Social enrichment reverses the isolation-induced deficits of neuronal plasticity in the hippocampus of male rats

Biggio, Francesca; Mostallino, Maria Cristina; Talani, Giuseppe; Locci, Valentina; Mostallino, Rafaela; Calandra, Gary B.; Sanna, Enrico; Biggio, Giovanni

doi:10.1016/j.neuropharm.2019.03.030

Cited by 54 publications

(47 citation statements)

References 62 publications

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“…Post-weaning environmental enrichment has been shown to increase BDNF in the hippocampus when compared to rats reared in standard or isolated conditions [59]. Furthermore, exposure to a socially enriched environment was able to restore the reduction in hippocampal BDNF induced by post-weaning social isolation [60] or by maternal separation [61]. Pre-weaning enrichment was also able to rescue animals from anxiety-like behaviors in adulthood induced by post-weaning maternal separation stress, while increasing BDNF content in the basolateral amygdala [62].…”

Section: Neurotrophic Proteinsmentioning

confidence: 96%

Neurosteroids and Neurotrophic Factors: What Is Their Promise as Biomarkers for Major Depression and PTSD?

Almeida

Barros

Pinna

2021

IJMS

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Even though major depressive disorder (MDD) and post-traumatic stress disorder (PTSD) are among the most prevalent and incapacitating mental illnesses in the world, their diagnosis still relies solely on the characterization of subjective symptoms (many of which are shared by multiple disorders) self-reported by patients. Thus, the need for objective measures that aid in the detection of and differentiation between psychiatric disorders becomes urgent. In this paper, we explore the potential of neurosteroids and neurotrophic proteins as biomarkers for MDD and PTSD. Circulating levels of the GABAergic neuroactive steroid, allopregnanolone, are diminished in MDD and PTSD patients, which corroborates the finding of depleted neurosteroid levels observed in animal models of these disorders. The neurotrophic protein, brain-derived neurotropic factor (BDNF), is also reduced in the periphery and in the brain of MDD patients and depressed-like animals that express lower neurosteroid levels. Although the role of BDNF in PTSD psychopathology seems less clear and merits more research, we propose a causal link between allopregnanolone levels and BDNF expression that could function as a biomarker axis for the diagnosis of both MDD and PTSD.

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Section: Neurotrophic Proteinsmentioning

confidence: 96%

Neurosteroids and Neurotrophic Factors: What Is Their Promise as Biomarkers for Major Depression and PTSD?

Almeida

Barros

Pinna

2021

IJMS

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“…Pre-op, pre-operation HDAC2 level was significantly decreased at 4 days after stroke in LV-shHDAC2-infected peri-infarct area (F 1,8 = 59.04, p < .001) (Figure 4b and c). Consistent with EE-mediated up-regulation of NGF and BDNF (Biggio et al, 2019), treatment with LV-shHDAC2 reversed stroke-induced down-regulation of NGF and BDNF in the peri-infarct area (For NGF: F 2,15 = 11.2, sham + LV-control vs. stroke + LV-control: p = .001; stroke + LV-control vs. stroke + LV-shHDAC2: p = .029. For BDNF: F 2,15 = 8.27, sham + LV-control vs. stroke + LV-control: p = .006; stroke + LV-control vs. stroke + LV-shHDAC2: p = .022) (Figure 4d).…”

Section: Hdac2 Knockdown Reverses Stroke-induced Neurotrophins Downmentioning

confidence: 59%

HDAC2 (Histone deacetylase 2): A critical factor in environmental enrichment‐mediated stroke recovery

Yang

Yao

et al. 2020

Journal of Neurochemistry

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Environmental enrichment (EE) is a generally accepted strategy to promote stroke recovery and its beneficial effect is positively correlated with neuroplasticity. However, the mechanisms underlying it remain elusive. Histone deacetylase 2 (HDAC2), a negative regulator of neuroplasticity, is up-regulated after stroke. Thus, we hypothesized that HDAC2 may participate in EE-mediated stroke recovery. In this study, focal stroke was induced by photothrombosis in male mice exposing to EE or standard housing (SH) conditions. Recombinant virus vectors, including Ad-HDAC2-Flag, AAV-CAG-EGFP-Cre, LV-shHDAC2, or their controls were microinjected into the motor cortex at 3 days before stroke. Grid-walking and cylinder tasks were conducted to assess motor function. Western blot and immunostaining were used to uncover the mechanisms underlying EE-mediated stroke recovery. We found that EE exposure reversed stroke-induced HDAC2 up-regulation, implicating HDAC2 in EE-mediated functional recovery. Importantly, EE-dependent stroke recovery was counteracted by over-expressing HDAC2, and HDAC2 knockdown promoted functional recovery from stroke to the similar extent as EE exposure. Moreover, the knockdown of HDAC2 epigenetically enhanced expressions of neurotrophins and neuroplasticityrelated proteins, with similar effects as EE, and consequently, whole brain and corticospinal tract (CST) rewiring. Together, our findings indicate that HDAC2 is critical for EE-dependent functional restoration. Precisely targeting HDAC2 may mimic EE and serve as a novel therapeutic strategy for stroke recovery.

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“…Indeed, it has been recently shown that, for example, social enrichment in the absence of further cognitive stimulation has a potent neurogenesis-stimulating potential (Moreno-Jiménez et al., 2019b) and might exert further beneficial effects on hippocampal plasticity. The exercise paradigm utilized in our study resembles social isolation due to housing in single cages, which has been associated with diminished neurogenesis (Dong et al., 2004), reduced DG, CA2/3 or total hippocampal volume (Fabricius et al., 2010), as well as altered neuronal tree arborization in the DG in rats (Biggio et al., 2019). However, the fact that observed DCX-positive neuron numbers in 6-month-old WT and Tg4-42 hom mice housed either under standard or isolation (BW) conditions were comparable argues against a major detrimental effect and supports studies that report no prolonged impact of social isolation on neurogenesis (Grégoire et al., 2014).…”

Section: Discussionmentioning

confidence: 99%

Physical Activity Ameliorates Impaired Hippocampal Neurogenesis in the Tg4-42 Mouse Model of Alzheimer’s Disease

et al. 2019

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There is growing evidence from epidemiological studies that especially midlife physical activity might exert a positive influence on the risk and progression of Alzheimer's disease. In this study, the Tg4-42 mouse model of Alzheimer's disease has been utilized to assess the effect of different housing conditions on structural changes in the hippocampus. Focusing on the dentate gyrus, we demonstrate that 6-month-old Tg4-42 mice have a reduced number of newborn neurons in comparison to age-matched wild-type mice. Housing these mice for 4 months with either unlimited or intermittent access to a running wheel resulted in a significant rescue of dentate gyrus neurogenesis. Although neither dentate gyrus volume nor neuron number could be modified in this Alzheimer's disease mouse model, unrestricted access to a running wheel significantly increased dentate gyrus volume and granule cell number in wild-type mice.

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Social enrichment reverses the isolation-induced deficits of neuronal plasticity in the hippocampus of male rats

Cited by 54 publications

References 62 publications

Neurosteroids and Neurotrophic Factors: What Is Their Promise as Biomarkers for Major Depression and PTSD?

Neurosteroids and Neurotrophic Factors: What Is Their Promise as Biomarkers for Major Depression and PTSD?

HDAC2 (Histone deacetylase 2): A critical factor in environmental enrichment‐mediated stroke recovery

Physical Activity Ameliorates Impaired Hippocampal Neurogenesis in the Tg4-42 Mouse Model of Alzheimer’s Disease

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