Sex-specific attentional deficits in adult vitamin D deficient BALB/c mice

Groves, Natalie J.; Burne, Thomas H. J.

doi:10.1016/j.physbeh.2016.01.033

Cited by 22 publications

(17 citation statements)

References 43 publications

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“…Vitamin D deficiency has also been examined in adult mice. Similar findings were observed here, as it was shown that males were the only sex affected, with vitamin D-deficient males showing an increase in reaction time, less accurate performance, and more inattentive errors in the 5CSRTT, while there were no adverse effects of vitamin D deficiency in females [34].…”

Section: Sex Differences In Animals In Attention and Impulsive Actionsupporting

confidence: 90%

Let’s call the whole thing off: evaluating gender and sex differences in executive function

Grissom

Reyes

2018

Neuropsychopharmacol

201

144

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The executive functions allow for purposeful, deliberate, and intentional interactions with the world-attention and focus, impulse control, decision making, and working memory. These measures have been correlated with academic outcomes and quality of life, and are impacted by deleterious environmental events throughout the life span, including gestational and early life insults. This review will address the topic of sex differences in executive function including a discussion of differences arising in response to developmental programming. Work on gender differences in human studies and sex differences in animal research will be reviewed. Overall, we find little support for significant gender or sex differences in executive function. An important variable that factors into the interpretation of potential sex differences include differing developmental trajectories. We conclude by discussing future directions for the field and a brief discussion of biological mechanisms.

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Section: Sex Differences In Animals In Attention and Impulsive Actionsupporting

confidence: 90%

Let’s call the whole thing off: evaluating gender and sex differences in executive function

Grissom

Reyes

2018

Neuropsychopharmacol

201

144

View full text Add to dashboard Cite

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“…Vitamin D deficiency during pregnancy results in sex‐specific dysregulation of placental inflammation in mice and rats [Ali, Cui, Alexander, & Eyles, ; Liu et al, ]. Gender differences in the metabolism of vitamin D3 and its interaction with estrogen production [Bertone‐Johnson, Chocano‐Bedoya, Zagarins, Micka, & Ronnenberg, ; Correale et al, ; Lee et al, ] are congruent with sex‐specific health effects induced by vitamin D deficiency [Stadlmayr et al, ; Verdoia et al, ] including attentional deficits [Groves & Burne, ] and sex‐specific effects of vitamin D supplementation [Al‐Daghri et al, ] and stronger protective effects in females against other conditions [Fereidan‐Esfahani, Ramagopalan, Etemadifar, Sadri, & Abtahi, ].…”

Section: Discussionmentioning

confidence: 99%

Neonatal vitamin D status in relation to autism spectrum disorder and developmental delay in the CHARGE case–control study

et al. 2019

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Vitamin D appears essential for normal neurodevelopment and cognitive and behavioral function. We examined neonatal vitamin D in relation to the child's later diagnosis of autism spectrum disorder (ASD) or developmental delay (DD). Children aged 24-60 months enrolled in the population-based CHARGE case-control study were evaluated clinically for ASD (n = 357), DD (n = 134), or typical development (TD, n = 234) at the MIND Institute (Sacramento, CA) using standardized assessments. Total 25-hydroxyvitamin D (25[OH]D) was measured using sensitive isotope dilution liquid chromatography-tandem mass spectrometry in archived dried blood spots collected for the California Department of Public Health's Newborn Screening Program. Multinomial logistic regression was used to calculate ORs as measures of the associations between 25 nmol/L change in 25(OH)D and ASD and DD. Associations between 25(OH)D and scores on Mullen Scales of Early Learning and Vineland Adaptive Behavior Scales were assessed using robust linear regression. Effect modification was examined using stratified models and interaction product terms.Unadjusted mean (SD) 25(OH)D was lower for DD (73.2 [37.6]) than for TD (82.7 [39.3]) and ASD (80.1 [37.4]). After adjustment for maternal prepregnancy body mass index and education, a 25 nmol/L increase in total 25(OH)D was not associated with ASD (OR = 0.97; CI: 0.87-1.08) or DD (OR = 0.91; 95% CI: 0.78-1.06). Neonatal 25(OH)D was associated with significantly reduced ASD only in females (adjusted OR = 0.74; 95% CI: 0.55-0.99, P interaction = 0.03), and significantly reduced DD only in non-Hispanic white children (adjusted OR = 0.79; 95% CI: 0.63-0.98, P interaction = 0.11 for Hispanic, P interaction = 0.31 for other), driven by DD children with trisomy 21. This study provides evidence that neonatal vitamin D could be associated with ASD in females and with DD in non-Hispanic white children. Autism Res 2019, 12: 976-988.Lay Summary: Vitamin D appears essential for brain development and function. We examined neonatal total 25hydroxyvitamin D (25[OH]D) measured in dried blood spots in relation to later diagnoses of autism spectrum disorder (ASD) or developmental delay (DD) and related assessment scores. Higher neonatal 25(OH)D was associated with a 26% reduction in the odds for ASD only in females. After taking into account factors that could contribute to vitamin D status, a significant association with 21% reduced odds for DD was found only in non-Hispanic white children. Though results were nonsignificant overall, certain subgroups might benefit from higher neonatal vitamin D.

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“…This VD3 action probably alters genes involved in glutamatergic and GABAergic neurotransmissions, calcium regulation, as well as neurotrophic factors and genes involved in neuroprotection [13]. VD3 deficiency may have a negative influence on critical processes necessary for brain function, as neurotransmission, synapse formation, synaptic plasticity, and dendritic arborization [14]. Furthermore, VD3 deficiency does act as a risk factor for PD development [15].…”

Section: Introductionmentioning

confidence: 99%

Vitamin D protects dopaminergic neurons against neuroinflammation and oxidative stress in hemiparkinsonian rats

Lima

Lopes

Costa

et al. 2018

J Neuroinflammation

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BackgroundThe deficiency in 1α, 25-dihydroxyvitamin D3 (VD3) seems to increase the risk for neurodegenerative pathologies, including Parkinson’s disease (PD). The majority of its actions are mediated by the transcription factor, VD3 receptor (VD3R).MethodsThe neuroprotective effects of VD3 were investigated on a PD model. Male Wistar rats were divided into the following groups: sham-operated (SO), 6-OHDA-lesioned (non-treated), and 6-OHDA-lesioned and treated with VD3 (7 days before the lesion, pre-treatment or for 14 days after the 6-OHDA striatal lesion, post-treatment). Afterwards, the animals were subjected to behavioral tests and euthanized for striatal neurochemical and immunohistochemical assays. The data were analyzed by ANOVA and the Tukey test and considered significant for p < 0.05.ResultsWe showed that pre- or post-treatments with VD3 reversed behavioral changes and improved the decreased DA contents of the 6-OHDA group. In addition, VD3 reduced the oxidative stress, increased (TH and DAT), and reduced (TNF-alpha) immunostainings in the lesioned striata. While significant decreases in VD3R immunoreactivity were observed after the 6-OHDA lesion, these changes were blocked after VD3 pre- or post-treatments. We showed that VD3 offers neuroprotection, decreasing behavioral changes, DA depletion, and oxidative stress. In addition, it reverses partially or completely TH, DAT, TNF-alpha, and VD3R decreases of immunoreactivities in the non-treated 6-OHDA group.ConclusionsTaken together, VD3 effects could result from its anti-inflammatory and antioxidant actions and from its actions on VD3R. These findings should stimulate translational research towards the VD3 potential for prevention or treatment of neurodegenerative diseases, as PD.Electronic supplementary materialThe online version of this article (10.1186/s12974-018-1266-6) contains supplementary material, which is available to authorized users.

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Sex-specific attentional deficits in adult vitamin D deficient BALB/c mice

Cited by 22 publications

References 43 publications

Let’s call the whole thing off: evaluating gender and sex differences in executive function

Let’s call the whole thing off: evaluating gender and sex differences in executive function

Neonatal vitamin D status in relation to autism spectrum disorder and developmental delay in the CHARGE case–control study

Vitamin D protects dopaminergic neurons against neuroinflammation and oxidative stress in hemiparkinsonian rats

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