Table 4. Summary of 14 studies investigating miRNA expression in animal models after AD use.
Abbreviations: CT - non-stressed control, CMS - chronic mild stress, CUS - chronic unpredictable stress, vDG - ventral dentate gyrus, NAc - nucleus accumbens, dDG - dorsal dentate gyrus, CUMS - chronic unpredictable mild stress, PFC - prefrontal cortex, miRNA - microRNA
| Author/year | Population | Treatment | Sample | MicroRNAs in depression | MicroRNAs after treatment |
| Issler et al. [25], 2014 (Israel) | Mice - social defeat, mice treated | Tricyclic, imipramine, fluoxetine or reboxetine | Raphe nuclei, blood | Reduced: miR-135a in blood | Imipramine and fluoxetine, increased: miR-135a in raphe nuclei SSRI, increased: miR-135a in blood |
| Patricio et al. [49], 2020 (Portugal) | Non-stressed control (N=10-12), CMS group (N=10-12), CMS+fluoxetine (N=10-12) | Fluoxetine | Brain, blood | Increased: miRNA-409-5p in the NAc | Increased: miR-409-5p in vDG, reduced: miR-411-5p in the dDG, reduced: miR-409-5p and miR-411-5p in blood |
| Lo Iacono et al. [50], 2021 (Italy) | Knockout (TKO) mice, wild-type (WT) mice | Fluoxetine | Dorsal raphe | Chronic treatment, increased: miR-34a in WT mice | |
| Zhang et al. [51], 2015 (China) | Normal control (NOR, n=15), maternal deprivation (MD, n=12), chronic unpredictable stress (CUS, n=11), MD with CUS (MD+CUS, n=11) | Escitalopram | NAc and the striatum | Increased: miR-326 in NAc, decreased: miR-9 in NAc and striatum, decreased: miR-326 in striatum | Reverted the miR-326 to normal levels in NAc |
| Song et al. [52], 2019 (China) | Control group (N=8), CUMS group + escitalopram (N=8), CUMS not treated (N=8) | Escitalopram | Nac | Reduced: miR-10b-5p, increased: miR- 214-3p | Increased: miR-10b-5p, reduced: miR-214-3p |
| Xie et al. [53], 2019 (China) | Controls (N=8), imipramine (N=8), fluoxetine (N=8) | Imipramine, fluoxetine, reboxetine | Dorsal raphe nucleus | Reduced: miR-26 | Imipramine and fluoxetine, increased: miR-26a-2 |
| Grieco et al. [54], 2017 (USA) | C57BL/6 wild-type and homozygous GSK3α/β 21A/21A/9A/9A knockin mice | Ketamine, 2,3-dihdroxyl-6-nitro-7-sulfamoylbenzo(f)quinoxaline-2, 3-dione or fluoxetine | Hippocampus and PFC | Ketamine Increased: miR-764-5p, miR-1912-3p, miR-1264-3p, miR-1298-5p, and miR-448-3p in the hippocampus | |
| Wan et al. [55], 2018 (China) | CUMS Controls | Ketamine | PFC | Reduced: miR-29b-3p | Increased: miR-29b-3p |
| Mingardi et al. [56], 2021 (Italy) | 72 Sprague-Dawley male rats, divided according to vulnerability or resilience to CMS, and CMS-vulnerable rats were evenly randomized to ketamine or saline | Racemic ketamine (10 mg/kg) - single dose | Hipoccampus (brain tissue and cell culture) | Ketamine restored original miR-9-5p levels, which was correlated with higher sucrose preference/less anhedonic phenotype in rats, and increased dendritic length in vitro | |
| Huang et al. [57], 2021 (China) | Control CSDS-resilient mice and saline- or ketamine administered CSDS-susceptible mice (n = 8 per group) | Ketamine (10 mg/kg), aline | Hippocampus and cortex | Reduced: miR-98-5p | Increased: miR-98-5p |
| Pan et al. [58],2015 (China) | 30 animals (mice): Control group Model group Duloxetine group CUMS | Duloxetine | Frontal lobe and hippocampus | Reduced: miR-132 and miR-18a in the hippocampus, increased: miR-134 and miR-124a | Increased: miR-132 and miR-18a in the hippocampus, decreased: miR-134 and miR-124a |
| Higuchi et al. [59], 2016 (Japan) | BALB mice CUMS, control | Imipramine | Hippocampus | Reduced: miR-124-1 and miR-29a | These effects were blocked by imipramine |
| Zeng et al. [60], 2023 (China) | Adult male BALB/c mice (18–22 g, 8 weeks old) CUMS | Fluoxetine | Hippocampus | Increased: miR-124 | Reduced: miR-124 levels |
| Guan et al. [61], 2023 (China) | Adult male C57BL6/J mice | Venlafaxine | Hippocampus | Increased: miR-204-5p | Reduced: miR-204-5p |