ArticleMolecular neurobiology2019
Modulation of Monoaminergic Systems by Antidepressants in the Frontal Cortex of Rats After Chronic Mild Stress Exposure.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- From Stress to Neurodegeneration: A New Look at the Pathogenesis of Parkinson's Disease.Biomedicines · 2026Review
- Studying the potential ameliorative effect of biosynthesized selenium nanoparticles using epigallocatechin gallate against depression in rats.Frontiers in pharmacology · 2025Article
- Pathogenesis of Depression in Alzheimer's Disease.Neurochemical research · 2024Review
- Article
- Antidepressant-like Effects of Representative Types of Food and Their Possible Mechanisms.Molecules (Basel, Switzerland) · 2023Review
- Does Sertraline Affect Hypothalamic Food Intake Peptides in the Rat Experimental Model of Chronic Mild Stress-Induced Depression?Neurochemical research · 2022Article
- The miRNome of Depression.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The standard pharmacological treatment of the major depressive disorder (MDD) is still grounded in a monoaminergic approach. Consequently, antidepressant treatments pursue to heighten serotonergic and noradrenergic neurotransmissions. Thus, the aim of this study was to assess the impact of exposure to a well-characterized animal model, the chronic mild stress (CMS) on serotonin (5-HT) and noradrenaline (NE) levels, and reuptake transporters and receptors in the frontal cortex (FC) of CMS-exposed rats. Moreover, considering the diverse pharmacological profiles of existing antidepressants and the large number of patients not responding to treatments, we have investigated whether generally utilized antidepressants can modulate their expression. Male Wistar rats were exposed to CMS and some of them treated with desipramine, escitalopram, or duloxetine. Possible changes in the described monoaminergic neurotransmission elements were evaluated. CMS induced differences in the expression of reuptake transporters and receptors involved in the monoaminergic neurotransmission pointing towards the weakening of their signaling. CMS antidepressant-treated rats showed an improvement of the monoaminergic tone, being desipramine and duloxetine more influential than escitalopram over noradrenergic elements and having the three antidepressant-tested effects on serotonergic transmission. In summary, there are molecular alterations on the monoaminergic neurotransmission in FC induced by CMS exposure. Besides, antidepressant treatments modulate the elements of these neurotransmission systems differentially.
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