Food and Behaviour Research

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

Becker A, Eyles DW, McGrath JJ, Grecksch G.  (2005) Behav Brain Res.  161(2): 306-12. 

Web URL: View this and related abstracts via PubMed here


Based on clues from epidemiology, low prenatal vitamin D has been proposed as a candidate risk factor for schizophrenia.

Recent animal experiments have demonstrated that transient prenatal vitamin D deficiency is associated with persistent alterations in brain morphology and neurotrophin expression. In order to explore the utility of the vitamin D animal model of schizophrenia, we examined different types of learning and memory in adult rats exposed to transient prenatal vitamin D deficiency.

Compared to control animals, the prenatally deplete animals had a significant impairment of latent inhibition, a feature often associated with schizophrenia. In addition, the deplete group was (a) significantly impaired on hole board habituation and (b) significantly better at maintaining previously learnt rules of brightness discrimination in a Y-chamber. In contrast, the prenatally deplete animals showed no impairment on the spatial learning task in the radial maze, nor on two-way active avoidance learning in the shuttle-box.

The results indicate that transient prenatal vitamin D depletion in the rat is associated with subtle and discrete alterations in learning and memory. The behavioural phenotype associated with this animal model may provide insights into the neurobiological correlates of the cognitive impairments of schizophrenia.


This study builds on previous work showing that transient Vitamin D deficiency during pregnancy can have long-term effects on brain development and behaviour in animals. See also:
As the authors note, these changes in nervous system reactivity resemble those associated with risks for neuropsychiatric disorders such as ADHD and schizophrenia.