Developmental vitamin D deficiency alters adult behaviour in 129/SvJ and C57BL/6J mice

  title={Developmental vitamin D deficiency alters adult behaviour in 129/SvJ and C57BL/6J mice},
  author={Lauren Harms and Darryl Walter Eyles and J J Mcgrath and Alan Mackay-Sim and Thomas H. J. Burne},
  journal={Behavioural Brain Research},

Attentional Processing in C57BL/6J Mice Exposed to Developmental Vitamin D Deficiency

Epidemiological evidence suggests that Developmental Vitamin D (DVD) deficiency is associated with an increased risk of schizophrenia. DVD deficiency in mice is associated with altered behaviour,

Developmental vitamin D deficiency alters MK-801-induced behaviours in adult offspring

It is suggested that a transient prenatal vitamin D deficiency has a long-lasting effect on NMDA-mediated signalling in the rodent brain and may be a plausible candidate risk factor for schizophrenia and other neuropsychiatric disorders.

Vitamin D Levels Are Not Associated with Hippocampal-Dependent Learning in Young Adult Male C57BL/6J Mice: A Negative Report

Vitamin D status did not affect spatial learning and memory, general behavioural domains, or catecholamine or protein expression in C57BL/6J mice, indicating that, in contrast to BALB/c mice, vitamin D status does not impact on hippocampal-dependent behaviour in young and healthy, adult male C57bl/ 6J mice.

The impact of vitamin D deficiency on behaviour and brain function in rodents

Vitamin D is crucial for maternal care and offspring social behaviour in rats.

As adults, males that had been exposed to vitamin D deficiency in early life exhibited decreased social behaviour, impaired learning and memory outcomes and increased grooming behaviour, but unaltered affective behaviours, highlighting that early life levels of vitamin D are an important consideration for maternal behavioural adaptations as well as offspring neuropsychiatry.



Developmental vitamin D deficiency alters brain protein expression in the adult rat: Implications for neuropsychiatric disorders

Nearly half of the molecules dysregulated in the animal model have also been shown to be misexpressed in either schizophrenia and/or multiple sclerosis and an impaired synaptic network may be a consequence of mitochondrial dysfunction.