Christoph Kellendonk, PhD

  • Professor of Molecular Pharmacology and Therapeutics (in Psychiatry)
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Overview

Dr. Kellendonk obtained his PhD in the laboratory of Günther Schütz at the German Cancer Research Center in Heidelberg where he studied the function of the glucocorticoid receptor. He then joined Eric Kandel's laboratory at Columbia University in New York as a post-doctoral research fellow where he became interested in using mouse genetics to study neuropsychiatric disorders. Since 2008 Dr. Kellendonk is an independent investigator in the Departments of Pharmacology and Psychiatry at Columbia University.

Academic Appointments

  • Professor of Molecular Pharmacology and Therapeutics (in Psychiatry)

Gender

  • Male

Research

The Kellendonk laboratory uses circuit dissection tools in the mouse to understand the biology that underlies cognitive, negative and positive symptoms of schizophrenia. To this end we have been manipulating the expression levels of dopamine D2 receptors and neuronal activity in genetically defined sub-circuits of the striatum and studied the consequences of these manipulations on behavior and circuit function. Using similar approaches, we have been studying the role of thalamo-prefrontal circuits in cognition and working memory. Recently, we began to address the role of dopamine in the generation of false percepts which has relevance to auditory hallucinations in humans.


Research Interests

  • Models of Psychiatric Disorders
  • Neurobiology of Cognitive and Motivated Behaviors
  • Neurobiology of Disease
  • Neurobiology of Learning and Memory
  • Neurobiology of Psychiatric Disorders
  • Neurogenetics
  • Thalamo-Cortical and Basal Ganglia Circuitry

Selected Publications

Labouesse M, Torres-Herraez A, Chohan M, Villarin J, Greenwald J, Sun X, Zahran M, Tang A, Lam S, Veenstra-VanderWeele J, Lacefield C, Bonaventura J, Michaelides M, Chan S, Yizhar O, Kellendonk C. (2023) A non-canonical striatopallidal "Go" pathway that supports motor control Nature Communications (in press)

Canetta S.E., Holt E.S., Benoit L.J., Teboul E., Ogden R.T., Harris A.Z., Kellendonk C. (2022) Mature parvalbumin interneuron function in prefrontal cortex requires activity during a postnatal sensitive period Elife. 2022 Dec 28;11:e80324

Benoit L., Holt. E., Pisano L., Fusi S., Harris A.Z, Canetta S., Kellendonk. C. (2022) Adolescent thalamic inhibition leads to long-lasting impairments in prefrontal cortex function Nature Neuroscience (25):714–725

Martyniuk K.M.,  Torres-Herraez A.,  Rubinstein M.,  Labouesse M.A., Kellendonk C. (2022) Dopamine D2Rs Coordinate Cue-Evoked Changes in Striatal Acetylcholine Levels eLife 2022 Jul 20;11:e76111

E.F. Gallo, J. Greenwald, E. Teboul, K. Martyniuk, N. Zarrelli, Y. Li, J.A. Javitch, P. Balsam, C. Kellendonk (2021) Dopamine D2 receptors modulate the cholinergic pause and inhibitory learning Molecular Psychiatry 27(3):1502-1514

Gallo E.F., Meszaros J., Sherman J.D., Chohan M.O., Teboul E., Choi C.S., Moore H., Javitch J.A., Kellendonk C. (2018) Accumbens Dopamine D2 Receptors increase motivation by decreasing inhibitory transmission to the ventral pallidum Nature Communications 14;9(1):1086.  

Bolkan S., Stujenske J.M., Parnaudeau S., Spellman T.J, Rauffenbart C., Abbas A., Harris A.Z., Gordon J.A., Kellendonk C. (2017) Thalamic projections sustain prefrontal activity during working memory maintenance Nature Neuroscience doi:10.1038/nn.4568 

S. Canetta, S. Bolkan, N. Padilla-Coreano, L.J. Song, R. Sahn, N.L. Harrison, J.A. Gordon, A. Brown, C. Kellendonk (2016) Maternal immune activation leads to selective functional deficits in offspring parvalbumin interneurons. Molecular Psychiatry 21(7):956-68  

Cazorla M, de Carvalho FD, Chohan MO, Shegda M, Chuhma N, Rayport S, Ahmari SE, Moore H, Kellendonk C. (2014) Dopamine D2 receptors regulate the anatomical and functional balance of basal ganglia circuitry. Neuron. 81:153-164. 

Parnaudeau S, O'Neill PK, Bolkan SS, Ward RD, Abbas AI, Roth BL, Balsam PD, Gordon JA, Kellendonk C. (2013) Inhibition of mediodorsal thalamus disrupts thalamofrontal connectivity and cognition. Neuron. 77:1151-1162.