Pharmacological treatment to augment hole board habituation in prenatal Vitamin D-deficient rats.

Neurocognitive impairment has consistently been considered a central and stable feature of schizophrenia. There is much controversy about the effects of neuroleptics on neurocognitive deficits. Thus, further investigations are needed to clarify the pathological substrate of cognitive deficits in schizophrenia as well as to identify pharmacological tools for treatment. Transient prenatal Vitamin D deficiency is considered a developmental model in schizophrenia research. Recently, it was reported that prenatal Vitamin D-depleted rats showed a habituation deficit in the hole board. Here, we tested the effect on hole board habituation of haloperidol (Hal, 0.075 mg/kg, i.p.), risperidone (Ris, 0.2 mg/kg, i.p.) and the mGluR5 agonist CHPG (0.1 mg, i.c.v.) after subchronic treatment. Hal was found to impair habituation in control animals, Ris restored hole board habituation, whereas Hal and CHPG normalised hole board habituation in the deplete animals completely. The results of the study demonstrate that (i) the Vitamin D model might be a valuable tool in the study of neurodevelopmental aspects of schizophrenia, (ii) the model is sensitive in detecting the effect of antipsychotic drugs and (iii) the model appears to be sensitive in differentiating between typical and atypical antipsychotic drug.