Tamang, Man Kumar, Ali, Asad, Pertile, Renata Nedel, Cui, Xiaoying, Alexander, Suzy, Nitert, Marloes Dekker, Palmieri, Chiara and Eyles, Darryl (2023). Developmental vitamin D-deficiency produces autism-relevant behaviours and gut-health associated alterations in a rat model. Translational Psychiatry, 13 (1) 204. doi: 10.1038/s41398-023-02513-3

The University of Queensland

  • Professor John McGrath, QBI
  • Associate Professor Tom Burne, QBI
  • Associate Professor Bruno Van Swinderen, QBI
  • Dr Ethan Scott


  • Prof Andrew Whitehouse Telethon Kids Institute Perth, WA
  • Dr. Jake Gratten TRI, Brisbane


  • E Fernell Karolinska, Sweden
  • B. Lee Drexel University, USA
  • U. Meyer, ETH Zurich, Switzerland
  • O. Howes Kings college London
  • R. Schmidt, University of California Davis, USA
  • G Windham, Division of Environmental and Occupational Disease Control, USA
  • P Hurst Massey University Auckland NZ.
  • D Kirik Lund University Sweden

We have developed a new animal model of schizophrenia. We elevate dopamine selectively in the dorsal striatum by stereotaxically delivering genetic constructs to the substantia. We call this model Elevated Dopamine in Prodromal Schizophrenia (EDiPs). Our aim is to follow the course and examine the alterations in brain connectivity induced by EDiPS. Our ultimate aim is to intervene to block the disease process.


Project 1:  How does EDiPS affect cortical and subcortical connectivity and can we intervene to block EDiPS induced abnormalities in connectivity and behavioural phenotypes?

Project 2:  This project will firstly establish a new and more dopaminergically-selective EDiPS model using a TH-Cre rat and DREADD technology. Secondly, the student will establish whether early post-natal or late (Puberty) stages of brain development represent the critical window for EDiPS-induced phenotypes.

In a second series of studies we have selectively blocked both early features of autism and late characteristic behaviours associated with schizophrenia in the well-described Maternal Immune Activation animal model using the hormonal form of vitamin D.

Project 3:  We now want to understand what neuroprotective mechanisms we have triggered in this model and if we could also replicate these findings using the dietary form of vitamin D.

How to apply