Τhe neuroprotective role of environmental enrichment against behavioral, morphological, neuroendocrine and molecular changes following chronic unpredictable mild stress: A systematic review

Dandi, Εvgenia; Spandou, Evangelia; Dalla, Christina; Tata, Despina Α.

doi:10.22541/au.166853524.46758325/v1

Cited by 1 publication

(1 citation statement)

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“…According to our initial hypothesis, long‐term VDD would exacerbate the detrimental effects of chronic stress on depressive‐like behaviour and memory in middle‐aged mice. This hypothesis was based on preclinical studies demonstrating decreased neuroplasticity and dysregulated neuroinflammation in response to UCMS (Dandi et al, 2023; Farooq et al, 2012; Koo et al, 2019; Mineur et al, 2007; Toth et al, 2008; Zhang et al, 2015) as well as the neuroprotective and anti‐inflammatory benefits of vitamin D (Boontanrart et al, 2016; Calvello et al, 2017; Dulla et al, 2016; Mayne & Burne, 2019). Although long‐term VDD during adulthood independently induced cognitive decline and reduced self‐care in middle‐aged mice, VDD did not exacerbate the negative effects of UCMS, disproving our initial hypothesis.…”

Section: Discussionmentioning

confidence: 99%

‘Unpredictable chronic mild stress does not exacerbate memory impairment or altered neuronal and glial plasticity in the hippocampus of middle‐aged vitamin D deficient mice’

Somelar‐Duracz,

Jürgenson,

Viil

et al. 2024

Eur J of Neuroscience

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Vitamin D deficiency is a worldwide health concern, especially in the elderly population. Much remains unknown about the relationship between vitamin D deficiency (VDD), stress‐induced cognitive dysfunctions and depressive‐like behaviour. In this study, 4‐month‐old male C57Bl/6J mice were fed with control or vitamin D free diet for 6 months, followed by unpredictable chronic stress (UCMS) for 8 weeks. VDD induced cognitive impairment and reduced grooming behaviour, but did not induce depressive‐like behaviour. While UCMS in vitamin D sufficient mice induced expected depressive‐like phenotype and impairments in the contextual fear memory, chronic stress did not manifest as an additional risk factor for memory impairments and depressive‐like behaviour in VDD mice. In fact, UCMS restored self‐care behaviour in VDD mice. At the histopathological level, VDD mice exhibited cell loss in the granule cell layer, reduced survival of newly generated cells, accompanied with an increased number of apoptotic cells and alterations in glial morphology in the hippocampus; however, these effects were not exacerbated by UCMS. Interestingly, UCMS reversed VDD induced loss of microglial cells. Moreover, tyrosine hydroxylase levels decreased in the striatum of VDD mice, but not in stressed VDD mice. These findings indicate that long‐term VDD in adulthood impairs cognition but does not augment behavioural response to UCMS in middle‐aged mice. While VDD caused cell loss and altered glial response in the DG of the hippocampus, these effects were not exacerbated by UCMS and could contribute to mechanisms regulating altered stress response.

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