Kimberly L. Stark

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.

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.

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.

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.

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.