Developmental vitamin D (DVD) deficiency in the rat alters adult behaviour independently of HPA function

Eyles, Darryl W.; Rogers, F.; Buller, Kathryn M.; McGrath, John J.; Ko, Pauline; French, K. R.; Burne, Thomas H. J.

doi:10.1016/j.psyneuen.2006.05.006

Cited by 60 publications

(48 citation statements)

References 29 publications

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“…42 However, the evidence derived from animal studies strongly suggests a crucial role of vitamin D in brain development and critical brain functions, 2,3 normal neurogenesis, 7 learning ability and behavior. [43][44][45] CONCLUSIONS In this prospective cohort higher circulating 25(OH)D 3 in pregnancy was associated with improved mental and psychomotor development in infants. Efforts to maintain an adequate vitamin D status in pregnancy could make a positive impact on infants' neuropsychological development if the associations are causal.…”

Section: Figurementioning

confidence: 66%

Circulating 25-Hydroxyvitamin D3 in Pregnancy and Infant Neuropsychological Development

et al. 2012

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Section: Figurementioning

confidence: 66%

Circulating 25-Hydroxyvitamin D3 in Pregnancy and Infant Neuropsychological Development

et al. 2012

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“…68 This is unlikely to be a stress-mediated mechanism because the animals have normal hypothalamic pituitary adrenal axis-mediated stress responses. 69 These animals are also selectively sensitive to the locomotor-enhancing effects of amphetamine, a drug that enhances DA release. 43 A relationship between vitamin D and DA in vivo is further supported via experiments where the active form of vitamin D, 1,25(OH) 2 D 3 is given to adult animals.…”

Section: Dvd-deficiency and Da Dysfunction In Adult Offspringmentioning

confidence: 99%

Schizophrenia: do all roads lead to dopamine or is this where they start? Evidence from two epidemiologically informed developmental rodent models

2012

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The idea that there is some sort of abnormality in dopamine (DA) signalling is one of the more enduring hypotheses in schizophrenia research. Opinion leaders have published recent perspectives on the aetiology of this disorder with provocative titles such as ‘Risk factors for schizophrenia—all roads lead to dopamine' or ‘The dopamine hypothesis of schizophrenia—the final common pathway'. Perhaps, the other most enduring idea about schizophrenia is that it is a neurodevelopmental disorder. Those of us that model schizophrenia developmental risk-factor epidemiology in animals in an attempt to understand how this may translate to abnormal brain function have consistently shown that as adults these animals display behavioural, cognitive and pharmacological abnormalities consistent with aberrant DA signalling. The burning question remains how can in utero exposure to specific (environmental) insults induce persistent abnormalities in DA signalling in the adult? In this review, we summarize convergent evidence from two well-described developmental animal models, namely maternal immune activation and developmental vitamin D deficiency that begin to address this question. The adult offspring resulting from these two models consistently reveal locomotor abnormalities in response to DA-releasing or -blocking drugs. Additionally, as adults these animals have DA-related attentional and/or sensorimotor gating deficits. These findings are consistent with many other developmental animal models. However, the authors of this perspective have recently refocused their attention on very early aspects of DA ontogeny and describe reductions in genes that induce or specify dopaminergic phenotype in the embryonic brain and early changes in DA turnover suggesting that the origins of these behavioural abnormalities in adults may be traced to early alterations in DA ontogeny. Whether the convergent findings from these two models can be extended to other developmental animal models for this disease is at present unknown as such early brain alterations are rarely examined. Although it is premature to conclude that such mechanisms could be operating in other developmental animal models for schizophrenia, our convergent data have led us to propose that rather than all roads leading to DA, perhaps, this may be where they start.

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“…Using the dietary restriction model, an Australian group (J. J. McGrath, D. W. Eyles, A. Mackay Sim, and collaborators) reported several other abnormalities, including hyperlocomotion in the holeboard or open-field tests (199,201), the absence of latent inhibition in a shuttle-box test (197), and less habituation as measured by head-dipping in the holeboard test (197,198). On the basis of these results, the Australian group recently suggested that the gestational vitamin D dietary restriction design may be a useful model for studying mechanisms of schizophrenia (198,201).…”

Section: Rodentsmentioning

confidence: 99%

Is there convincing biological or behavioral evidence linking vitamin D deficiency to brain dysfunction?

McCann¹,

Ames²

2007

FASEB j.

357

286

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Vitamin D insufficiency is common in the United States; the elderly and African-Americans are at particularly high risk of deficiency. This review, written for a broad scientific readership, presents a critical overview of scientific evidence relevant to a possible causal relationship between vitamin D deficiency and adverse cognitive or behavioral effects. Topics discussed are 1) biological functions of vitamin D relevant to cognition and behavior; 2) studies in humans and rodents that directly examine effects of vitamin D inadequacy on cognition or behavior; and 3) immunomodulatory activity of vitamin D relative to the proinflammatory cytokine theory of cognitive/behavioral dysfunction. We conclude there is ample biological evidence to suggest an important role for vitamin D in brain development and function. However, direct effects of vitamin D inadequacy on cognition/behavior in human or rodent systems appear to be subtle, and in our opinion, the current experimental evidence base does not yet fully satisfy causal criteria. Possible explanations for the apparent inconsistency between results of biological and cognitive/behavioral experiments, as well as suggested areas for further research are discussed. Despite residual uncertainty, recommendations for vitamin D supplementation of at-risk groups, including nursing infants, the elderly, and African-Americans appear warranted to ensure adequacy.

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Developmental vitamin D (DVD) deficiency in the rat alters adult behaviour independently of HPA function

Cited by 60 publications

References 29 publications

Circulating 25-Hydroxyvitamin D3 in Pregnancy and Infant Neuropsychological Development

Circulating 25-Hydroxyvitamin D3 in Pregnancy and Infant Neuropsychological Development

Schizophrenia: do all roads lead to dopamine or is this where they start? Evidence from two epidemiologically informed developmental rodent models

Is there convincing biological or behavioral evidence linking vitamin D deficiency to brain dysfunction?

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