TY - JOUR
T1 - A biomarker to differentiate between primary and cocaine-induced major depression in cocaine use disorder: The role of platelet IRAS/nischarin (I1-imidazoline receptor)
AU - Keller, Benjamin
AU - Mestre-Pinto, Joan Ignasi
AU - álvaro-Bartolomé, María
AU - Martinez-Sanvisens, Diana
AU - Farre, Magí
AU - García-Fuster, M. Julia
AU - García-Sevilla, Jesús A.
AU - Torrens, Marta
AU - Fonseca, F.
AU - Mateus, J.
AU - Papaseit, E.
AU - Pérez-Mañá, C.
AU - Rodríguez-Minguela, R.
AU - Rossi, P.
AU - Tamarit, C.
AU - Vallecillo, G.
PY - 2017/12/1
Y1 - 2017/12/1
N2 - © 2017 Keller, Mestre-Pinto, álvaro-Bartolomé, Martinez-Sanvisens, Farre, García-Fuster, García-Sevilla and Torrens. 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.
AB - © 2017 Keller, Mestre-Pinto, álvaro-Bartolomé, Martinez-Sanvisens, Farre, García-Fuster, García-Sevilla and Torrens. 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.
KW - Acute tryptophan depletion
KW - Antidepressant drugs
KW - Cocaine use disorder
KW - Cocaine-induced depression
KW - IRAS/nischarin
KW - Major depressive disorder
KW - Platelet biomarker
U2 - https://doi.org/10.3389/fpsyt.2017.00258
DO - https://doi.org/10.3389/fpsyt.2017.00258
M3 - Article
VL - 8
IS - DEC
M1 - 258
ER -