Transient prenatal vitamin D deficiency is associated with subtle alterations in learning and memory functions in adult rats

Becker, Axel; Eyles, Darryl W.; McGrath, John J.; Grecksch, Gisela

doi:10.1016/j.bbr.2005.02.015

Cited by 162 publications

(126 citation statements)

References 41 publications

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“…In support of these findings, vitamin D depletion in utero resulted in reduced levels of NGF and GDNF in addition to morphological brain changes in newborn rodents (Becker, Eyles et al 2005). These deleterious characteristics remained through adulthood (Becker, Eyles et al 2005).…”

Section: 25(oh) 2 D 3 and Neuronal Protectionmentioning

confidence: 53%

“…In animal models, treatment with 1, 25(OH) 2 D 3 increased GDNF concentrations and reduced oxidative stress in Parkinson's disease (Wang, Wu et al 2001). In support of these findings, vitamin D depletion in utero resulted in reduced levels of NGF and GDNF in addition to morphological brain changes in newborn rodents (Becker, Eyles et al 2005). These deleterious characteristics remained through adulthood (Becker, Eyles et al 2005).…”

Section: 25(oh) 2 D 3 and Neuronal Protectionmentioning

confidence: 67%

“…BsmI and TaqI carriers experienced impairments in memory and attention--domains most vulnerable to age related deterioration. Interestingly, the haplotype associated with better cognitive performance, ApaI in haplotype 1 (baT), is the same haplotype associated with increased risk of fractures (Uitterlinden, Pols et al 1996;Turner, Chen et al 2004;Uitterlinden, Fang et al 2004;Becker, Eyles et al 2005). Calcium concentrations did not vary across the phenotypes and suggest that vitamin D may be neuroprotective beyond its role in calcium regulation.…”

Section: Vitamin D and Neuronal Calcium Regulationmentioning

confidence: 99%

“…While some studies reported no observed impairments in working memory or anxiety in the VDR-KO model (Burne, JJ et al 2005), others showed anxiety-like behavior and behavioral impairment (Kalueff, Lou et al 2004;Kalueff, Keisala et al 2006). In embryonic animal models, vitamin D deficiency during fetal development resulted in morphological brain changes (Eyles, Brown et al 2003), motor impairments (Burne, Becker et al 2004) and memory and learning impairments (McGrath, Eyles et al 2003;Becker, Eyles et al 2005).…”

Section: Vitamin D and Neurocognitive Function: Deciphering The Evidencementioning

confidence: 99%

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Vitamin D and neurocognitive dysfunction: Preventing “D”ecline?

Buell

Dawson‐Hughes

2008

Molecular Aspects of Medicine

310

222

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Section: 25(oh) 2 D 3 and Neuronal Protectionmentioning

confidence: 53%

Section: 25(oh) 2 D 3 and Neuronal Protectionmentioning

confidence: 67%

Section: Vitamin D and Neuronal Calcium Regulationmentioning

confidence: 99%

Section: Vitamin D and Neurocognitive Function: Deciphering The Evidencementioning

confidence: 99%

See 2 more Smart Citations

Vitamin D and neurocognitive dysfunction: Preventing “D”ecline?

Buell

Dawson‐Hughes

2008

Molecular Aspects of Medicine

310

222

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“…Human vitamin D deficiency may result in an active mood disorder and worse cognitive functioning (38,39). In animals, it has been demonstrated that prenatal vitamin D deficiency resulted in alterations in brain morphology, learning and memory (40,41). In addition, mice lacking a functional VDR gene exhibited anxiety-like behavior, indicating that vitamin D may affect cognitive functioning and the prevalence of depressive symptoms (13 (42).…”

Section: Discussionmentioning

confidence: 99%

Changes in the expression of the vitamin D receptor and LVSCC-A1C in the rat hippocampus submitted to single prolonged stress

Tong

Peng

et al. 2014

Molecular Medicine Reports

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Abstract. Vitamin D signaling not only controls calcium (Ca 2+ ) and phosphorus uptake and transport, but also correlates with neurocognitive decline and neurodegenerative diseases. Almost all actions of Vitamin D are mediated by the transcription factor, vitamin D receptor (VDR), which has been widely identified in the central nervous system. Although previous studies have substantially advanced the understanding of the action of VDR in the brain, much remains unknown concerning how VDR relates to stress. Multiple lines of evidence indicate that the downregulation of L-type voltage-sensitive Ca 2+ -channels α-1C (LVSCC-A1C) by vitamin D in hippocampal neurons is able to reduce the influx and excitotoxic effects of Ca 2+ to neurons. Along these lines, the purpose of the present study was to analyze the relative expression of VDR in the hippocampus of rats exposed to single prolonged stress (SPS) as a putative animal model for human post-traumatic stress disorder (PTSD). Furthermore, changes in the levels of expression of LVSCC-A1C and Ca 2+ (neurotransmitter content) were examined during the onset periods of PTSD. The results revealed an increase in the expression of VDR at 1, 3 and 7 days post-stress compared with the control group. The intracellular free Ca 2+ levels in the hippocampus increased 1 day after SPS exposure, and then decreased gradually to the normal level at 14 days, consistent with the expression pattern of LVSCC-A1C. These results indicated that VDR may be involved in the pathogenesis of SPS rats, thereby providing an alternative preparation to search for optimal therapeutic strategies for PTSD. IntroductionPost-traumatic stress disorder (PTSD) is a severe anxiety disorder that may develop following exposure to any threat or injury that results in psychological trauma. Diagnostic symptoms for PTSD include re-experiencing the original trauma through flashbacks or nightmares, avoidance of stimuli associated with the trauma and increased arousal. Single-prolonged stress (SPS), an animal model of PTSD, has been extensively developed and employed in the investigation of PTSD (1-3). The three areas of the brain whose function may be altered in PTSD have been identified as the prefrontal cortex, the amygdala and the hippocampus, among which, the hippocampus is a key organ of the limbic system involved in learning and memory, as well as being a regulatory center for the stress response (4).Alterations in brain neurochemistry have been linked with neuropsychiatric disorders, including schizophrenia, Alzheimer's disease, depression and cognitive decline. Previous studies have identified a positive association between vitamin D signaling and cognitive function (5). Vitamin D may regulate neurotransmission, neuroprotection and neuroimmunomodulation as a neurosteroid hormone (5,6), in addition to its critical role in calcium (Ca 2+ ) and phosphorous regulation and skeletal mineralization (7). Hypovitaminosis D is associated with several neuropsychiatric disorders, including dementia, Parkinson's d...

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The Surprisingly Rich Contours of Schizophrenia Epidemiology

McGrath¹

2007

Arch Gen Psychiatry

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References 1. Ron M. A., Harvey I. The brain in schizophrenia. in incidence rates of schizophrenia and other psychotic syndromes: findings from the 3-center AeSOP study. Arch Gen Psychiatry 2006; 63: 250-8. 5. Semple D. M., McIntosh A. M., Lawrie S. M. Cannabis as a risk factor for psychosis: systematic review. J Psychopharmacol 2005; 19: 187-94. 6. Degenhardt L., Hall W. Is cannabis use a contributory cause of psychosis? Can J Psychiatry 2006; 51: 556-65. 7. Barendregt J. J., Ott A. Consistency of epidemiologic estimates. Eur J Epidemiol 2005; 20: 827-32. 8. Kruijshaar M. E., Barendregt J. J., Hoeymans N. The use of models in the estimation of disease epidemiology. Bull World Health Organ 2002; 80: 622-8. 9. Kruijshaar M. E., Barendregt J. J., Van De Poll-Franse L. V. Estimating the prevalence of breast cancer using a disease model: data problems and trends. Popul Health Metr 2003; 1: 5. 10. Hickman M., Vickerman P., Macleod J., Kirkbride J., Jones P. B. Cannabis and schizophrenia: model projections of the impact of the rise in cannabis use on historical and future trends in schizophrenia in England and Wales. Addiction 2007; 102: 597-606. 11. Henquet C., Murray R., Linszen D., Van Os J. The environment and schizophrenia: the role of cannabis use. Schizophr Bull 2005; 31: 608-12. 12. Linszen D. H., Dingemans P. M., Lenior M. E. Cannabis abuse and the course of recent-onset schizophrenic disorders. Arch Gen Psychiatry 1994; 51: 273-9. 13. Andrews G., Sanderson K., Corry J., Issakidis C., Lapsley H.Cost-effectiveness of current and optimal treatment for schizophrenia.

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Transient prenatal vitamin D deficiency is associated with subtle alterations in learning and memory functions in adult rats

Cited by 162 publications

References 41 publications

Vitamin D and neurocognitive dysfunction: Preventing “D”ecline?

Vitamin D and neurocognitive dysfunction: Preventing “D”ecline?

Changes in the expression of the vitamin D receptor and LVSCC-A1C in the rat hippocampus submitted to single prolonged stress

The Surprisingly Rich Contours of Schizophrenia Epidemiology

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