Abnormally reduced glutamate is associated with many symptoms in schizophrenia. Indeed, in both healthy humans and animal models, application of drugs that block the glutamate NMDA receptor, to simulate loss of glutamate, reproduced phenotypes such as psychosis and neurocognitive disturbances similar to those observed in schizophrenia. In schizophrenia patients, the gene expression for the GluNR2D receptor subunit has been found to be abnormally increased . In the GluNR2D knockout mouse, our international collaborator, Prof. Kazutaka Ikeda, observed that the psychosis-inducing effects of phencyclidine (PCP), a drug which blocks NMDA receptors, is reduced . These findings suggest that the GluNR2D-containing NMDA receptors are major players in mediating schizophrenia-related psychosis. However, to date the cognitive profile and response to NMDA antagonist (PCP or ketamine) challenge in GluNR2D knock-out mice has not been characterised. Using highly innovative cognitive testing units (touchscreens) newly established in our laboratory this project will thoroughly test the involvement of this receptor in mediating drug-induced cognitive disturbances, which are analogous to cognitive disturbances found in schizophrenia.
neuroscience, behavioural neuroscience, schizophrenia, psychiatry, mental health
School of Clinical Sciences at Monash Health / Hudson Institute of Medical Research
Masters by research
Top-up scholarship funding available
Monash Medical Centre Clayton