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Pavel Osten

Associate Professor
M.D., Medical School of Charles University, Prague, 1991
Ph.D., SUNY Downstate Brooklyn, 1995

(516) 367-6990 (p)
To understand what’s going wrong in illnesses like autism and schizophrenia, we need to know more about how neural circuits are connected in the healthy brain. We’ve developed advanced imaging methods to draw the first whole-brain activation map in the mouse.  Now we’re applying that technology to study changes in brain activity in mice whose behavior models human autism and schizophrenia. 

Pavel Osten’s lab works on identification and analysis of brain regions, neural circuits, and connectivity pathways that are disrupted in genetic mouse models of autism and schizophrenia. Osten hypothesizes that (1) systematic comparison of multiple genetic mouse models will allow determination of overlaps in pathology—neural circuit endophenotypes—responsible for the manifestation of neuropsychiatric disorders and (2) neural circuit-based classification of autism and schizophrenia will provide key circuit targets for detailed mechanistic studies and therapeutic development. Osten and colleagues have developed the first systematic approach to the study of neural circuits in mouse models of psychiatric diseases, based on a pipeline of anatomical and functional methods for analysis of mouse brain circuits. An important part of this pipeline is high-throughput microscopy for whole-mouse brain imaging, called serial two-photon (STP) tomography. This year, they used this method to describe the first whole-brain activation map representing social behavior in normal mice. They are currently focusing on using this approach to study brain activation changes in two mouse models of autism: the 16p11.2 df/+ mouse model, which shows an increased propensity to seizures and hyperactivity, and the CNTNAP2 knockout mouse model, which shows abnormal social behavior.

Kim, Y. and Pradhan, K. and Fitzgerald, G. and Umadevi Venkataraju, K and Osten, P. (2013) Serial two-photon tomography-based whole-brain activity mapping in cntnap2 ko mouse model of autism. pp. 719.04.

Glajch, K. E. and Fleming, S. M. and Surmeier, D. J. and Osten, P. (2012) Sensorimotor assessment of the unilateral 6-hydroxydopamine mouse model of Parkinson's disease. Behavioural Brain Research 230(2) pp. 309-316.

Chan, C. S. and Glajch, K. E. and Gertler, T. S. and Guzman, J. N. and Mercer, J. N. and Lewis, A. S. and Goldberg, A. B. and Tkatch, T. and Shigemoto, R. and Fleming, S. M. and Chetkovich, D. M. and Osten, P. and Kita, H. and Surmeier, D. J. (2011) HCN channelopathy in external globus pallidus neurons in models of Parkinson's disease. Nature Neuroscience 14(1) pp. 85-U117.

Komai, S. and Licznerski, P. and Cetin, A. and Waters, J. and Denk, W. and Brecht, M. and Osten, P. (2006) Postsynaptic excitability is necessary for strengthening of cortical sensory responses during experience-dependent development. Nature Neuroscience 9(9) pp. 1125-33.

Cetin, A. and Komai, S. and Eliava, M. and Seeburg, P. H. and Osten, P. (2006) Stereotaxic gene delivery in the rodent brain. Nature Protocols 1(6)

Additional materials of the author at
CSHL Institutional Repository