Kally O’Reilly earned her PhD in Cellular and Molecular Biology at the University of Texas at Austin in Texas in 2008. Her thesis work focused on pharmacological induced changes in depression-related behaviors and neural network interactions in the adolescent mouse brain. She then started her postdoctoral work with Menno Witter at the Kavli Institute for Systems Neuroscience/Centre for the Biology of Memory at the Norwegian University of Science and Technology (NTNU) in Trondheim Norway. Her postdoctoral research examines the development of hippocampal/parahippocampal regions. She has focused on early postnatal development of connections using traditional retrograde and anterograde tracing techniques. The need to delineate hippocampal/parahippocampal regions for her studies has led to the synthesis of the neonatal atlas with chemoarchitectonic markers.
Contact Details
Kally C. O’Reilly, PhD
Postdoctor – Witter Group
Kavli Institute for Systems Neuroscience, Centre for the Biology of Memory
MTFS, Norwegian University of Science and Technology (NTNU)
NO-7489 Trondheim, Norway
Email: kally.oreilly at(@)ntnu.no
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A social encounter drives gene expression changes linked to neuronal function, brain development, and related disorders in mice expressing the serotonin transporter Ala56 variant.
A social encounter drives gene expression changes linked to neuronal function, brain development, and related disorders in mice expressing the serotonin transporter Ala56 variant. Neurosci Lett. 2020 May 08;:135027 Authors: O'Reilly KC, Anacker AMJ, Rogers TD, Forsberg CG, Wang J, Zhang B, Blakely RD, Veenstra-VanderWeele J Abstract Multiple lines of evidence implicate the serotonin (5-HT) system in social function, including biomarker findings in autism spectrum disorder. In mice, knock-in of a rare Gly56Ala substitution in the serotonin transporter (SERT) causes elevated whole blood 5-HT levels, increased 5-HT clearance in the brain, and altered social and repetitive behavior. To further examine the molecular impact of this variant on social response, SERT Ala56 mutant mice and wildtype littermate controls were exposed to a social or non-social stimulus. We examined the differential activation of the prefrontal cortex, lateral amygdala, and medial amygdala, to social stimuli through RNA sequencing. Differentially expressed genes were enriched in axonal guidance signaling pathways, networks related to nervous system development and function, neurological and psychiatric disorders, and behavior. These identified pathways and networks may shed light on the molecular cascades underlying the impact of altered SERT function on social behavior. PMID: 32437898 [PubMed - as supplied by publisher]
