Table 2.
Effects of diet on brain plasticity in animal studies of mood/anxiety from 2010 onwards.
Model | Dietary factor | Intervention | Cellular and molecular mechanisms | Effects on behavior | Conclusion/proposed mechanism | Reference |
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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] |
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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] |
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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] |
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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] |
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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-α, IL-6, and NF-κB in the PFC and hippocampus | [183] |
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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] |
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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] |
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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] |
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8-9-month-old C57BL/6J and SIRT1 mutant mice | RES | Intraventricular injection of RES (5 µg/µL 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] |
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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] |
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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] |
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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] |
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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] |
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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] |
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8-week-old BAFF Tg | PUFAs | 12 weeks | PUFAs restored AHN and LTP | N/A | PUFA can restore AHN in autoimmune mouse model | [181] |
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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] |
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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] |
Effects of different proneural plasticity dietary interventions (CR, IF, and polyphenolic/fatty acid supplementation) on brain function and behavior in in recent animal studies (2010 onwards) of mood/anxiety. AHN: adult hippocampal neurogenesis; BDNF: brain-derived neurotrophic factor; BNST: bed nucleus of the stria terminalis; CORT: corticosterone; CREB: cAMP responsive-element binding; CRF: corticotropin-releasing factor; CRS: chronic restraint stress; CSA: continuous spontaneous alternation task; CUR: curcumin; DCX: doublecortin; DG: dentate gyrus; DHA: docosahexaenoic acid; DOI: serotoninergic 5-HT2A/2C receptor agonist (±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride; EPM: elevated plus maze test; 5-HT: 5-hydroxytryptamine; 5-HT1A: 5-hydroxytryptamine type 1A receptor; FLU: fluoxetine; FO: fish oil-supplemented diet; FPI: fluid percussion injury; FST: forced swimming test; GAP-43: growth-associated protein 43; GR: glucocorticoid receptor; HFD: high fat diet; IL-6: interleukin 6; IMI: imipramine; i.p.: interaperitoneal injection; LTP: long term potentiation; MAO-A: monoamine oxidase-A; MCH: melanin-concentrating hormone (MCH); MWM: Morris water maze; N/A: not assessed; NE: noradrenaline; NF-κB: nuclear factor kappa B; NORT: novel object recognition test; NPY-1: neuropeptide Y type 1 receptor; n-3 def: n-3 deficient diet; n-3 diet: n-3 adequate diet; OFT: open field test; p-CAMKii: Ca2+/calmodulin-dependent protein kinase II; pERK: phosphorylated extracellular signal-regulated kinase; PFC: prefrontal cortex; p-syn: phospho-synapsin; PUFA: polyunsaturated fatty acid-enriched diet; RES: resveratrol supplementation; SP: sucrose preference; TNF-α: tumor necrosis factor alpha; TPs: tea polyphenols; Trans-RES: trans-resveratrol; TrkB: tyrosine kinase receptor B; TST: tail suspension test; UCMS: unpredictable chronic mild stress; WD: western diet.