Show simple item record Fonseca Casals, Francina, 1972- Mestre-Pintó, Juan Ignacio Gómez-Gómez, Àlex Martínez-Sanvisens, Diana Rodríguez-Minguela, Rocío Papaseit Fontanet, Esther Pérez Mañá, Clara Langohr, Klaus Valverde Granados, Olga Pozo Mendoza, Óscar J., 1975- Farré Albaladejo, Magí Pérez Mañá, Clara Neurodep Group 2021-10-19T07:08:13Z 2021-10-19T07:08:13Z 2020
dc.identifier.citation Fonseca F, Mestre-Pintó JI, Gómez-Gómez À, Martinez-Sanvisens D, Rodríguez-Minguela R, Papaseit E, et al. The tryptophan system in cocaine-induced depression. J Clin Med. 2020 Dec 19; 9(12): 4103. DOI: 10.3390/jcm9124103
dc.identifier.issn 2077-0383
dc.description.abstract Major depression disorder (MDD) is the most prevalent psychiatric comorbid condition in cocaine use disorder (CUD). The comorbid MDD might be primary-MDD (CUD-primary-MDD) or cocaine-induced MDD (CUD-induced-MDD), and their accurate diagnoses and treatment is a challenge for improving prognoses. This study aimed to assess the tryptophan/serotonin (Trp/5-HT) system with the acute tryptophan depletion test (ATD), and the kynurenine pathway in subjects with CUD-primary-MDD, CUD-induced-MDD, MDD and healthy controls. The ATD was performed with a randomized, double-blind, crossover, and placebo-controlled design. Markers of enzymatic activity of indoleamine 2,3-dioxygenase/tryptophan 2,3-dioxygenase, kynurenine aminotransferase (KAT) and kynureninase were also established. Following ATD, we observed a decrease in Trp levels in all groups. Comparison between CUD-induced-MDD and MDD revealed significant differences in 5-HT plasma concentrations (512 + 332 ng/mL vs. 107 + 127 ng/mL, p = 0.039) and the Kyn/5-HT ratio (11 + 15 vs. 112 + 136; p = 0.012), whereas there were no differences between CUD-primary-MDD and MDD. Effect size coefficients show a gradient for all targeted markers (d range 0.72-1.67). Results suggest different pathogenesis for CUD-induced-MDD, with lower participation of the tryptophan system, probably more related to other neurotransmitter pathways and accordingly suggesting the need for a different pharmacological treatment approach.
dc.description.sponsorship This work was supported by grants from the Instituto de Salud Carlos III–ISCIII Red de Trastornos Adictivos 2016 (RD16/0017/0010, RD16/0017/0003; Fondo de Investigación Sanitaria (FIS) (PI09/02121, PI12/01838, PI14/00178, PI16/00603); National R + D+I and funded by the Instituto de Salud Carlos III (ISCIII) and the European Regional Development Fund (FEDER) grant Juan Rodes (JR 16/00020); Ministerio de Sanidad, Política Social e Igualdad, Plan Nacional Sobre Drogas (PNSD) (2012I054); Suport Grups de Recerca AGAUR-Gencat (2017 SGR 316, 2017 SGR 530); Acció instrumental d’Intensificació de Professionals de la Salut - Facultatius especialistes (PERIS) (SLT006/17/00014); and Ministerio de Economía y Competitividad (MTM2015-64465-C2-1-R). The funding agencies had no role in study design, data collection, interpretation, or had influence on the writing.
dc.format.mimetype application/pdf
dc.language.iso eng
dc.publisher MDPI
dc.rights Copyright © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (
dc.title The tryptophan system in cocaine-induced depression
dc.type info:eu-repo/semantics/article
dc.subject.keyword Cocaine use disorder
dc.subject.keyword Kynurenine
dc.subject.keyword Primary/substance-induced depression
dc.subject.keyword Serotonin
dc.subject.keyword Tryptophan
dc.relation.projectID info:eu-repo/grantAgreement/ES/1PE/MTM2015-64465-C2-1-R
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/publishedVersion


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