Clinical studies in 2011 showed a completely novel genetic link between the VIPR2 gene and both schizophrenia and autism. In addition to providing a new clue to the pathophysiology of these mental health disorders, this finding is particularly exciting because the implicated gene encodes a cell surface neuropeptide receptor — a type of molecule that is generally targetable with drugs.
James Waschek and his colleagues at the University of California, Los Angeles plan to use several original strains of genetically engineered mice to investigate exactly how the VIPR2 mutation acts in the brain to increase the risk of developing autism and schizophrenia. Waschek and his team aim to determine whether the increased risk of developing these disorders is due to overactivity of VIPR2 at a critical stage of brain development and/or to altered action in the mature brain.
The researchers plan to perform a variety of autism-relevant tests on mice with altered VIPR2 activity: ultrasonic vocalization (pups calling) to their mothers after temporary isolation, socialization with other mice, startle response, cognition and memory tests relevant to autism, and studies of brain structure.
The results could provide new insights into the molecular and neurochemical mechanisms underlying the etiology of these disorders. They could also lead to a valuable new animal model and the discovery of novel therapeutic treatments.