Our laboratory uses mouse genetic tools in an effort to understand the biology that underlies the symptoms of schizophrenia. Schizophrenia is characterized by three symptom clusters: the cognitive, negative and positive symptoms. While the positive symptoms – which include disordered thought processes, hallucinations and delusions – are the most characteristic feature of the disorder, such symptoms are more difficult to model in the mouse. In contrast, cognitive and negative symptoms of the disorder – including deficits in working memory and motivation – have behavioral readouts homologous to humans in the mouse. These symptoms are poorly understood, difficult to treat and their severities are a better predictor for the long-term prognosis of patients than the degree of positive symptoms.
Our approach uses observations made in patients with schizophrenia (e.g. with brain imaging) and then seeks to “model” these observations as closely as possible in the mouse. This allows for establishing causality between a specific brain alteration and changes in behavior. We use transgenic and viral approaches to expresses dopamine D2 receptors or optogenetic and chemo-genetic tools in defined circuits of the brain. We then combine behavioral analyses with slice and in vivo physiological outcome measures to understand how circuit function regulates behavior.
The position will involve studying how the thalamus regulates prefrontal maturation during adolescence (https://assets.researchsquare.com/files/rs-730508/v1/72d959c6-9aad-45de-ac4c-a7cba8d8d912.pdf?c=1631887842) and will be NIH funded with a salary of $60,000 inculding health benefits.
Experience in slice or in vivo physiology would be preferred.
How to apply ?
Please contact Christoph Kellendonk, Ph.D.: email@example.com