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Sylvie Ramboz

Researcher at Columbia University

Publications -  28
Citations -  3638

Sylvie Ramboz is an academic researcher from Columbia University. The author has contributed to research in topics: Huntington's disease & Receptor. The author has an hindex of 16, co-authored 25 publications receiving 3440 citations. Previous affiliations of Sylvie Ramboz include French Institute of Health and Medical Research.

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Serotonin1A receptor acts during development to establish normal anxiety-like behaviour in the adult.

TL;DR: Findings show that postnatal developmental processes help to establish adult anxiety-like behaviour, and the normal role of the serotonin1A receptor during development may be different from its function when this receptor is activated by therapeutic intervention in adulthood.
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Enhanced aggressive behavior in mice lacking 5-HT1B receptor

TL;DR: In this article, mutant mice lacking the 5-HT1B receptor were generated by homologous recombination, and they did not exhibit any obvious developmental or behavioral defects, and when confronted with an intruder, mutant mice attacked the intruder faster and more intensely than did wild-type mice.
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Serotonin receptor 1A knockout: an animal model of anxiety-related disorder.

TL;DR: It is demonstrated that mice without 5-HT1A receptors display decreased exploratory activity and increased fear of aversive environments (open or elevated spaces) and suggested that reductions in 5- HT1A receptor density due to genetic defects or environmental stressors might result in heightened anxiety.
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Comprehensive behavioral and molecular characterization of a new knock-in mouse model of Huntington's disease: zQ175

TL;DR: A new mouse line, the zQ175 knock-in mouse, derived from a spontaneous expansion of the CAG copy number in the authors' CAG 140 knock- in colony is described, which carries a significantly higher CAG repeat length and is expected to be more significantly impaired than the parent line.
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5-HT1B receptor knock out--behavioral consequences.

TL;DR: In this paper, mutant mice lacking the 5-HT1B receptor were generated by homologous recombination, and they exhibited no obvious developmental or behavioral defect, and when confronted with an intruder, isolated mutant mice attacked the intruder faster and more intensely than wild-type mice.