gradually increased to a maximum, by week-6, of 26% higher than baseline (p < 0.01 compared to baseline). Two weeks after desipramine discontinuation, there was a decline in alpha(2)-adrenoceptor binding and 33 kDa band's immunodensity (p = 0.04).
conclusionsThe findings support the hypothesis that platelet IR-1 binding sites are a marker of mood state rather than of antidepressant-induced pharmacological regulation. By comparison, platelet alpha(2)-adrenoceptors appear to be regulated by desipramine as a pharmacological effect independent of mood state.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.