A Biomarker to Differentiate between Primary and Cocaine-Induced Major Depression in Cocaine Use Disorder: The Role of Platelet IRAS/Nischarin (I1-Imidazoline Receptor)
The association of cocaine use disorder (CUD) and comorbid major depressive disorder (MDD; CUD/MDD) is characterized by high prevalence and poor treatment outcomes. CUD/MDD may be primary (primary MDD) or cocaine-induced (CUD-induced MDD). Specific biomarkers are needed to improve diagnoses and ther...
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| Published in | Frontiers in psychiatry Vol. 8; p. 258 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
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01.12.2017
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| Abstract | The association of cocaine use disorder (CUD) and comorbid major depressive disorder (MDD; CUD/MDD) is characterized by high prevalence and poor treatment outcomes. CUD/MDD may be primary (primary MDD) or cocaine-induced (CUD-induced MDD). Specific biomarkers are needed to improve diagnoses and therapeutic approaches in this dual pathology. Platelet biomarkers [5-HT
receptor and imidazoline receptor antisera selected (IRAS)/nischarin] were assessed by Western blot in subjects with CUD and primary MDD (
= 16) or CUD-induced MDD (
= 9; antidepressant free, AD-; antidepressant treated, AD+) and controls (
= 10) at basal level and/or after acute tryptophan depletion (ATD). Basal platelet 5-HT
receptor (monomer) was reduced in comorbid CUD/MDD subjects (all patients: 43%) compared to healthy controls, and this down-regulation was independent of AD medication (decreases in AD-: 47%, and in AD+: 40%). No basal differences were found for IRAS/nischarin contents in AD+ and AD- comorbid CUD/MDD subjects. The comparison of IRAS/nischarin in the different subject groups during/after ATD showed opposite modulations (i.e., increases and decreases) in response to low plasma tryptophan levels with significant differences discriminating between the subgroups of CUD with primary MDD and CUD-induced MDD. These specific alterations suggested that platelet IRAS/nischarin might be useful as a biomarker to discriminate between primary and CUD-induced MDD in this dual pathology. |
|---|---|
| AbstractList | The association of cocaine use disorder (CUD) and comorbid major depressive disorder (MDD; CUD/MDD) is characterized by high prevalence and poor treatment outcomes. CUD/MDD may be primary (primary MDD) or cocaine-induced (CUD-induced MDD). Specific biomarkers are needed to improve diagnoses and therapeutic approaches in this dual pathology. Platelet biomarkers [5-HT
2A
receptor and imidazoline receptor antisera selected (IRAS)/nischarin] were assessed by Western blot in subjects with CUD and primary MDD (
n
= 16) or CUD-induced MDD (
n
= 9; antidepressant free, AD−; antidepressant treated, AD+) and controls (
n
= 10) at basal level and/or after acute tryptophan depletion (ATD). Basal platelet 5-HT
2A
receptor (monomer) was reduced in comorbid CUD/MDD subjects (all patients: 43%) compared to healthy controls, and this down-regulation was independent of AD medication (decreases in AD−: 47%, and in AD+: 40%). No basal differences were found for IRAS/nischarin contents in AD+ and AD− comorbid CUD/MDD subjects. The comparison of IRAS/nischarin in the different subject groups during/after ATD showed opposite modulations (i.e., increases and decreases) in response to low plasma tryptophan levels with significant differences discriminating between the subgroups of CUD with primary MDD and CUD-induced MDD. These specific alterations suggested that platelet IRAS/nischarin might be useful as a biomarker to discriminate between primary and CUD-induced MDD in this dual pathology. The association of cocaine use disorder (CUD) and comorbid major depressive disorder (MDD; CUD/MDD) is characterized by high prevalence and poor treatment outcomes. CUD/MDD may be primary (primary MDD) or cocaine-induced (CUD-induced MDD). Specific biomarkers are needed to improve diagnoses and therapeutic approaches in this dual pathology. Platelet biomarkers [5-HT2A receptor and imidazoline receptor antisera selected (IRAS)/nischarin] were assessed by Western blot in subjects with CUD and primary MDD (n = 16) or CUD-induced MDD (n = 9; antidepressant free, AD-; antidepressant treated, AD+) and controls (n = 10) at basal level and/or after acute tryptophan depletion (ATD). Basal platelet 5-HT2A receptor (monomer) was reduced in comorbid CUD/MDD subjects (all patients: 43%) compared to healthy controls, and this down-regulation was independent of AD medication (decreases in AD-: 47%, and in AD+: 40%). No basal differences were found for IRAS/nischarin contents in AD+ and AD- comorbid CUD/MDD subjects. The comparison of IRAS/nischarin in the different subject groups during/after ATD showed opposite modulations (i.e., increases and decreases) in response to low plasma tryptophan levels with significant differences discriminating between the subgroups of CUD with primary MDD and CUD-induced MDD. These specific alterations suggested that platelet IRAS/nischarin might be useful as a biomarker to discriminate between primary and CUD-induced MDD in this dual pathology.The association of cocaine use disorder (CUD) and comorbid major depressive disorder (MDD; CUD/MDD) is characterized by high prevalence and poor treatment outcomes. CUD/MDD may be primary (primary MDD) or cocaine-induced (CUD-induced MDD). Specific biomarkers are needed to improve diagnoses and therapeutic approaches in this dual pathology. Platelet biomarkers [5-HT2A receptor and imidazoline receptor antisera selected (IRAS)/nischarin] were assessed by Western blot in subjects with CUD and primary MDD (n = 16) or CUD-induced MDD (n = 9; antidepressant free, AD-; antidepressant treated, AD+) and controls (n = 10) at basal level and/or after acute tryptophan depletion (ATD). Basal platelet 5-HT2A receptor (monomer) was reduced in comorbid CUD/MDD subjects (all patients: 43%) compared to healthy controls, and this down-regulation was independent of AD medication (decreases in AD-: 47%, and in AD+: 40%). No basal differences were found for IRAS/nischarin contents in AD+ and AD- comorbid CUD/MDD subjects. The comparison of IRAS/nischarin in the different subject groups during/after ATD showed opposite modulations (i.e., increases and decreases) in response to low plasma tryptophan levels with significant differences discriminating between the subgroups of CUD with primary MDD and CUD-induced MDD. These specific alterations suggested that platelet IRAS/nischarin might be useful as a biomarker to discriminate between primary and CUD-induced MDD in this dual pathology. The association of cocaine use disorder (CUD) and comorbid major depressive disorder (MDD; CUD/MDD) is characterized by high prevalence and poor treatment outcomes. CUD/MDD may be primary (primary MDD) or cocaine-induced (CUD-induced MDD). Specific biomarkers are needed to improve diagnoses and therapeutic approaches in this dual pathology. Platelet biomarkers [5-HT receptor and imidazoline receptor antisera selected (IRAS)/nischarin] were assessed by Western blot in subjects with CUD and primary MDD ( = 16) or CUD-induced MDD ( = 9; antidepressant free, AD-; antidepressant treated, AD+) and controls ( = 10) at basal level and/or after acute tryptophan depletion (ATD). Basal platelet 5-HT receptor (monomer) was reduced in comorbid CUD/MDD subjects (all patients: 43%) compared to healthy controls, and this down-regulation was independent of AD medication (decreases in AD-: 47%, and in AD+: 40%). No basal differences were found for IRAS/nischarin contents in AD+ and AD- comorbid CUD/MDD subjects. The comparison of IRAS/nischarin in the different subject groups during/after ATD showed opposite modulations (i.e., increases and decreases) in response to low plasma tryptophan levels with significant differences discriminating between the subgroups of CUD with primary MDD and CUD-induced MDD. These specific alterations suggested that platelet IRAS/nischarin might be useful as a biomarker to discriminate between primary and CUD-induced MDD in this dual pathology. The association of cocaine use disorder (CUD) and comorbid major depressive disorder (MDD; CUD/MDD) is characterized by high prevalence and poor treatment outcomes. CUD/MDD may be primary (primary MDD) or cocaine-induced (CUD-induced MDD). Specific biomarkers are needed to improve diagnoses and therapeutic approaches in this dual pathology. Platelet biomarkers [5-HT2A receptor and imidazoline receptor antisera selected (IRAS)/nischarin] were assessed by Western blot in subjects with CUD and primary MDD (n = 16) or CUD-induced MDD (n = 9; antidepressant free, AD−; antidepressant treated, AD+) and controls (n = 10) at basal level and/or after acute tryptophan depletion (ATD). Basal platelet 5-HT2A receptor (monomer) was reduced in comorbid CUD/MDD subjects (all patients: 43%) compared to healthy controls, and this down-regulation was independent of AD medication (decreases in AD−: 47%, and in AD+: 40%). No basal differences were found for IRAS/nischarin contents in AD+ and AD− comorbid CUD/MDD subjects. The comparison of IRAS/nischarin in the different subject groups during/after ATD showed opposite modulations (i.e., increases and decreases) in response to low plasma tryptophan levels with significant differences discriminating between the subgroups of CUD with primary MDD and CUD-induced MDD. These specific alterations suggested that platelet IRAS/nischarin might be useful as a biomarker to discriminate between primary and CUD-induced MDD in this dual pathology. |
| Author | Keller, Benjamin García-Sevilla, Jesús A. Torrens, Marta Martinez-Sanvisens, Diana Mestre-Pinto, Joan-Ignasi Farre, Magí García-Fuster, M. Julia Álvaro-Bartolomé, María |
| AuthorAffiliation | 1 Laboratori de Neurofarmacologia, IUNICS, Universitat de les Illes Balears (UIB), Fundació Institut d’Investigació Sanitària Illes Balears (IdISBa) , Palma, Majorca , Spain 2 Redes Temáticas de Investigación Cooperativa en Salud – Red de Trastornos Adictivos (RETICS-RTA), Instituto de Salud Carlos III (ISCIII) , Madrid , Spain 4 Hospital Universitari Germans Trias i Pujol (IGTP) , Badalona , Spain 5 Universitat Autònoma de Barcelona (UAB) , Barcelona , Spain 3 Hospital del Mar Medical Research Institute (IMIM), Institut de Neuropsiquiatria i addiccions (INAD) , Barcelona , Spain |
| AuthorAffiliation_xml | – name: 1 Laboratori de Neurofarmacologia, IUNICS, Universitat de les Illes Balears (UIB), Fundació Institut d’Investigació Sanitària Illes Balears (IdISBa) , Palma, Majorca , Spain – name: 2 Redes Temáticas de Investigación Cooperativa en Salud – Red de Trastornos Adictivos (RETICS-RTA), Instituto de Salud Carlos III (ISCIII) , Madrid , Spain – name: 3 Hospital del Mar Medical Research Institute (IMIM), Institut de Neuropsiquiatria i addiccions (INAD) , Barcelona , Spain – name: 4 Hospital Universitari Germans Trias i Pujol (IGTP) , Badalona , Spain – name: 5 Universitat Autònoma de Barcelona (UAB) , Barcelona , Spain |
| Author_xml | – sequence: 1 givenname: Benjamin surname: Keller fullname: Keller, Benjamin – sequence: 2 givenname: Joan-Ignasi surname: Mestre-Pinto fullname: Mestre-Pinto, Joan-Ignasi – sequence: 3 givenname: María surname: Álvaro-Bartolomé fullname: Álvaro-Bartolomé, María – sequence: 4 givenname: Diana surname: Martinez-Sanvisens fullname: Martinez-Sanvisens, Diana – sequence: 5 givenname: Magí surname: Farre fullname: Farre, Magí – sequence: 6 givenname: M. Julia surname: García-Fuster fullname: García-Fuster, M. Julia – sequence: 7 givenname: Jesús A. surname: García-Sevilla fullname: García-Sevilla, Jesús A. – sequence: 8 givenname: Marta surname: Torrens fullname: Torrens, Marta |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29326609$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_1371_journal_pone_0213791 crossref_primary_10_3390_jcm9124103 crossref_primary_10_1016_j_jare_2023_01_020 crossref_primary_10_1038_s41388_021_02150_4 |
| Cites_doi | 10.1176/appi.ajp.2012.12010112 10.1001/archpsyc.1990.01810170011002 10.1136/jnnp.23.1.56 10.1111/j.1360-0443.2012.04010.x 10.1196/annals.1304.001 10.1002/jbm.820270516 10.1176/appi.ajp.161.7.1231 10.1016/j.drugalcdep.2004.09.004 10.1016/j.biopsych.2011.06.010 10.1016/j.jpsychires.2006.10.011 10.1016/S0025-7753(03)73814-7 10.1016/j.jad.2016.10.007 10.1016/j.ejphar.2017.02.028 10.5498/wjp.v2.i6.114 10.1016/j.drugalcdep.2010.07.013 10.1016/j.ejphar.2017.09.011 10.1016/0006-3223(90)90576-N 10.20882/adicciones.868 10.1038/nn.2529 10.1016/j.bbamcr.2010.08.010 10.1371/journal.pone.0118610 10.1016/0006-3223(94)90033-7 10.1046/j.1471-4159.1999.721641.x 10.1038/sj.npp.1300356 10.1089/10445490050043290 10.3109/10826084.2012.663296 10.1016/0024-3205(74)90440-8 10.1111/adb.12107 10.1016/j.jad.2005.11.016 10.3389/fpsyt.2015.00017 10.1503/jpn.120209 10.1016/j.jemermed.2005.01.019 10.1016/j.psychres.2012.07.043 10.1176/ajp.2006.163.4.689 10.1016/j.ejphar.2011.03.038 10.1111/adb.12156 10.1016/S0006-3223(96)00493-3 10.1177/0269881115586936 10.1083/jcb.151.6.1141 |
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| Copyright | Copyright © 2017 Keller, Mestre-Pinto, Álvaro-Bartolomé, Martinez-Sanvisens, Farre, García-Fuster, García-Sevilla and Torrens. 2017 Keller, Mestre-Pinto, Álvaro-Bartolomé, Martinez-Sanvisens, Farre, García-Fuster, García-Sevilla and Torrens |
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| Keywords | acute tryptophan depletion cocaine use disorder major depressive disorder IRAS/nischarin antidepressant drugs cocaine-induced depression platelet biomarker |
| Language | English |
| License | This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These senior authors have equally supervised the research. Reviewed by: Noelia Weisstaub, Institute of Cognitive and Translational Neuroscience (INCYT), Argentina; Domenico De Berardis, NHS England, United Kingdom Edited by: Marijn Lijffijt, Baylor College of Medicine, United States NEURODEP Group: F. Fonseca, J. Mateus, E. Papaseit, C. Pérez-Mañá, R. Rodríguez-Minguela, P. Rossi, C. Tamarit, G. Vallecillo. Specialty section: This article was submitted to Addictive Disorders, a section of the journal Frontiers in Psychiatry |
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| SubjectTerms | acute tryptophan depletion cocaine use disorder cocaine-induced depression IRAS/nischarin major depressive disorder platelet biomarker Psychiatry |
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| Title | A Biomarker to Differentiate between Primary and Cocaine-Induced Major Depression in Cocaine Use Disorder: The Role of Platelet IRAS/Nischarin (I1-Imidazoline Receptor) |
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