K
Kimberly L. Stark
Researcher at Columbia University
Publications - 21
Citations - 3102
Kimberly L. Stark is an academic researcher from Columbia University. The author has contributed to research in topics: Receptor & Internal medicine. The author has an hindex of 15, co-authored 18 publications receiving 2858 citations.
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Journal ArticleDOI
Serotonin1A receptor acts during development to establish normal anxiety-like behaviour in the adult.
Cornelius Gross,Xiaoxi Zhuang,Xiaoxi Zhuang,Kimberly L. Stark,Sylvie Ramboz,Ronald Oosting,Lynn G. Kirby,Luca Santarelli,Sheryl G. Beck,René Hen +9 more
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.
Journal ArticleDOI
Impaired hippocampal–prefrontal synchrony in a genetic mouse model of schizophrenia
TL;DR: It is suggested that deficits in functional connectivity observed in patients with schizophrenia may be realized at the single-neuron level and impaired long-range synchrony of neural activity is one consequence of the 22q11.2 deletion.
Journal ArticleDOI
Altered brain microRNA biogenesis contributes to phenotypic deficits in a 22q11-deletion mouse model
Kimberly L. Stark,Bin Xu,Anindya Bagchi,Wen-Sung Lai,Hui Liu,Ruby Hsu,Xiang Wan,Paul Pavlidis,Alea A. Mills,Maria Karayiorgou,Joseph A. Gogos +10 more
TL;DR: Evidence is provided that the abnormal miRNA biogenesis emerges because of haploinsufficiency of the Dgcr8 gene, which encodes an RNA-binding moiety of the 'microprocessor' complex and contributes to the behavioral and neuronal deficits associated with the 22q11.2 microdeletion.
Journal ArticleDOI
Palmitoylation-dependent neurodevelopmental deficits in a mouse model of 22q11 microdeletion
Jun Mukai,Alefiya Dhilla,Liam Drew,Kimberly L. Stark,Luxiang Cao,Amy B. MacDermott,Maria Karayiorgou,Joseph A. Gogos +7 more
TL;DR: Evidence is provided that primary hippocampal neurons from a mouse model of 22q11.2 deletion have decreased density of dendritic spines and glutamatergic synapses, as well as impaired dendedritic growth, and evidence that PSD95 is one of the substrates of ZDHHC8.
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Derepression of a Neuronal Inhibitor due to miRNA Dysregulation in a Schizophrenia-Related Microdeletion
TL;DR: A drastic reduction of miR-185 is shown, which resides within the 22q11.2 locus, to levels more than expected by a hemizygous deletion, and it is demonstrated that this reduction alters dendritic and spine development.