Model Dietary factor Intervention Cellular and molecular mechanisms Effects on behavior Conclusion/proposed mechanism Reference ICR strain male mice Acute fasting 3 h, 9 h, and 18 h or 9 h + i.p. injection of IMI (30 mg/kg) or 9 h + i.p. injection of IMI (30 mg/kg) + DOI (5 mg/kg) ↑ratio of p-CREB/CREB in 9 h fasting mice ↓depressive-like behavior (FST) in 9 h fasting mice, which was more pronounced in 9 h + IMI. Effects reversed by DOI Antidepressant-like effects of acute fasting possibly occur via ↑p-CREB/CREB ratio, and additive effects with IMI via modulation of 5-HT2 receptors [111 ] C57BL/6J mice 7-8 weeks of age CR Moderate 10–15% CR for 3 weeks after CR, a subset of mice was refed either with a high-fat or chow diet AL CR ↑stress-induced corticosterone levels, ↓BNST CRF levels and ↑BNST CRF promoter methylation ↑MCH and orexin among post-CR mice transitioned to high-fat diet CR ↑depressive-like behaviour (TST) ↑binge eating of palatable high-fat foods after CR MCH receptor-1 antagonist ↓total caloric intake in post-CR mice on high-fat diet Moderate CR reprogrammes pathways involved in regulating stress responsivity and orexigenic drives. Management of stress during diet may be beneficial in long-term maintenance [64 ] 20–22 g male ICR mice Trans-RES 10 mg/kg, 20 mg/kg, 40 mg/kg or 80 mg/kg via gavage, acute ↑hippocampal 5-HT and ↓MAO-A activity (40 or 80 mg/kg) ↓depressive-like behavior (FST: 20, 40, and 80 mg/kg; TST: 40 and 80 mg/kg) Antidepressant-like effects of trans-RES might be related, among others, to modulation of the 5-HT system [142 ] 180 g–200 g male Wistar rats RES or UCMS + RES 80 mg/kg, i.p., once daily for 5 weeks Prevented UCMS-induced ↑serum CORT, and ↓BDNF, pERK, and pCREB levels in the PFC and hippocampus Prevented UCMS-induced cognitive deficits (MWM; NORT) RES prevents UCMS-induced cognitive impairment partly via normalizing serum CORT levels and upregulating BDNF, pERK, and pCREB in the PFC and hippocampus [137 ] 200–250 g male Wistar rats CUR or UCMS + CUR 10 mg/kg via oral gavage, once daily for 3 weeks N/A Prevented UCMS-induced depressive phenotype (SP; OFT) CUR exerts antidepressant effects partially by preventing UCMS-induced ↑of TNF-
, IL-6, and NF-
B in the PFC and hippocampus [183 ] 18–22 g male Kun-Ming mice TPs or UCMS + TPs 25 mg/kg or 50 mg/kg by gavage once daily for 3 weeks from 3rd week on of UCMS Reversed hippocampal and prefrontal cortex alterations of 5-HT and NE Reversed UCMS-induced depressive-like behavior (FST, TST, SP, and OFT) Antidepressant action of TPs might be related to modulation of monoaminergic responses and ↑antioxidant defenses [143 ] 22–25 g male Kun-Ming mice RES or FLU 20 mg/kg or 40 mg/kg or 80 mg/kg (RES); 10 mg/kg (FLU), i.p., once daily for 21 days ↑BDNF and ERK levels in the hippocampus and PFC, ↓serum CORT ↓depressive-like behavior (FST and TST) Antidepressant-like actions of RES are probably mediated by modulation of the HPA axis, BDNF, and Erk levels in the hippocampal and PFC [138 ] 190 g–200 g male Sprague-Dawley rats Trans-RES 10 mg/kg, 20 mg/kg, 40 mg/kg or 80 mg/kg via gavage 30 min before the chronic stress for 21 days ↑5-HT levels in the frontal cortex, hippocampus, and hypothalamus (80 mg/kg); inhibited MAO-A activity in the frontal cortex and hippocampus (10–80 mg/kg) ↓depressive-like behavior (SP and shuttle box test: 40 and 80 mg/kg) Antidepressant-like effects of trans-resveratrol involves, among others, the regulation of 5-HT levels and MAO-A activity [144 ] 8-9-month-old C57BL/6J and SIRT1 mutant mice RES Intraventricular injection of RES (5
g/
L for a week) ↑LTP in CA1; ↑BDNF and CREB in hippocampal slices; ↓miR-134 and miR-124; effects blocked in SIRT1 mutant mice ↑fear memory (contextual and tone-dependent memory test); effects blocked in SIRT1 mutant mice RES exerts its effects via regulation of microRNA-CREB-BDNF mechanism, likely in a SIRT1 dependent way [130 ] 3-4-month-old female Wistar rats and PND40 offspring RES or RES + CRS 10 mg/kg orally administered throughout pregnancy ↑hippocampal DCX and BDNF N/A Resveratrol neuroprotects against prenatal stress likely via AHN improvement [140 ] 280–300 g female pregnant Sprague-Dawley rats; 15-week-old male offspring n-3 diet or n-3 def Gestation, lactation, and postnatal week 15 n-3 def ↓levels of DHA, NPY-1, BDNF and CREB; ↑GR in the frontal cortex, hypothalamus and hippocampus n-3 def ↑anxiety-like behavior in the OFT and EPM DHA deficiency during gestational and postnatal development ↓brain plasticity and compromises brain function in adulthood [184 ] 10-week-old virgin female Wistar rats and PND90 male offspring FO Adaptation period (15 days), mating (8 days), pregnancy (21 days), and nursing (21 days) ↑hippocampal and cortical BDNF; ↑hippocampal 5-HT ↓depressive phenotype (FST); effects reversed by 5-HT1A antagonist n-3 PUFA exert antidepressant effects likely via increase in hippocampal 5-HT transmission [185 ] 6-month-old male Wistar rats n-3 diet or n-3 def or n-3 diet + CRS or n-3 def + CRS 25 g/day from weaning to 3 months; 20 g/day until 6 months; CRS for 21 days N/A n-3 def ↓locomotor activity induced by CRS and ↑startle response n-3 deficiency may contribute to vulnerability to stress [186 ] 280–300 g female pregnant Sprague-Dawley rats; 12-week-old male offspring DHA or HFD DHA = from gestation to postnatal week 15; HFD = DHA from gestation to postnatal week 12 + HFD until 15 weeks Switch from DHA to HFD ↓DHA levels, NPY, BDNF, pCREB, GAP-43, pCAMKii, and p-syn expression in frontal cortex, and hippocampus Switch from DHA to HFD ↓locomotor activity in the OPF and ↑anxiety-like behavior in one of the measures of the EPM Transition from DHA to HFD ↓plasticity markers and is associated with increased anxiety [187 ] 8-week-old BAFF Tg PUFAs 12 weeks PUFAs restored AHN and LTP N/A PUFA can restore AHN in autoimmune mouse model [181 ] Female Sprague-Dawley rats and PND7 offspring n-3 PUFAs (dam) or n-3 PUFAs (dam) + sevoflurane (offspring) from pregnancy to PND14 (n-3 PUFAs); 6 h at PND7 (sevoflurane) n-3 PUFAs attenuated sevoflurane-induced neuronal apoptosis; ↑cell proliferation in the DG n-3 PUFAs restored fear response to footshock and ↑working and short-term memory (MWM) PUFA can improve altered memory and fear response in sevoflurane-treated rats via ↓apoptosis and ↑AHN [182 ] 280–300 g female pregnant Sprague-Dawley rats; 15-week-old male offspring n-3 diet or n-3 def or n-3 diet + WD or n-3 def + WD or n-3 diet + WD + FPI or n-3 def + WD + FPI n-3 diet or n-3 def during brain maturation; WD for 6 weeks at 8 weeks of age n-3 def + WD disrupted BDNF signaling (TrkB, CaMKII, Akt, and CREB) and ↓NPY-1 in the frontal cortex; more pronounced after FPI n-3 def + WD ↑anxiety-like behavior (EPM); more pronounced after FPI n-3 def + transition to WD might lower the threshold for neurological disorders via BDNF and NPY-1 signaling disruption [188 ]