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Christoph Kellendonk
Researcher at Columbia University
Publications - 97
Citations - 12760
Christoph Kellendonk is an academic researcher from Columbia University. The author has contributed to research in topics: Prefrontal cortex & Dopamine receptor D2. The author has an hindex of 49, co-authored 94 publications receiving 11320 citations. Previous affiliations of Christoph Kellendonk include German Cancer Research Center & Howard Hughes Medical Institute.
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Journal ArticleDOI
Disruption of the glucocorticoid receptor gene in the nervous system results in reduced anxiety
François Tronche,Christoph Kellendonk,Oliver Kretz,Peter Gass,Katrin Anlag,Paul C. Orban,Rudolf Bock,Rüdiger Klein,Günther Schütz +8 more
TL;DR: Conditional mutagenesis of Gr in the nervous system provides genetic evidence for the importance of Gr signalling in emotional behaviour because mutant animals show an impaired behavioural response to stress and display reduced anxiety.
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Resetting of circadian time in peripheral tissues by glucocorticoid signaling.
Aurélio Balsalobre,Steven A. Brown,Lysiane Marcacci,François Tronche,Christoph Kellendonk,Holger M. Reichardt,Günther Schütz,Ueli Schibler +7 more
TL;DR: It is shown that the glucocorticoid hormone analog dexamethasone induces circadian gene expression in cultured rat-1 fibroblasts and transiently changes the phase of circadian gene Expression in liver, kidney, and heart, however, dexamETHasone does not affect cyclic geneexpression in neurons of the suprachiasmatic nucleus.
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Disruption of CREB function in brain leads to neurodegeneration
Theo Mantamadiotis,Thomas Lemberger,Susanne C. Bleckmann,Heidrun Kern,Oliver Kretz,Ana Martin Villalba,François Tronche,Christoph Kellendonk,Daniel Gau,Josef P. Kapfhammer,Christiane Otto,Wolfgang Schmid,Günther Schütz +12 more
TL;DR: Mice with a Crem−/− background and lacking Creb in the central nervous system during development show extensive apoptosis of postmitotic neurons, and mice in which both Creb1 and Crem are disrupted in the postnatal forebrain show progressive neurodegeneration in the hippocampus and in the dorsolateral striatum.
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Transient and selective overexpression of dopamine D2 receptors in the striatum causes persistent abnormalities in prefrontal cortex functioning.
Christoph Kellendonk,Eleanor H. Simpson,H. Jonathan Polan,Gaël Malleret,Svetlana Vronskaya,Vanessa Winiger,Holly Moore,Eric R. Kandel +7 more
TL;DR: It is found that D2R overexpression in the striatum impacts dopamine levels, rates of dopamine turnover, and activation of D1 receptors in the prefrontal cortex, measures that are critical for working memory.
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A Possible Role for the Striatum in the Pathogenesis of the Cognitive Symptoms of Schizophrenia
TL;DR: It is suggested how mouse models might test ideas about the contribution of early striatal dysfunction to the cognitive symptoms of schizophrenia and how the striatum and its cortical connections are critical for complex cognition are reviewed.